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1. Differences in the neural correlates of schizophrenia with positive and negative formal thought disorder in patients with schizophrenia in the ENIGMA dataset

Author

Sharkey, Rachel J., Bacon, Chelsea, Peterson, Zeru, Rootes-Murdy, Kelly, Salvador, Raymond, Pomarol-Clotet, Edith, Karuk, Andriana, Homan, Philipp, Ji, Ellen, Omlor, Wolfgang, Homan, Stephanie, Georgiadis, Foivos, Kaiser, Stefan, Kirschner, Matthias, Ehrlich, Stefan, Dannlowski, Udo, Grotegerd, Dominik, Goltermann, Janik, Meinert, Susanne, Kircher, Tilo, Stein, Frederike, Brosch, Katharina, Krug, Axel, Nenadic, Igor, Sim, Kang, Spalletta, Gianfranco, Banaj, Nerisa, Sponheim, Scott R., Demro, Caroline, Ramsay, Ian S., King, Margaret, Quidé, Yann, Green, Melissa Jane, Nguyen, Dana, Preda, Adrian, Calhoun, Vince, Turner, Jessica, van Erp, Theo, and Nickl-Jockschat, Thomas

Published
2024
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2. Neurostructural subgroup in 4291 individuals with schizophrenia identified using the subtype and stage inference algorithm

Author

Jiang, Yuchao, Luo, Cheng, Wang, Jijun, Palaniyappan, Lena, Chang, Xiao, Xiang, Shitong, Zhang, Jie, Duan, Mingjun, Huang, Huan, Gaser, Christian, Nemoto, Kiyotaka, Miura, Kenichiro, Hashimoto, Ryota, Westlye, Lars T., Richard, Genevieve, Fernandez-Cabello, Sara, Parker, Nadine, Andreassen, Ole A., Kircher, Tilo, Nenadić, Igor, Stein, Frederike, Thomas-Odenthal, Florian, Teutenberg, Lea, Usemann, Paula, Dannlowski, Udo, Hahn, Tim, Grotegerd, Dominik, Meinert, Susanne, Lencer, Rebekka, Tang, Yingying, Zhang, Tianhong, Li, Chunbo, Yue, Weihua, Zhang, Yuyanan, Yu, Xin, Zhou, Enpeng, Lin, Ching-Po, Tsai, Shih-Jen, Rodrigue, Amanda L., Glahn, David, Pearlson, Godfrey, Blangero, John, Karuk, Andriana, Pomarol-Clotet, Edith, Salvador, Raymond, Fuentes-Claramonte, Paola, Garcia-León, María Ángeles, Spalletta, Gianfranco, Piras, Fabrizio, Vecchio, Daniela, Banaj, Nerisa, Cheng, Jingliang, Liu, Zhening, Yang, Jie, Gonul, Ali Saffet, Uslu, Ozgul, Burhanoglu, Birce Begum, Uyar Demir, Aslihan, Rootes-Murdy, Kelly, Calhoun, Vince D., Sim, Kang, Green, Melissa, Quidé, Yann, Chung, Young Chul, Kim, Woo-Sung, Sponheim, Scott R., Demro, Caroline, Ramsay, Ian S., Iasevoli, Felice, de Bartolomeis, Andrea, Barone, Annarita, Ciccarelli, Mariateresa, Brunetti, Arturo, Cocozza, Sirio, Pontillo, Giuseppe, Tranfa, Mario, Park, Min Tae M., Kirschner, Matthias, Georgiadis, Foivos, Kaiser, Stefan, Van Rheenen, Tamsyn E., Rossell, Susan L., Hughes, Matthew, Woods, William, Carruthers, Sean P., Sumner, Philip, Ringin, Elysha, Spaniel, Filip, Skoch, Antonin, Tomecek, David, Homan, Philipp, Homan, Stephanie, Omlor, Wolfgang, Cecere, Giacomo, Nguyen, Dana D., Preda, Adrian, Thomopoulos, Sophia I., Jahanshad, Neda, Cui, Long-Biao, Yao, Dezhong, Thompson, Paul M., Turner, Jessica A., van Erp, Theo G. M., Cheng, Wei, and Feng, Jianfeng

Published
2024
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3. Connectome architecture shapes large-scale cortical alterations in schizophrenia: a worldwide ENIGMA study

Author

Georgiadis, Foivos, Larivière, Sara, Glahn, David, Hong, L. Elliot, Kochunov, Peter, Mowry, Bryan, Loughland, Carmel, Pantelis, Christos, Henskens, Frans A., Green, Melissa J., Cairns, Murray J., Michie, Patricia T., Rasser, Paul E., Catts, Stanley, Tooney, Paul, Scott, Rodney J., Schall, Ulrich, Carr, Vaughan, Quidé, Yann, Krug, Axel, Stein, Frederike, Nenadić, Igor, Brosch, Katharina, Kircher, Tilo, Gur, Raquel, Gur, Ruben, Satterthwaite, Theodore D., Karuk, Andriana, Pomarol- Clotet, Edith, Radua, Joaquim, Fuentes-Claramonte, Paola, Salvador, Raymond, Spalletta, Gianfranco, Voineskos, Aristotle, Sim, Kang, Crespo-Facorro, Benedicto, Tordesillas Gutiérrez, Diana, Ehrlich, Stefan, Crossley, Nicolas, Grotegerd, Dominik, Repple, Jonathan, Lencer, Rebekka, Dannlowski, Udo, Calhoun, Vince, Rootes-Murdy, Kelly, Demro, Caroline, Ramsay, Ian S., Sponheim, Scott R., Schmidt, Andre, Borgwardt, Stefan, Tomyshev, Alexander, Lebedeva, Irina, Höschl, Cyril, Spaniel, Filip, Preda, Adrian, Nguyen, Dana, Uhlmann, Anne, Stein, Dan J., Howells, Fleur, Temmingh, Henk S., Diaz Zuluaga, Ana M., López Jaramillo, Carlos, Iasevoli, Felice, Ji, Ellen, Homan, Stephanie, Omlor, Wolfgang, Homan, Philipp, Kaiser, Stefan, Seifritz, Erich, Misic, Bratislav, Valk, Sofie L., Thompson, Paul, van Erp, Theo G. M., Turner, Jessica A., Bernhardt, Boris, and Kirschner, Matthias

Published
2024
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4. Robust, fully-automated assessment of cerebral perivascular spaces and white matter lesions: a multicentre MRI longitudinal study of their evolution and association with risk of dementia and accelerated brain atrophy

Author

Weiner, Michael, Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Saykin, Andrew J., Morris, John, Shaw, Leslie M., Liu, Enchi, Montine, Tom, Thomas, Ronald G., Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Jiminez, Gus, Harvey, Danielle, Bernstein, Matthew, Fox, Nick, Thompson, Paul, Schuff, Norbert, DeCarli, Charles, Borowski, Bret, Gunter, Jeff, Senjem, Matt, Vemuri, Prashanthi, Jones, David, Kantarci, Kejal, Ward, Chad, Koeppe, Robert A., Foster, Norm, Reiman, Eric M., Chen, Kewei, Mathis, Chet, Landau, Susan, Cairns, Nigel J., Householder, Erin, Reinwald, Lisa Taylor, Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M., Potkin, Steven, Shen, Li, Kelley, Faber, Kim, Sungeun, Nho, Kwangsik, Kachaturian, Zaven, Frank, Richard, Snyder, Peter J., Molchan, Susan, Kaye, Jeffrey, Quinn, Joseph, Lind, Betty, Carter, Raina, Dolen, Sara, Schneider, Lon S., Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Fleisher, Adam, Heidebrink, Judith L., Lord, Joanne L., Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Doody, Rachelle S., Meyer, Javier Villanueva, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Ances, Beau, Morris, John C., Carroll, Maria, Leon, Sue, Mintun, Mark A., Schneider, Stacy, Oliver, Angela, Marson, Daniel, Griffith, Randall, Clark, David, Geld-macher, David, Brockington, John, Roberson, Erik, Grossman, Hillel, Mitsis, Effie, Leyla deToledo-Morrell, Shah, Raj C., Duara, Ranjan, Varon, Daniel, Greig, Maria T., Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, D’Agostino, Daniel, Kielb, Stephanie, Galvin, James E., Pogorelec, Dana M., Cerbone, Brittany, Michel, Christina A., Rusinek, Henry, de Leon, Mony J., Glodzik, Lidia, De Santi, Susan, Doraiswamy, P. Murali, Petrella, Jeffrey R., Wong, Terence Z., Arnold, Steven E., Karlawish, Jason H., Wolk, David, Smith, Charles D., Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Lopez, Oscar L., Oakley, MaryAnn, Simpson, Donna M., Porsteinsson, Anton P., Goldstein, Bonnie S., Martin, Kim, Makino, Kelly M., Ismail, M. Saleem, Brand, Connie, Mulnard, Ruth A., Thai, Gaby, Adams Ortiz, Catherine Mc, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Arrastia, Ramon Diaz, King, Richard, Weiner, Myron, Cook, Kristen Martin, DeVous, Michael, Levey, Allan I., Lah, James J., Cellar, Janet S., Burns, Jeffrey M., Anderson, Heather S., Swerdlow, Russell H., Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H.S., Lu, Po H., Bartzokis, George, Graff Radford, Neill R., Parfitt, Francine, Kendall, Tracy, Johnson, Heather, Farlow, Martin R., Hake, AnnMarie, Matthews, Brandy R., Herring, Scott, Hunt, Cynthia, van Dyck, Christopher H., Carson, Richard E., MacAvoy, Martha G., Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Robin Hsiung, Ging-Yuek, Feldman, Howard, Mudge, Benita, Assaly, Michele, Kertesz, Andrew, Rogers, John, Trost, Dick, Bernick, Charles, Munic, Donna, Kerwin, Diana, Mesulam, Marek Marsel, Lipowski, Kristine, Wu, Chuang Kuo, Johnson, Nancy, Sadowsky, Carl, Martinez, Walter, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Frey, Meghan, Yesavage, Jerome, Taylor, Joy L., Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N., Belden, Christine M., Jacobson, Sandra A., Sirrel, Sherye A., Kowall, Neil, Killiany, Ronald, Budson, Andrew E., Norbash, Alexander, Johnson, Patricia Lynn, Obisesan, Thomas O., Wolday, Saba, Allard, Joanne, Lerner, Alan, Ogrocki, Paula, Hudson, Leon, Fletcher, Evan, Carmichael, Owen, Olichney, John, Kittur, Smita, Borrie, Michael, Lee, T.Y., Bartha, Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Potkin, Steven G., Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W., Kataki, Maria, Adeli, Anahita, Zimmerman, Earl A., Celmins, Dzintra, Brown, Alice D., Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Santulli, Robert B., Kitzmiller, Tamar J., Schwartz, Eben S., Sink, Kaycee M., Williamson, Jeff D., Garg, Pradeep, Watkins, Franklin, Ott, Brian R., Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J., Miller, Bruce L., Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Finger, Elizabeth, Pasternak, Stephen, Rachinsky, Irina, Drost, Dick, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Schultz, Susan K., Boles Ponto, Laura L., Shim, Hyungsub, Smith, Karen Elizabeth, Relkin, Norman, Chaing, Gloria, Raudin, Lisa, Smith, Amanda, Fargher, Kristin, Raj, Balebail Ashok, Barisano, Giuseppe, Iv, Michael, Choupan, Jeiran, and Hayden-Gephart, Melanie

Published
2025
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6. Insomnia Symptoms Are Associated with Measures of Functional Deterioration and Dementia Status in Adults with Down Syndrome at High Risk for Alzheimer's Disease.

Author

Desai, Shivum, Chen, Ivy Y., Hom, Christy, Doran, Eric, Nguyen, Dana D., Benca, Ruth M., Lott, Ira T., and Mander, Bryce A.

Subjects
DISEASE risk factors, ALZHEIMER'S disease, DEMENTIA, DOWN syndrome, INSOMNIA, VASCULAR dementia, INTELLECTUAL disabilities
Abstract

Background: While obstructive sleep apnea (OSA) and insomnia symptoms in neurotypical populations are associated with Alzheimer's disease (AD), their association with dementia in adults with Down syndrome (DS) remains less clear, even though these symptoms are prevalent and treatable in DS. Understanding their associations with AD-related dementia status, cognitive impairment, and functional deterioration may lead to interventions to slow decline or disease progression in adults with DS. Objective: To characterize differences in OSA and insomnia symptom expression by dementia status, and to determine which sleep factors support dementia diagnosis. Methods: Multimodal consensus conference was used to determine dementia status in 52 adults with DS (52.2 ± 6.4 years, 21 women). Cognitive impairment, adaptive behavior skills, and symptoms of OSA and insomnia were quantified using validated assessments for adults with DS and their primary informants. Results: A sex by dementia status interaction demonstrated that older women with DS and dementia had more severe terminal insomnia but not OSA symptoms relative to older women with DS who were cognitively stable (CS). Greater insomnia symptom severity was associated with greater functional impairments in social and self-care domains adjusting for age, sex, premorbid intellectual impairment, and dementia status. Conclusions: Insomnia symptoms are more severe in women with DS with dementia than in women with DS and no dementia, and regardless of dementia status or sex, more severe insomnia symptoms are associated with greater impairment in activities of daily living. These findings underscore the potential importance of early insomnia symptom evaluation and treatment in women with DS at risk of developing AD. [ABSTRACT FROM AUTHOR]

Published
2024
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9. Neurofilament light chain concentration mediates the association between regional medial temporal lobe structure and memory in adults with Down syndrome.

Author

DiProspero, Natalie, Sathishkumar, Mithra, Janecek, John, Smith, Anna, McMillan, Liv, Petersen, Melissa, Tustison, Nicholas, Keator, David B., Doran, Eric, Hom, Christy L., Nguyen, Dana, Andrews, Howard, Krinsky‐McHale, Sharon, Brickman, Adam M., Rosas, H. Diana, Lai, Florence, Head, Elizabeth, Mapstone, Mark, Silverman, Wayne, and Lott, Ira T.

Subjects
TEMPORAL lobe, EPISODIC memory, RECOLLECTION (Psychology), DOWN syndrome, GRAY matter (Nerve tissue), ENTORHINAL cortex
Abstract

INTRODUCTION: Virtually all people with Down syndrome (DS) develop neuropathology associated with Alzheimer's disease (AD). Atrophy of the hippocampus and entorhinal cortex (EC), as well as elevated plasma concentrations of neurofilament light chain (NfL) protein, are markers of neurodegeneration associated with late‐onset AD. We hypothesized that hippocampus and EC gray matter loss and increased plasma NfL concentrations are associated with memory in adults with DS. METHODS: T1‐weighted structural magnetic resonance imaging (MRI) data were collected from 101 participants with DS. Hippocampus and EC volume, as well as EC subregional cortical thickness, were derived. In a subset of participants, plasma NfL concentrations and modified Cued Recall Test scores were obtained. Partial correlation and mediation were used to test relationships between medial temporal lobe (MTL) atrophy, plasma NfL, and episodic memory. RESULTS: Hippocampus volume, left anterolateral EC (alEC) thickness, and plasma NfL were correlated with each other and were associated with memory. Plasma NfL mediated the relationship between left alEC thickness and memory as well as hippocampus volume and memory. DISCUSSION: The relationship between MTL gray matter and memory is mediated by plasma NfL levels, suggesting a link between neurodegenerative processes underlying axonal injury and frank gray matter loss in key structures supporting episodic memory in people with DS. [ABSTRACT FROM AUTHOR]

Published
2024
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11. A multi-scanner study of subcortical brain volume abnormalities in schizophrenia

Author

van Erp, Theo G.M., Greve, Douglas N., Rasmussen, Jerod, Turner, Jessica, Calhoun, Vince D., Young, Sarah, Mueller, Bryon, Brown, Gregory G., McCarthy, Gregory, Glover, Gary H., Lim, Kelvin O., Bustillo, Juan R., Belger, Aysenil, McEwen, Sarah, Voyvodic, James, Mathalon, Daniel H., Keator, David, Preda, Adrian, Nguyen, Dana, Ford, Judith M., Potkin, Steven G., and FBIRN

Published
2014
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12. Schizophrenia miR-137 Locus Risk Genotype Is Associated with Dorsolateral Prefrontal Cortex Hyperactivation

Author

van Erp, Theo G.M., Guella, Ilaria, Vawter, Marquis P., Turner, Jessica, Brown, Gregory G., McCarthy, Gregory, Greve, Douglas N., Glover, Gary H., Calhoun, Vince D., Lim, Kelvin O., Bustillo, Juan R., Belger, Aysenil, Ford, Judith M., Mathalon, Daniel H., Diaz, Michele, Preda, Adrian, Nguyen, Dana, Macciardi, Fabio, and Potkin, Steven G.

Published
2014
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14. Obesity Risk Among West Point Graduates Later in Life.

Author

Szivak, Tunde K., Thomas, Melissa M., Pietrzak, Robert H., Nguyen, Dana R., Ryan, Diane M., and Mazure, Carolyn M.

Subjects
OBESITY risk factors, ENERGY metabolism, BODY composition, PHYSICAL fitness, HEALTH status indicators, DIET, RISK assessment, SEX distribution, SURVEYS, PHYSICAL activity, QUESTIONNAIRES, DESCRIPTIVE statistics, BODY mass index, MILITARY personnel, PSYCHOLOGICAL resilience
Abstract

The purpose of this investigation was to evaluate sex differences in health and fitness outcomes among United States Military Academy (USMA) graduates (class years 1980-2011). Subjects (n = 701 men, 641 women, age: 45.7 ± 9.3 years) were surveyed as a part of a larger investigation on risk and resiliency factors among USMA graduates. Physical activity was assessed using the International Physical Activity Questionnaire (IPAQ) short form and calculation of weekly metabolic equivalents (METs). Overweight and obesity status were assessed by body mass index (BMI). Significance for the study was set at p ≤ 0.05. Obesity rates for men (30.1%) were significantly higher than for women (16.6%). Men reported significantly higher (p = 0.01) vigorous METs·wk-1 (1,214.6 ± 1,171.6) than women (1,046.8 ± 1,133.2) despite significantly higher (p = 0.00) BMI values (28.75 ± 4.53 kg·m-2) than women (25.90 ± 5.48 kg·m-2). Women were 89% more likely to have ever been on a diet and reported higher (15.2%) Army Body Composition Program enrollment rates than men (6.3%). Obesity rates among men reflect trends seen in the broader military, Veteran, and U.S. adult populations, whereas obesity rates among women were lower. Men may be at a greater risk for obesity later in life despite higher self-reported physical activity; however, lean body mass and self-report bias should be considered. Because lifetime obesity may be influenced by factors other than physical activity, health initiatives should use a comprehensive approach early in the career of military officers. [ABSTRACT FROM AUTHOR]

Published
2023
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19. Joint‐label fusion brain atlases for dementia research in Down syndrome.

Author

Queder, Nazek, Phelan, Michael J., Taylor, Lisa, Tustison, Nicholas, Doran, Eric, Hom, Christy, Nguyen, Dana, Lai, Florence, Pulsifer, Margaret, Price, Julie, Kreisl, William C., Rosas, Herminia D., Krinsky‐McHale, Sharon, Brickman, Adam M., Yassa, Michael A., Schupf, Nicole, Silverman, Wayne, Lott, Ira T., Head, Elizabeth, and Mapstone, Mark

Subjects
DOWN syndrome, POSITRON emission tomography, ALZHEIMER'S disease, MAGNETIC resonance imaging, DEMENTIA, CEREBRAL amyloid angiopathy
Abstract

Research suggests a link between Alzheimer's Disease in Down Syndrome (DS) and the overproduction of amyloid plaques. Using Positron Emission Tomography (PET) we can assess the in‐vivo regional amyloid load using several available ligands. To measure amyloid distributions in specific brain regions, a brain atlas is used. A popular method of creating a brain atlas is to segment a participant's structural Magnetic Resonance Imaging (MRI) scan. Acquiring an MRI is often challenging in intellectually‐imparied populations because of contraindications or data exclusion due to significant motion artifacts or incomplete sequences related to general discomfort. When an MRI cannot be acquired, it is typically replaced with a standardized brain atlas derived from neurotypical populations (i.e. healthy individuals without DS) which may be inappropriate for use in DS. In this project, we create a series of disease and diagnosis‐specific (cognitively stable (CS‐DS), mild cognitive impairment (MCI‐DS), and dementia (DEM‐DS)) probabilistic group atlases of participants with DS and evaluate their accuracy of quantifying regional amyloid load compared to the individually‐based MRI segmentations. Further, we compare the diagnostic‐specific atlases with a probabilistic atlas constructed from similar‐aged cognitively‐stable neurotypical participants. We hypothesized that regional PET signals will best match the individually‐based MRI segmentations by using DS group atlases that aligns with a participant's disorder and disease status (e.g. DS and MCI‐DS). Our results vary by brain region but generally show that using a disorder‐specific atlas in DS better matches the individually‐based MRI segmentations than using an atlas constructed from cognitively‐stable neurotypical participants. We found no additional benefit of using diagnose‐specific atlases matching disease status. All atlases are made publicly available for the research community. Highlight: Down syndrome (DS) joint‐label‐fusion atlases provide accurate positron emission tomography (PET) amyloid measurements.A disorder‐specific DS atlas is better than a neurotypical atlas for PET quantification.It is not necessary to use a disease‐state–specific atlas for quantification in aged DS.Dorsal striatum results vary, possibly due to this region and dementia progression. [ABSTRACT FROM AUTHOR]

Published
2022
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20. Psychological Resilience in West Point Graduates: Results From a Nationally Representative Study.

Author

Thomas, Melissa M., Pietrzak, Robert H., Nguyen, Dana R., Ryan, Diane, Southwick, Steven M., and Mazure, Carolyn M.

Subjects
PSYCHOSOCIAL factors, PSYCHOLOGICAL resilience, MENTAL depression, POST-traumatic stress disorder, MEDICAL personnel, PSYCHOLOGICAL distress, PSYCHOLOGICAL factors
Abstract

Background: The purpose of this study was to examine factors associated with psychological resilience in a nationally representative sample of West Point graduates. Aims: The aims of this study were to (a) employ a dimensional approach to operationalizing psychological resilience in a trauma-exposed population that had been highly trained and educated in persisting in the face of stress, was previously unstudied, and in which we could examine correlates of resilience, (b) identify key psychosocial factors, character traits, health variables, military experiences, and coping strategies as potential correlates of psychological resilience; and (c) examine whether reported gender moderated any of these associations in this population. Methods: A nationally representative sample of 1342 West Point graduates after gender integration from classes 1980 to 2011 were surveyed. Psychological resilience was operationalized using a discrepancy-based approach in which a measure of composite psychological distress (current posttraumatic stress disorder, generalized anxiety and depression symptoms) was regressed on measures of cumulative trauma burden. A multivariable linear regression model was then employed to identify factors that were independently associated with psychological resilience scores. Results: Purpose in life (29.8% of relative variance explained [RVE]), fewer perceived negative experiences in the military (20.6% RVE), social support (9.6% RVE), and grit (9.5% RVE) were the strongest correlates of psychological resilience scores for both women and men. Time in service was positively associated with resilience in women only. Conclusion: This study identifies key correlates of psychological resilience in West Point graduates, individuals who are highly trained to persevere in the face of stress and then were trauma-exposed. Most of these factors are modifiable and can be targeted in stress prevention and treatment interventions, especially for high-stress professions such as the military, frontline health care providers, and first responders. [ABSTRACT FROM AUTHOR]

Published
2021
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22. Association Between Neuroimaging Biomarkers, Plasma NfL, and Memory Performance in Adults With Down Syndrome With and Without Dementia.

Author

Queder, Nazek, Adams, Jenna N., Keator, David B., McMillan, Liv, Sathishkumar, Mithra, Taylor, Lisa M., Doran, Eric, Nguyen, Dana, Hom, Christy, Krinsky‐McHale, Sharon J, Price, Julie C, Lai, Florence, Rosas, H. Diana, Petersen, Melissa, O'Bryant, Sid E., Brickman, Adam M., Head, Elizabeth, Mapstone, Mark, Schupf, Nicole, and Silverman, Wayne

Abstract

Background: Down syndrome (DS) is associated with early development of Alzheimer's disease pathology. Both the severity of tau pathology and the increase of neurofilament light chain (NfL) protein are correlated with cognitive decline in the neurotypical populations. Here, we assessed whether tau accumulation in the hippocampus and entorhinal cortex and plasma NfL concentrations were associated with memory performance in adults with DS. Method: We used 18F‐AV‐1451 (FTP) positron emission tomography (PET) to assess tau accumulation in 44 participants enrolled in the multi‐site Alzheimer's Disease in Down syndrome (ADDS) study (age 50.72 + 6.21). FTP‐PET scans were partial volume‐corrected, and weighted standardized uptake value ratio (SUVR) were calculated for each of the following regions of interests (ROIs): entorhinal cortex, hippocampus, and the precentral gyrus (control). Participants' plasma NfL concentration (in pg/mL) was measured on a single plex plate using the ultra‐sensitive single molecule array (Simoa) technology platform HD‐X. Memory performance was measured with the modified Cued Recall Test. We evaluated the relationship between FTP SUVRs, NfL, and memory performance using linear regression analysis. Sex and site were used as covariates. Result: Increased FTP SUVR in the hippocampus and entorhinal cortex were associated with lower scores on free recall (hippocampus: r2 = 0.53, p <0.001; entorhinal: r2 = 0.35, p <0.001) and total recall (hippocampus: r2 = 0.46, p <0.001; entorhinal: r2 = 0.29, p <0.01). As expected, no association between FTP SUVRs and memory performance was found in the precentral gyrus. Additionally, higher plasma NfL concentrations were associated with lower free recall (r2 = 0.35, p <0.001) and total recall (r2 = 0.29, p <0.01). Further, increased levels of plasma NfL were associated with increased FTP SUVRs in the hippocampus (r2 = 0.38, p <0.001), entorhinal cortex (r2 = 0.28, p<0.01), and precentral gyrus (r2 = 0.19, p<0.05). Conclusion: Increased levels of both in‐vivo tau in medial temporal ROIs and NfL in plasma were associated with worse memory performance, consistent with observations in the neurotypical population. Future work will investigate the impact of tau accumulation and NfL concentration on longitudinal cognitive decline in older adults with DS. [ABSTRACT FROM AUTHOR]

Published
2023
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23. Brief screening for co-occurring disorders among women entering substance abuse treatment

Author

Chernoff Miriam, Liebschutz Jane M, Lincoln Alisa K, Nguyen Dana, and Amaro Hortensia

Subjects
Public aspects of medicine, RA1-1270, Social pathology. Social and public welfare. Criminology, HV1-9960
Abstract

Abstract Background Despite the importance of identifying co-occurring psychiatric disorders in substance abuse treatment programs, there are few appropriate and validated instruments available to substance abuse treatment staff to conduct brief screen for these conditions. This paper describes the development, implementation and validation of a brief screening instrument for mental health diagnoses and trauma among a diverse sample of Black, Hispanic and White women in substance abuse treatment. With input from clinicians and consumers, we adapted longer existing validated instruments into a 14 question screen covering demographics, mental health symptoms and physical and sexual violence exposure. All women entering treatment (methadone, residential and out-patient) at five treatment sites were screened at intake (N = 374). Results Eighty nine percent reported a history of interpersonal violence, and 70% reported a history of sexual assault. Eighty-eight percent reported mental health symptoms in the last 30 days. The screening questions administered to 88 female clients were validated against in-depth psychiatric diagnostic assessments by trained mental health clinicians. We estimated measures of predictive validity, including sensitivity, specificity and predictive values positive and negative. Screening items were examined multiple ways to assess utility. The screen is a useful and valid proxy for PTSD but not for other mental illness. Conclusion Substance abuse treatment programs should incorporate violence exposure questions into clinical use as a matter of policy. More work is needed to develop brief screening tools measures for front-line treatment staff to accurately assess other mental health needs of women entering substance abuse treatment

Published
2006
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24. Career Satisfaction of Military Medical Officers.

Author

Song, Kaoru H, Nguyen, Dana R, Dietrich, Erich J, Powers, John E, and Barrett, John P

Subjects
*JOB satisfaction, *MILITARY officers, *WORKING hours, *MILITARY service, *FAMILY services, *CROSS-sectional method, *MENTORING, *JOB Descriptive Index, *MILITARY personnel
Abstract

Introduction: Having a mentor is associated with higher job satisfaction among U.S. physicians. The objective of this study was to assess satisfaction among military medical officers and to assess if mentorship and job satisfaction are associated with intention to continue military service.Materials and Methods: This is a cross-sectional study using voluntary, anonymous data from 2018 Uniformed Services Academy of Family Physicians Annual Meeting registered attendees who completed an online Omnibus Survey. Outcome measures: satisfaction with work hours and workload; voice in organizational decision-making; amount of teaching, research, and other administrative tasks; being and having a mentor; and likelihood of remaining in the military beyond current service obligation. Statistical analysis: descriptive statistics, chi-square, and logistic regression.Results: There was a 66% response rate (310/568) among registered attendees. Respondents reported being satisfied with work hours-workload (53.3%), voice in organizational decision-making (47.4%), and amount of teaching-research-other administrative tasks (55.7%). About 64.6% of respondents reported being a mentor, and 80.7% reported having a mentor. About 53.4% reported being likely/very likely to continue military service beyond their current service obligation. Adjustment for demographic and occupational factors, with significance defined as P ≤ 0.05, revealed that higher percent time in clinical care was negatively associated with satisfaction with voice in organizational decision-making; being a mentor and working in an academic practice setting were positively associated with satisfaction in amount of time with teaching, research, and administrative tasks; and having a mentor was the only factor associated with being likely/very likely to continue military service beyond current service obligation (odd ratio 3.9, 95% confidence interval 1.2-12.1).Conclusions: Having a mentor was the only factor associated with intention to remain in the military among 2018 Uniformed Services Academy of Family Physicians Omnibus Survey respondents. These results support enhancing mentorship among military medical officers. [ABSTRACT FROM AUTHOR]

Published
2020
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25. fmCASES National Examination as a Pretest in a Family Medicine Clerkship.

Author

Nguyen, Dana R., Servey, Jessica T., Scott, LaTraia S., and Nguyen, Dana

Abstract

Background and Objectives: Pretests have been shown to contribute to improved performance on standardized tests by serving to facilitate development of individualized study plans. fmCASES is an existing validated examination used widely in family medicine clerkships throughout the country. Our study aimed to determine if implementation of the fmCASES National Examination as a pretest decreased overall failure rates on the end-of-clerkship National Board of Medical Examiners (NBME) subject examination, and to assess if fmCASES pretest scores correlate with student NBME scores.Methods: One hundred seventy-one and 160 clerkship medical students in different class years at a single institution served as the control and intervention groups, respectively. The intervention group took the fmCASES National Examination as a pretest at the beginning of the clerkship and received educational prescriptions based on the results. Chi-square analysis, Pearson correlation, and receiver operating curve analysis were used to evaluate the effectiveness and correlations for the intervention.Results: Students completing an fmCASES National Examination as a pretest failed the end-of-clerkship NBME exam at significantly lower rates than those students not taking the pretest. The overall failure rate for the intervention group was 8.1% compared to 17.5% for the control group (P=0.01). Higher pretest scores correlated with higher NBME examination scores (r=0.55, P<0.001).Conclusions: fmCASES National Examination is helpful as a formative assessment tool for students beginning their family medicine clerkship. This tool introduces students to course learning objectives, assists them in identifying content areas most in need of study, and can be used to help students design individualized study plans. [ABSTRACT FROM AUTHOR]

Published
2018
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26. Body mass index is associated with biological CSF markers of core brain pathology of Alzheimer's disease

Author

Ewers, Michael, Schmitz, Susanne, Vellas, Bruno, Morris, John C, Ances, Beau, Carroll, Maria, Leon, Sue, Mintun, Mark A, Schneider, Stacy, Marson, Daniel, Griffith, Randall, Clark, David, Grossman, Hillel, Dubois, Bruno, Mitsis, Effie, Romirowsky, Aliza, deToledo-Morrell, Leyla, Shah, Raj C, Duara, Ranjan, Varon, Daniel, Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, Kielb, Stephanie, Blennow, Kaj, Rusinek, Henry, de Leon, Mony J, Glodzik, Lidia, Doraiswamy, P Murali, Petrella, Jeffrey R, Coleman, R Edward, Arnold, Steven E, Karlawish, Jason H, Wolk, David, Smith, Charles D, Buerger, Katharina, Jicha, Greg, Hardy, Peter, Lopez, Oscar L, Oakley, MaryAnn, Simpson, Donna M, Porsteinsson, Anton P, Goldstein, Bonnie S, Martin, Kim, Makino, Kelly M, Ismail, M Saleem, Teipel, Stefan J, Brand, Connie, Mulnard, Ruth A, Thai, Gaby, Mc-Adams-Ortiz, Catherine, Diaz-Arrastia, Ramon, Martin-Cook, Kristen, DeVous, Michael, Levey, Allan I, Lah, James J, Cellar, Janet S, Weiner, Michael, Burns, Jeffrey M, Anderson, Heather S, Swerdlow, Russell H, Apostolova, Liana, Lu, Po H, Bartzokis, George, Silverman, Daniel H S, Graff-Radford, Neill R, Parfitt, Francine, Johnson, Heather, Hampel, Harald, Farlow, Martin, Herring, Scott, Hake, Ann M, van Dyck, Christopher H, Carson, Richard E, MacAvoy, Martha G, Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Initiative, Alzheimer's Disease Neuroimaging, Stefanovic, Bojana, Caldwell, Curtis, Hsiung, Ging-Yuek Robin, Feldman, Howard, Assaly, Michele, Kertesz, Andrew, Rogers, John, Trost, Dick, Bernick, Charles, Munic, Donna, Kerwin, Diana, Mesulam, Marek-Marsel, Lipowski, Kristina, Wu, Chuang-Kuo, Johnson, Nancy, Sadowsky, Carl, Martinez, Walter, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Aisen, Paul, Reynolds, Brigid, Sperling, Reisa A, Johnson, Keith A, Marshall, Gad, Frey, Meghan, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan, Belden, Christine, Jacobson, Sandra, Hansson, Oskar, Kowall, Neil, Killiany, Ronald, Budson, Andrew E, Norbash, Alexander, Johnson, Patricia Lynn, Obisesan, Thomas O, Wolday, Saba, Bwayo, Salome K, Lerner, Alan, Hudson, Leon, Ogrocki, Paula, Fletcher, Evan, Carmichael, Owen, Olichney, John, DeCarli, Charles, Kittur, Smita, Borrie, Michael, Lee, T-Y, Bartha, Rob, Johnson, Sterling, Petersen, Ronald, Asthana, Sanjay, Carlsson, Cynthia M, Potkin, Steven G, Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Fleisher, Adam, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Jack, Clifford R, Rainka, Michelle, Hendin, Barry A, Scharre, Douglas W, Kataki, Maria, Zimmerman, Earl A, Celmins, Dzintra, Brown, Alice D, Pearlson, Godfrey D, Blank, Karen, Anderson, Karen, Jagust, William, Saykin, Andrew J, Santulli, Robert B, Schwartz, Eben S, Sink, Kaycee M, Williamson, Jeff D, Garg, Pradeep, Watkins, Franklin, Ott, Brian R, Querfurth, Henry, Tremont, Geoffrey, Trojanowki, John Q, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J, Miller, Bruce L, Mintzer, Jacobo, Longmire, Crystal Flynn, Spicer, Kenneth, Toga, Arthur W, Beckett, Laurel, Green, Robert C, Walsh, Cathal, Morris, John, Liu, Enchi, Montine, Tom, Gamst, Anthony, Thomas, Ronald G, Donohue, Michael, Walter, Sarah, Fitzpatrick, Annette, Gessert, Devon, Sather, Tamie, Harvey, Danielle, Kornak, John, Dale, Anders, Bernstein, Matthew, Bennett, David, Felmlee, Joel, Fox, Nick, Thompson, Paul, Schuff, Norbert, Alexander, Gene, Bandy, Dan, Koeppe, Robert A, Foster, Norm, Minthon, Lennart, Reiman, Eric M, Chen, Kewei, Mathis, Chet, Cairns, Nigel J, Taylor-Reinwald, Lisa, Trojanowki, J. Q., Shaw, Les, Lee, Virginia M Y, Korecka, Magdalena, Trojanowski, John Q, Crawford, Karen, Neu, Scott, Foroud, Tatiana M, Potkin, Steven, Shen, Li, Kachaturian, Zaven, Frank, Richard, Snyder, Peter J, Shaw, Leslie M, Molchan, Susan, Kaye, Jeffrey, Quinn, Joseph, Lind, Betty, Dolen, Sara, Schneider, Lon S, Pawluczyk, Sonia, Spann, Bryan M, Brewer, James, Vanderswag, Helen, Faluyi, Yetunde O, Heidebrink, Judith L, Lord, Joanne L, Johnson, Kris, Doody, Rachelle S, Villanueva-Meyer, Javier, Chowdhury, Munir, Stern, Yaakov, Honig, Lawrence S, and Bell, Karen L

Subjects
Male, Apolipoprotein E, Aging, Pathology, Neurology, epidemiology [Alzheimer Disease], Statistics as Topic, cerebrospinal fluid [Amyloid beta-Peptides], Comorbidity, Body Mass Index, Cerebrospinal fluid, pathology [Brain], Prevalence, Aged, 80 and over, biology, General Neuroscience, Brain, Middle Aged, Prognosis, amyloid beta-protein (1-42), cerebrospinal fluid [Cognition Disorders], cerebrospinal fluid [Alzheimer Disease], cerebrospinal fluid [Biomarkers], Biomarker (medicine), Female, epidemiology [United States], Alzheimer's disease, Psychology, Alzheimer's Disease Neuroimaging Initiative, epidemiology [Cognition Disorders], medicine.medical_specialty, Tau protein, tau Proteins, Alzheimer Disease, medicine, Humans, ddc:610, cerebrospinal fluid [Peptide Fragments], Aged, Amyloid beta-Peptides, medicine.disease, United States, Peptide Fragments, cerebrospinal fluid [tau Proteins], metabolism [Brain], biology.protein, pathology [Cognition Disorders], Neurology (clinical), Geriatrics and Gerontology, Cognition Disorders, Body mass index, Biomarkers, Developmental Biology
Abstract

Weight changes are common in aging and Alzheimer's disease (AD) and postmortem findings suggest a relation between lower body mass index (BMI) and increased AD brain pathology. In the current multicenter study, we tested whether lower BMI is associated with higher core AD brain pathology as assessed by cerebrospinal fluid (CSF)-based biological markers of AD in 751 living subjects: 308 patients with AD, 296 subjects with amnestic mild cognitive impairment (MCI), and 147 elderly healthy controls (HC). Based upon a priori cutoff values on CSF concentration of total tau and beta-amyloid (Aβ(1-42)), subjects were binarized into a group with abnormal CSF biomarker signature (CSF+) and those without (CSF-). Results showed that BMI was significantly lower in the CSF+ when compared with the CSF- group (F = 27.7, df = 746, p0.001). There was no interaction between CSF signature and diagnosis or apolipoprotein E (ApoE) genotype. In conclusion, lower BMI is indicative of AD pathology as assessed with CSF-based biomarkers in demented and nondemented elderly subjects.

Published
2012
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27. Testing Quick Response (QR) Codes as an Innovation to Improve Feedback Among Geographically-Separated Clerkship Sites.

Author

Snyder, Matthew J., Nguyen, Dana R., Womack, Jasmyne J., Bunt, Christopher W., Westerfield, Katie L., Bell, Adriane E., and Ledford, Christy J. W.

Abstract

Background and Objectives: Collection of feedback regarding medical student clinical experiences for formative or summative purposes remains a challenge across clinical settings. The purpose of this study was to determine whether the use of a quick response (QR) code-linked online feedback form improves the frequency and efficiency of rater feedback.Methods: In 2016, we compared paper-based feedback forms, an online feedback form, and a QR code-linked online feedback form at 15 family medicine clerkship sites across the United States. Outcome measures included usability, number of feedback submissions per student, number of unique raters providing feedback, and timeliness of feedback provided to the clerkship director.Results: The feedback method was significantly associated with usability, with QR code scoring the highest, and paper second. Accessing feedback via QR code was associated with the shortest time to prepare feedback. Across four rotations, separate repeated measures analyses of variance showed no effect of feedback system on the number of submissions per student or the number of unique raters.Conclusions: The results of this study demonstrate that preceptors in the family medicine clerkship rate QR code-linked feedback as a high usability platform. Additionally, this platform resulted in faster form completion than paper or online forms. An overarching finding of this study is that feedback forms must be portable and easily accessible. Potential implementation barriers and the social norm for providing feedback in this manner need to be considered. [ABSTRACT FROM AUTHOR]

Published
2018
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29. Improving Coding Accuracy in an Academic Practice.

Author

Nguyen, Dana, O'Mara, Heather, and Powell, Robert

Subjects
*GRADUATE medical education, *PHYSICIANS, *MEDICAL practice, *MILITARY medicine, STUDY & teaching of medicine
Abstract

Practice management has become an increasingly important component of graduate medical education. This applies to every practice environment; private, academic, and military. One of the most critical aspects of practice management is documentation and coding for physician services, as they directly affect the financial success of any practice. Our quality improvement project aimed to implement a new and innovative method for teaching billing and coding in a longitudinal fashion in a family medicine residency. We hypothesized that implementation of a new teaching strategy would increase coding accuracy rates among residents and faculty. Methods Design: single group, pretest-posttest. Setting: military family medicine residency clinic. Study populations: 7 faculty physicians and 18 resident physicians participated as learners in the project. Educational intervention: monthly structured coding learning sessions in the academic curriculum that involved learner-presented cases, small group case review, and large group discussion. Main outcome measures: overall coding accuracy (compliance) percentage and coding accuracy per year group for the subjects that were able to participate longitudinally. Statistical tests used: average coding accuracy for population; paired t test to assess improvement between 2 intervention periods, both aggregate and by year group. Results Overall coding accuracy rates remained stable over the course of time regardless of the modality of the educational intervention. A paired t test was conducted to compare coding accuracy rates at baseline (mean (M)=26.4%, SD=10%) to accuracy rates after all educational interventions were complete (M=26.8%, SD=12%); t24=-0.127, P=.90. Conclusions Didactic teaching and small group discussion sessions did not improve overall coding accuracy in a residency practice. Future interventions could focus on educating providers at the individual level. [ABSTRACT FROM AUTHOR]

Published
2017

31. Doing What Is Right.

Author

Weber, Lauren A and Nguyen, Dana R

Subjects
*HELICOPTER ambulances, *COMMAND of troops, *MILITARY physicians, *MEDICAL care of military personnel, *AERONAUTICS in medicine, *LEADERSHIP, *PSYCHOLOGY of military personnel
Abstract

Junior officers have an obligation to "lead up." They help senior officers successfully complete missions while maintaining accountability to core values and taking care of those they lead. The following case highlights one junior officer's challenge "leading up" in a very ambiguous situation. [ABSTRACT FROM AUTHOR]

Published
2019
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32. Default mode network and medial temporal lobe functional connectivity changes with Alzheimer's disease severity and cognitive impairment in individuals with Down syndrome.

Author

DiProspero, Natalie, Sathishkumar, Mithra, McMillan, Liv, Keator, David B., Doran, Eric, Hom, Christy, Nguyen, Dana, Rosas, H. Diana, Lai, Florence, Brickman, Adam M., Schupf, Nicole, Silverman, Wayne, Lott, Ira T, and Yassa, Michael A.

Abstract

Background: By age 40, virtually all people with Down syndrome (DS) have sufficient beta‐amyloid and tau pathologies present to meet the criteria for pathological Alzheimer's disease (AD). Determining the timing and location of neurobiological changes caused by AD is critically important for effective intervention within this high‐risk population and more broadly in the general population, but little is known about the brain changes associated with clinical onset of AD in DS. Previous studies in sporadic AD suggest that functional connectivity of the default mode network (DMN) and medial temporal lobe (MTL) is vulnerable to AD pathology‐related impairment. Method: Seventy‐five individuals with DS (mean age 49.9±6.6, 36% women) from a subset of the Alzheimer's Biomarkers Consortium ‐ Down Syndrome study underwent MRI, including an MPRAGE scan and a resting state functional scan. Participants completed a battery of neuropsychological tests and were assigned a consensus diagnosis for the presence or absence of mild cognitive impairment (MCI‐DS) or AD dementia. Forty‐eight participants were classified as cognitively stable (CS) (mean age 48±6.1, 42% women), 16 participants had MCI‐DS (mean age 50.8±4.2, 19% women), and 11 participants had dementia (mean age 57.2±6.6, 36% women). Result: Participants with dementia had lower functional connectivity between the posterior DMN and the MTL relative to the CS and MCI‐DS groups. MCI‐DS participants had greater functional connectivity within the MTL relative to the CS group. Functional connectivity differences in these networks tracked with memory performance as well. Conclusion: Changes in DMN and MTL functional connectivity are related to the progression of clinical symptoms of AD‐DS and may reflect synaptic changes stemming from AD pathology. [ABSTRACT FROM AUTHOR]

Published
2022
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33. Correspondence between cortical tau and atrophy in aged non‐demented adults with Down syndrome.

Author

Taylor, Lisa, Doran, Eric, Poline, Jean‐Baptiste, Nguyen, Dana, Krinsky‐McHale, Sharon J., Price, Julie C., Sathishkumar, Mithra, Kreisl, William Charles, Hom, Christy, Pulsifer, Margaret, Lai, Florence, Rosas, H. Diana, Brickman, Adam M., Schupf, Nicole, Silverman, Wayne, Lott, Ira T., Yassa, Michael A., and Keator, David

Abstract

Background: Individuals with Down syndrome (DS) have a higher likelihood of developing early‐onset Alzheimer’s disease which has been associated with abnormal tau proteins and atrophy in the brain [1]. Prior research has shown a spatial relationship between tau and atrophy in neurotypicals with dementia [2]. Although tau and atrophy certainly contribute independently to dementia, the synergistic relationship in a non‐demented population with DS is not well understood. This study aims to identify cortical regions with high tau and atrophy in aged, non‐demented participants with DS. Method: Analysis included 28 non‐demented participants (49.8 +/‐ 6.4 years; 17 males) with DS from the Alzheimer’s Disease in Down Syndrome (ADDS) study. Tau PET (18F‐AV1451) and MRI scans were acquired within the same timeframe (1.8 months +/‐1.5). Gray‐matter cortical ribbons were extracted from T1 MRI segmentations with Freesurfer (RRID: SCR_001847). The cortical ribbons were used to mask the coregistered PET scan data and converted to standard uptake value ratio (SUVR) units using the cerebellar cortex reference region. The tau and gray‐matter images were converted to z‐score images using the group mean and standard deviation. We defined high tau as voxels with z‐scores >=2.0 and high atrophy as voxels with gray matter z‐scores <= ‐2.0. The z‐score images were spatially normalized into MNI space with ANTs (RRID: SCR_004757) and a voxel‐based correspondence analysis was performed. Voxels surviving the high tau and high atrophy thresholds were evaluated to determine anatomical localization using the Desikan/Killiany atlas [3]. Result: We found high correspondence between tau and atrophy in the following regions (figure 1): entorhinal cortex, insula, fusiform, pars orbitalis, paracentral, precentral, superior temporal, medial orbitofrontal, lateral orbitofrontal, temporal pole, rostral middle frontal, superior frontal, pars triangularis, lingual, and the amygdala. Conclusion: Our study demonstrated a correspondence between atrophy and tau in deep cortical structures, as well as frontotemporal regions in aged, non‐demented adults with DS. Many of these regions are consistent with findings in neurotypical populations and shown in our prior work to be regions associated with increased amyloid (18F‐AV‐45) as a function of disease severity in DS [4]. [ABSTRACT FROM AUTHOR]

Published
2021
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34. Implementation of a Transition of Care Coordinator at a Military Treatment Facility.

Author

Nguyen, Dana, Strickland, Sarah, Busey, Blake, Roselle, Ashley, Stackle, Mark, Hahn, Scott, Donoway, Tammy, and Bennett, Nick

Subjects
*MEDICAL care, *MEDICAL errors, *FAMILY medicine, *MEDICAL care costs, *PEARSON correlation (Statistics)
Abstract

A patient's transition from the inpatient to the outpatient setting is complex and prone to medical errors. This subsequently increases patient morbidity and cost to the healthcare system. Methods: Our quality improvement initiative used a licensed clinical social worker from within a Family Medicine residency clinic to serve as a Transitions of Care Coordinator (TOCC) with the goal of decreasing patient morbidity and system cost. Results: The number of documented patient contacts by our primary care office in the postdischarge period increased significantly after implementation of the TOCC (3.1% vs 40.2%, P=.01). Pearson correlation during our postimplementation period suggested an inverse relationship between contact by a TOCC and emergency department (ED) and hospital utilization rates (r=-0.68, P=.05 and r=0.062, P=.005, respectively). However, the percentage of ED visits (11.9% vs 20.8%, P=.02) and hospital readmissions (5.6% vs 13.7%, P=.01) significantly increased overall between the pre-and postimplementation periods. Conclusions: The implementation of a TOCC within a military Family Medicine residency clinic significantly increased the frequency of ED visits and readmissions to the inpatient service for patients discharged from the Family Medicine inpatient service. [ABSTRACT FROM AUTHOR]

Published
2016

35. The Effects of Military Deployment on Early Child Development.

Author

Nguyen, Dana R., Ee, Juliana, Berry-Cabán, Cristóbal S., and Hoedebecke, Kyle

Subjects
*DEPLOYMENT (Military strategy), *CHILD development, *COGNITIVE development, *SOCIAL development, *PSYCHOLOGY of preschool children, *DEVELOPMENTAL delay, *PSYCHOLOGY
Abstract

Purpose: The purpose of this observational, point prevalence study is to determine if parental deployment affects the cognitive, social and emotional development of preschool age children in the military family. Methods: Demographic information was collected and an age-appropriate Ages and Stages Questionnaire (ASQ-3) and Ages and Stages Social-Emotional Inventory (ASQ:SE) were administered. The primary outcome measure was the failure rates on the developmental instruments. Results: We identified 151 parents of eligible children; 95 children had a parent that deployed during their lifetime. We found a significant difference in ASQ-3 failure rates for children in the deployed group compared to those in the nondeployed group. Children of deployed parents were at least twice as often to fail the ASQ-3 or ASQ:SE developmental screen compared to children whose parents did not deploy. 30.5% of children in the deployed group failed the ASQ-3 screen while 12.5% of children who did not have a deployed parent failed (P=.009). On the ASQ:SE developmental screen, 16.8% of children who had a parent deploy failed versus 5.4% of children who did not have a parent deploy (P=.031). Conclusions: This study suggests that parental deployment is related to adverse risk for developmental delays in children in military families. The psychological burden on military children could be life-long or require significant resources to address. These adverse outcomes could be possibly mitigated by early detection of developmental delay and firm attention to aggressive screening techniques in military communities. [ABSTRACT FROM AUTHOR]

Published
2014

36. Mining Outcome-relevant Brain Imaging Genetic Associations via Three-way Sparse Canonical Correlation Analysis in Alzheimer’s Disease

Author

Hao, Xiaoke, Li, Chanxiu, Du, Lei, Yao, Xiaohui, Yan, Jingwen, Risacher, Shannon L., Saykin, Andrew J., Shen, Li, Zhang, Daoqiang, Weiner, Michael W., Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Farlow, Martin R., Marie Hake, Ann, Matthews, Brandy R., Brosch, Jared R., Herring, Scott, Hunt, Cynthia, Shaw, Leslie M., Ances, Beau, Morris, John C., Carroll, Maria, Creech, Mary L., Franklin, Erin, Mintun, Mark A., Schneider, Stacy, Oliver, Angela, Kaye, Jeffrey, Quinn, Joseph, Silbert, Lisa, Lind, Betty, Carter, Raina, Dolen, Sara, Schneider, Lon S., Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Fleisher, Adam, Tariot, Pierre, Burke, Anna, Trncic, Nadira, Reeder, Stephanie, Heidebrink, Judith L., Lord, Joanne L., Doody, Rachelle S., Villanueva-Meyer, Javier, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Marson, Daniel, Griffith, Randall, Clark, David, Geldmacher, David, Brockington, John, Roberson, Erik, Love, Marissa Natelson, Grossman, Hillel, Mitsis, Effie, Shah, Raj C., deToledo-Morrell, Leyla, Duara, Ranjan, Varon, Daniel, Greig, Maria T., Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, D’Agostino, Daniel, Kielb, Stephanie, Galvin, James E., Cerbone, Brittany, Michel, Christina A., Pogorelec, Dana M., Rusinek, Henry, de Leon, Mony J., Glodzik, Lidia, De Santi, Susan, Doraiswamy, P. Murali, Petrella, Jeffrey R., Borges-Neto, Salvador, Wong, Terence Z., Coleman, Edward, Smith, Charles D., Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Porsteinsson, Anton P., Goldstein, Bonnie S., Martin, Kim, Makino, Kelly M., Ismail, M. Saleem, Brand, Connie, Mulnard, Ruth A., Thai, Gaby, Mc-Adams-Ortiz, Catherine, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Levey, Allan I., Lah, James J., Cellar, Janet S., Burns, Jeffrey M., Swerdlow, Russell H., Brooks, William M., Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H. S., Lu, Po H., Bartzokis, George, Graff-Radford, Neill R., Parfitt, Francine, Kendall, Tracy, Johnson, Heather, van Dyck, Christopher H., Carson, Richard E., MacAvoy, Martha G., Varma, Pradeep, Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Hsiung, Ging-Yuek Robin, Feldman, Howard, Mudge, Benita, Assaly, Michele, Finger, Elizabeth, Pasternack, Stephen, Rachisky, Irina, Trost, Dick, Kertesz, Andrew, Bernick, Charles, Munic, Donna, Mesulam, Marek-Marsel, Lipowski, Kristine, Weintraub, Sandra, Bonakdarpour, Borna, Kerwin, Diana, Wu, Chuang-Kuo, Johnson, Nancy, Sadowsky, Carl, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Yesavage, Jerome, Taylor, Joy L., Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N., Belden, Christine M., Jacobson, Sandra A., Sirrel, Sherye A., Kowall, Neil, Killiany, Ronald, Budson, Andrew E., Norbash, Alexander, Johnson, Patricia Lynn, Obisesan, Thomas O., Wolday, Saba, Allard, Joanne, Lerner, Alan, Ogrocki, Paula, Tatsuoka, Curtis, Fatica, Parianne, Fletcher, Evan, Maillard, Pauline, Olichney, John, DeCarli, Charles, Carmichael, Owen, Kittur, Smita, Borrie, Michael, Lee, T.-Y., Bartha, Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Potkin, Steven G., Preda, Adrian, Nguyen, Dana, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W., Kataki, Maria, Adeli, Anahita, Zimmerman, Earl A., Celmins, Dzintra, Brown, Alice D., Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Flashman, Laura A., Seltzer, Marc, Hynes, Mary L., Santulli, Robert B., Sink, Kaycee M., Gordineer, Leslie, Williamson, Jeff D., Garg, Pradeep, Watkins, Franklin, Ott, Brian R., Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J., Miller, Bruce L., Perry, David, Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Relkin, Norman, Chaing, Gloria, Lin, Michael, Ravdin, Lisa, Smith, Amanda, Raj, Balebail Ashok, and Fargher, Kristin

Abstract

Neuroimaging genetics is an emerging field that aims to identify the associations between genetic variants (e.g., single nucleotide polymorphisms (SNPs)) and quantitative traits (QTs) such as brain imaging phenotypes. In recent studies, in order to detect complex multi-SNP-multi-QT associations, bi-multivariate techniques such as various structured sparse canonical correlation analysis (SCCA) algorithms have been proposed and used in imaging genetics studies. However, associations between genetic markers and imaging QTs identified by existing bi-multivariate methods may not be all disease specific. To bridge this gap, we propose an analytical framework, based on three-way sparse canonical correlation analysis (T-SCCA), to explore the intrinsic associations among genetic markers, imaging QTs, and clinical scores of interest. We perform an empirical study using the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort to discover the relationships among SNPs from AD risk gene APOE, imaging QTs extracted from structural magnetic resonance imaging scans, and cognitive and diagnostic outcomes. The proposed T-SCCA model not only outperforms the traditional SCCA method in terms of identifying strong associations, but also discovers robust outcome-relevant imaging genetic patterns, demonstrating its promise for improving disease-related mechanistic understanding.

Published
2017
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37. Longitudinal measurement and hierarchical classification framework for the prediction of Alzheimer’s disease

Author

Huang, Meiyan, Yang, Wei, Feng, Qianjin, Chen, Wufan, Weiner, Michael W., Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Saykin, Andrew J., Morris, John, Shaw, Leslie M., Kaye, Jeffrey, Quinn, Joseph, Silbert, Lisa, Lind, Betty, Carter, Raina, Dolen, Sara, Schneider, Lon S., Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Fleisher, Adam, Heidebrink, Judith L., Lord, Joanne L., Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Doody, Rachelle S., Villanueva-Meyer, Javier, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Ances, Beau, Morris, John C., Carroll, Maria, Creech, Mary L., Franklin, Erin, Mintun, Mark A., Schneider, Stacy, Oliver, Angela, Marson, Daniel, Griffith, Randall, Clark, David, Geldmacher, David, Brockington, John, Roberson, Erik, Love, Marissa Natelson, Grossman, Hillel, Mitsis, Effie, Shah, Raj C., deToledo-Morrell, Leyla, Duara, Ranjan, Varon, Daniel, Greig, Maria T., Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, D’Agostino, Daniel, Kielb, Stephanie, Galvin, James E., Cerbone, Brittany, Michel, Christina A., Pogorelec, Dana M., Rusinek, Henry, de Leon, Mony J., Glodzik, Lidia, De Santi, Susan, Doraiswamy, P. Murali, Petrella, Jeffrey R., Borges-Neto, Salvador, Wong, Terence Z., Coleman, Edward, Smith, Charles D., Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Porsteinsson, Anton P., Goldstein, Bonnie S., Martin, Kim, Makino, Kelly M., Ismail, M. Saleem, Brand, Connie, Mulnard, Ruth A., Thai, Gaby, Mc-Adams-Ortiz, Catherine, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Levey, Allan I., Lah, James J., Cellar, Janet S., Burns, Jeffrey M., Swerdlow, Russell H., Brooks, William M., Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H. S., Lu, Po H., Bartzokis, George, Graff-Radford, Neill R., Parfitt, Francine, Kendall, Tracy, Johnson, Heather, Farlow, Martin R., Hake, Ann Marie, Matthews, Brandy R., Brosch, Jared R., Herring, Scott, Hunt, Cynthia, van Dyck, Christopher H., Carson, Richard E., MacAvoy, Martha G., Varma, Pradeep, Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Hsiung, Ging-Yuek Robin, Feldman, Howard, Mudge, Benita, Assaly, Michele, Finger, Elizabeth, Pasternack, Stephen, Rachisky, Irina, Trost, Dick, Kertesz, Andrew, Bernick, Charles, Munic, Donna, Mesulam, Marek Marsel, Lipowski, Kristine, Weintraub, Sandra, Bonakdarpour, Borna, Kerwin, Diana, Wu, Chuang-Kuo, Johnson, Nancy, Sadowsky, Carl, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Yesavage, Jerome, Taylor, Joy L., Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N., Belden, Christine M., Jacobson, Sandra A., Sirrel, Sherye A., Kowall, Neil, Killiany, Ronald, Budson, Andrew E., Norbash, Alexander, Johnson, Patricia Lynn, Obisesan, Thomas O., Wolday, Saba, Allard, Joanne, Lerner, Alan, Ogrocki, Paula, Tatsuoka, Curtis, Fatica, Parianne, Fletcher, Evan, Maillard, Pauline, Olichney, John, DeCarli, Charles, Carmichael, Owen, Kittur, Smita, Borrie, Michael, Lee, T-Y, Bartha, Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Potkin, Steven G., Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Burke, Anna, Trncic, Nadira, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W., Kataki, Maria, Adeli, Anahita, Zimmerman, Earl A., Celmins, Dzintra, Brown, Alice D., Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Flashman, Laura A., Seltzer, Marc, Hynes, Mary L., Santulli, Robert B., Sink, Kaycee M., Gordineer, Leslie, Williamson, Jeff D., Garg, Pradeep, Watkins, Franklin, Ott, Brian R., Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J., Miller, Bruce L., Perry, David, Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Relkin, Norman, Chaing, Gloria, Lin, Michael, Ravdin, Lisa, Smith, Amanda, Raj, Balebail Ashok, and Fargher, Kristin

Abstract

Accurate prediction of Alzheimer’s disease (AD) is important for the early diagnosis and treatment of this condition. Mild cognitive impairment (MCI) is an early stage of AD. Therefore, patients with MCI who are at high risk of fully developing AD should be identified to accurately predict AD. However, the relationship between brain images and AD is difficult to construct because of the complex characteristics of neuroimaging data. To address this problem, we present a longitudinal measurement of MCI brain images and a hierarchical classification method for AD prediction. Longitudinal images obtained from individuals with MCI were investigated to acquire important information on the longitudinal changes, which can be used to classify MCI subjects as either MCI conversion (MCIc) or MCI non-conversion (MCInc) individuals. Moreover, a hierarchical framework was introduced to the classifier to manage high feature dimensionality issues and incorporate spatial information for improving the prediction accuracy. The proposed method was evaluated using 131 patients with MCI (70 MCIc and 61 MCInc) based on MRI scans taken at different time points. Results showed that the proposed method achieved 79.4% accuracy for the classification of MCIc versus MCInc, thereby demonstrating very promising performance for AD prediction.

Published
2017
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40. Anterolateral entorhinal cortical thinning as a biomarker for Alzheimer's disease in Down syndrome: Imaging: Pathological correlations.

Author

Sathishkumar, Mithra, Janecek, John, Smith, Anna, Phelan, Michael, Tustison, Nick, Keator, David, Doran, Eric, Hom, Christy, Nguyen, Dana, Petersen, Melissa, Rosas, H. Diana, Lai, Florence, Brickman, Adam M, Schupf, Nicole, Silverman, Wayne, Lott, Ira T, O'Bryant, Sid, and Yassa, Michael A.

Abstract

Background: Virtually all adults with Down syndrome (DS) develop Alzheimer's disease (AD) associated neuropathology by the age of 40 and the majority of them develop dementia by age 60. Atrophy of the anterolateral entorhinal cortex (aLEC) has been previously associated with cognitive decline. Here, we sought to determine whether aLEC thinning is associated with clinical impairment in older adults with DS as well as whether it is associated with blood neurofilament light chain (NfL), another biomarker of neurodegeneration in AD. Method: 103 older adults with DS enrolled in the Alzheimer's Disease in Down Syndrome (ADDS) study were included in this analysis. Scans were classified into 3 groups based on consensus diagnosis: 14 (6F) possible/definite dementia (DEM), 19 (5F) mild cognitive impairment (MCI‐DS) and 70 (28F) cognitively stable (CS). Images were processed through the joint label fusion (JLF) pipeline in ANTs to obtain medial temporal lobe subregional volumes and thickness. Cortical reconstruction was performed using Freesurfer 6.0 to obtain total intracranial volume (ICV). We used a multiple linear regression model to fit left aLEC thickness using diagnostic group as the independent variable, correcting for age, gender, ICV and scan site differences. For a subset of these data (N = 89), plasma NfL was quantified using a Simoa platform and we and tested whether left aLEC thickness was associated with NfL. Result: Cortical thickness in left aLEC was a significant predictor of clinical status. Thickness values were highest in the CS group, followed by MCI‐DS, followed by DEM. Groupwise differences were significant in DEM vs. CS and DEM vs. MCI‐DS comparisons. We also found a significant correlation between NfL and left aLEC thickness specifically in the DEM group. Finally, random forest classification showed that both NfL and left aLEC thickness were important features in predicting clinical diagnosis DEM vs MCI‐DS. Their estimates provided a diagnosis ROC curve with sensitivity of 0.79 and specificity of 0.92. Conclusion: In older adults with DS, left aLEC cortical thickness atrophy may be a primary feature of structural neurodegeneration that is associated with MCI‐DS and a blood‐based measurement of NfL may be informative as to this structural degeneration. [ABSTRACT FROM AUTHOR]

Published
2020
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41. Anterolateral entorhinal cortical thinning as a biomarker for Alzheimer's disease in Down syndrome: Neuroimaging / Optimal neuroimaging measures for early detection.

Author

Sathishkumar, Mithra, Janecek, John, Smith, Anna, Phelan, Michael, Tustison, Nick, Keator, David, Doran, Eric, Hom, Christy, Nguyen, Dana, Petersen, Melissa, Rosas, H. Diana, Lai, Florence, Brickman, Adam M., Schupf, Nicole, Silverman, Wayne, Lott, Ira T., O'Bryant, Sid, and Yassa, Michael A.

Abstract

Background: Virtually all adults with Down syndrome (DS) develop Alzheimer's disease (AD) associated neuropathology by the age of 40 and the majority of them develop dementia by age 60. Atrophy of the anterolateral entorhinal cortex (aLEC) has been previously associated with cognitive decline. Here, we sought to determine whether aLEC thinning is associated with clinical impairment in older adults with DS as well as whether it is associated with blood neurofilament light chain (NfL), another biomarker of neurodegeneration in AD. Method: 103 older adults with DS enrolled in the Alzheimer's Disease in Down Syndrome (ADDS) study were included in this analysis. Scans were classified into 3 groups based on consensus diagnosis: 14 (6F) possible/definite dementia (DEM), 19 (5F) mild cognitive impairment (MCI‐DS) and 70 (28F) cognitively stable (CS). Images were processed through the joint label fusion (JLF) pipeline in ANTs to obtain medial temporal lobe subregional volumes and thickness. Cortical reconstruction was performed using Freesurfer 6.0 to obtain total intracranial volume(ICV). We used a multiple linear regression model to fit left aLEC thickness using diagnostic group as the independent variable, correcting for age, gender, ICV and scan site differences. For a subset of these data (N=89), plasma NfL was quantified using a Simoa platform and we and tested whether left aLEC thickness was associated with NfL. Result: Cortical thickness in left aLEC was a significant predictor of clinical status. Thickness values were highest in the CS group, followed by MCI‐DS, followed by DEM. Groupwise differences were significant in DEM vs. CS and DEM vs. MCI‐DS comparisons. We also found a significant correlation between NfL and left aLEC thickness specifically in the DEM group. Finally, random forest classification showed that both NfL and left aLEC thickness were important features in predicting clinical diagnosis DEM vs MCI‐DS. Their estimates provided a diagnosis ROC curve with sensitivity of 0.79 and specificity of 0.92. Conclusion: In older adults with DS, left aLEC cortical thickness atrophy may be a primary feature of structural neurodegeneration that is associated with MCI‐DS and a blood‐based measurement of NfL may be informative as to this structural degeneration. [ABSTRACT FROM AUTHOR]

Published
2020
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42. Brief screening for co-occurring disorders among women entering substance abuse treatment.

Author

Lincoln, Alisa K., Liebschutz, Jane M., Chernoff, Miriam, Nguyen, Dana, and Amaro, Hortensia

Subjects
MEDICAL screening, WOMEN'S mental health, SUBSTANCE abuse treatment, PATHOLOGICAL psychology, MENTAL health, METHADONE abuse, POST-traumatic stress disorder
Abstract

Background: Despite the importance of identifying co-occurring psychiatric disorders in substance abuse treatment programs, there are few appropriate and validated instruments available to substance abuse treatment staff to conduct brief screen for these conditions. This paper describes the development, implementation and validation of a brief screening instrument for mental health diagnoses and trauma among a diverse sample of Black, Hispanic and White women in substance abuse treatment. With input from clinicians and consumers, we adapted longer existing validated instruments into a 14 question screen covering demographics, mental health symptoms and physical and sexual violence exposure. All women entering treatment (methadone, residential and out-patient) at five treatment sites were screened at intake (N = 374). Results: Eighty nine percent reported a history of interpersonal violence, and 70% reported a history of sexual assault. Eighty-eight percent reported mental health symptoms in the last 30 days. The screening questions administered to 88 female clients were validated against in-depth psychiatric diagnostic assessments by trained mental health clinicians. We estimated measures of predictive validity, including sensitivity, specificity and predictive values positive and negative. Screening items were examined multiple ways to assess utility. The screen is a useful and valid proxy for PTSD but not for other mental illness. Conclusion: Substance abuse treatment programs should incorporate violence exposure questions into clinical use as a matter of policy. More work is needed to develop brief screening tools measures for front-line treatment staff to accurately assess other mental health needs of women entering substance abuse treatment [ABSTRACT FROM AUTHOR]

Published
2006
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43. A Double-Blind, placebo-Controlled Trial of Sibutramine for Olanzapine-Associated Weight Gain.

Author

Cather, Corrine, Eden#Evins, A., Freudenreich, Oliver, Hayden, Doug, Henderson, David C., Paul M.Copeland, Daley, Tara B., Borba, Christina P., Nguyen, Dana D., Louie, Pearl M., and Goff, Donald C.

Subjects
WEIGHT gain, OBESITY, OLANZAPINE, HYPERTENSION, SCHIZOPHRENIA, CARDIOVASCULAR diseases
Abstract

Objective: Weight gain is commonly observed with olanzapine treatment and can increase the risk for obesity, cardiovascular disease, hypertension, and diabetes mellitus. This study examined the effectiveness of sibutramine, an approved weight loss agent, in overweight and obese subjects taking olanza pine for schizophrenia or schizoaffective disorder. Method: Each subject had a DSM-IV diagnosis of schizophrenia or schizoaffective disorder, had been taking a stable dose of olanzapine for at least 4 months, and had a body mass index of &ges;30 kg/m² or &ges;27 kg/m² plus at least one cardiovascular risk factor. In a 12-week double-blind, randomized, placebo-controlled study, 37 subjects received placebo or sibutramine (up to 15 mg/day). For the first 8 weeks all subjects participated in weekly group sessions focused on nutrition and behavioral modification. Results: The sibutramine and placebo groups had no significant baseline differences on age, gender, education, ethnicity, diagnosis, weight, body mass index, and blood pressure. At week 12 the sibutramine group had significantly greater losses than the placebo group in weight (mean=8.3 lb, SD=2.4, versus mean=1.8 Ib, SD=1.6), waist circumference, body mass index, and hemoglobin A1C. There were no significant differences on most side effects, although the sibutramine group exhibited a mean increase in systolic blood pressure of 2.1 mmHg (SD=8,5), and anticholinergic side effects and sleep disturbances were at least twice as common in the sibutramine group. conclusions: Sibutramine was an effective and well-tolerated adjunct to behavior modification for weight loss in patients with schizophrenia and schizoaffective disorder being treated with olanzapine. [ABSTRACT FROM AUTHOR]

Published
2005

44. Basal forebrain degeneration precedes and predicts the cortical spread of Alzheimer's pathology

Author

Schmitz, Taylor W., Nathan Spreng, R., Weiner, Michael W., Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Saykin, Andrew J., Morris, John, Shaw, Leslie M., Khachaturian, Zaven, Sorensen, Greg, Kuller, Lew, Raichle, Marc, Paul, Steven, Davies, Peter, Fillit, Howard, Hefti, Franz, Holtzman, Davie, Mesulam, M Marcel, Potter, William, Snyder, Peter, Schwartz, Adam, Montine, Tom, Thomas, Ronald G., Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Jiminez, Gus, Harvey, Danielle, Bernstein, Matthew, Fox, Nick, Thompson, Paul, Schuff, Norbert, Borowski, Bret, Gunter, Jeff, Senjem, Matt, Vemuri, Prashanthi, Jones, David, Kantarci, Kejal, Ward, Chad, Koeppe, Robert A., Foster, Norm, Reiman, Eric M., Chen, Kewei, Mathis, Chet, Landau, Susan, Cairns, Nigel J., Householder, Erin, Taylor-Reinwald, Lisa, Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M., Potkin, Steven, Shen, Li, Faber, Kelley, Kim, Sungeun, Nho, Kwangsik, Thal, Leon, Buckholtz, Neil, Albert, Marylyn, Frank, Richard, Hsiao, John, Kaye, Jeffrey, Quinn, Joseph, Lind, Betty, Carter, Raina, Dolen, Sara, Schneider, Lon S., Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Fleisher, Adam, Heidebrink, Judith L., Lord, Joanne L., Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Doody, Rachelle S., Villanueva-Meyer, Javier, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Ances, Beau, Carroll, Maria, Leon, Sue, Mintun, Mark A., Schneider, Stacy, Oliver, Angela, Marson, Daniel, Griffith, Randall, Clark, David, Geldmacher, David, Brockington, John, Roberson, Erik, Grossman, Hillel, Mitsis, Effie, de Toledo-Morrell, Leyla, Shah, Raj C., Duara, Ranjan, Varon, Daniel, Greig, Maria T., Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, D'Agostino, Daniel, Kielb, Stephanie, Galvin, James E., Cerbone, Brittany, Michel, Christina A., Rusinek, Henry, de Leon, Mony J., Glodzik, Lidia, De Santi, Susan, Doraiswamy, P. Murali, Petrella, Jeffrey R., Wong, Terence Z., Arnold, Steven E., Karlawish, Jason H., Wolk, David, Smith, Charles D., Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Lopez, Oscar L., Oakley, MaryAnn, Simpson, Donna M., Porsteinsson, Anton P., Goldstein, Bonnie S., Martin, Kim, Makino, Kelly M., Ismail, M. Saleem, Brand, Connie, Mulnard, Ruth A., Thai, Gaby, Mc-Adams-Ortiz, Catherine, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Diaz-Arrastia, Ramon, King, Richard, Weiner, Myron, Martin-Cook, Kristen, DeVous, Michael, Levey, Allan I., Lah, James J., Cellar, Janet S., Burns, Jeffrey M., Anderson, Heather S., Swerdlow, Russell H., Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H. S., Lu, Po H., Bartzokis, George, Graff-Radford, Neill R., Parfitt, Francine, Kendall, Tracy, Johnson, Heather, Farlow, Martin R., Hake, AnnMarie, Matthews, Brandy R., Herring, Scott, Hunt, Cynthia, van Dyck, Christopher H., Carson, Richard E., MacAvoy, Martha G., Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Robin Hsiung, Ging-Yuek, Feldman, Howard, Mudge, Benita, Assaly, Michele, Kertesz, Andrew, Rogers, John, Bernick, Charles, Munic, Donna, Kerwin, Diana, Mesulam, Marek-Marsel, Lipowski, Kristine, Wu, Chuang-Kuo, Johnson, Nancy, Sadowsky, Carl, Martinez, Walter, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Frey, Meghan, Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N., Belden, Christine M., Jacobson, Sandra A., Sirrel, Sherye A., Kowall, Neil, Killiany, Ronald, Budson, Andrew E., Norbash, Alexander, Johnson, Patricia Lynn, Allard, Joanne, Lerner, Alan, Ogrocki, Paula, Hudson, Leon, Fletcher, Evan, Carmichael, Owen, Olichney, John, DeCarli, Charles, Kittur, Smita, Borrie, Michael, Lee, T.-Y., Bartha, Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Potkin, Steven G., Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W., Kataki, Maria, Adeli, Anahita, Zimmerman, Earl A., Celmins, Dzintra, Brown, Alice D., Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Santulli, Robert B., Kitzmiller, Tamar J., Schwartz, Eben S., Sink, Kaycee M., Williamson, Jeff D., Garg, Pradeep, Watkins, Franklin, Ott, Brian R., Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J., Miller, Bruce L., Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Finger, Elizabether, Pasternak, Stephen, Rachinsky, Irina, Drost, Dick, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Schultz, Susan K., Boles Ponto, Laura L., Shim, Hyungsub, Smith, Karen Elizabeth, Relkin, Norman, Chaing, Gloria, Raudin, Lisa, Smith, Amanda, Fargher, Kristin, Raj, Balebail Ashok, Neylan, Thomas, Grafman, Jordan, Davis, Melissa, Morrison, Rosemary, Hayes, Jacqueline, Finley, Shannon, Friedl, Karl, Fleischman, Debra, Arfanakis, Konstantinos, James, Olga, Massoglia, Dino, Fruehling, J. Jay, Harding, Sandra, Peskind, Elaine R., Petrie, Eric C., Li, Gail, Yesavage, Jerome A., Taylor, Joy L., and Furst, Ansgar J.

Abstract

There is considerable debate whether Alzheimer's disease (AD) originates in basal forebrain or entorhinal cortex. Here we examined whether longitudinal decreases in basal forebrain and entorhinal cortex grey matter volume were interdependent and sequential. In a large cohort of age-matched older adults ranging from cognitively normal to AD, we demonstrate that basal forebrain volume predicts longitudinal entorhinal degeneration. Models of parallel degeneration or entorhinal origin received negligible support. We then integrated volumetric measures with an amyloid biomarker sensitive to pre-symptomatic AD pathology. Comparison between cognitively matched normal adult subgroups, delineated according to the amyloid biomarker, revealed abnormal degeneration in basal forebrain, but not entorhinal cortex. Abnormal degeneration in both basal forebrain and entorhinal cortex was only observed among prodromal (mildly amnestic) individuals. We provide evidence that basal forebrain pathology precedes and predicts both entorhinal pathology and memory impairment, challenging the widely held belief that AD has a cortical origin.

Published
2016
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45. A semi-mechanism approach based on MRI and proteomics for prediction of conversion from mild cognitive impairment to Alzheimer’s disease

Author

Liu, Haochen, Zhou, Xiaoting, Jiang, Hao, He, Hua, Liu, Xiaoquan, Weiner, Michael W., Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Saykin, Andrew J., Morris, John, Shaw, Leslie M., Khachaturian, Zaven, Sorensen, Greg, Carrillo, Maria, Kuller, Lew, Raichle, Marc, Paul, Steven, Davies, Peter, Fillit, Howard, Hefti, Franz, Holtzman, Davie, Mesulam, M. Marcel, Potter, William, Snyder, Peter, Montine, Tom, Thomas, Ronald G., Donohue, Michael, Walter, Sarah, Sather, Tamie, Jiminez, Gus, Balasubramanian, Archana B., Mason, Jennifer, Sim, Iris, Harvey, Danielle, Bernstein, Matthew, Fox, Nick, Thompson, Paul, Schuff, Norbert, DeCArli, Charles, Borowski, Bret, Gunter, Jeff, Senjem, Matt, Vemuri, Prashanthi, Jones, David, Kantarci, Kejal, Ward, Chad, Koeppe, Robert A., Foster, Norm, Reiman, Eric M., Chen, Kewei, Mathis, Chet, Landau, Susan, Cairns, Nigel J., Householder, Erin, Taylor-Reinwald, Lisa, Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M., Potkin, Steven, Shen, Li, Faber, Kelley, Kim, Sungeun, Nho, Kwangsik, Thal, Lean, Frank, Richard, Hsiao, John, Kaye, Jeffrey, Quinn, Joseph, Silbert, Lisa, Lind, Betty, Carter, Raina, Dolen, Sara, Ances, Beau, Carroll, Maria, Creech, Mary L., Franklin, Erin, Mintun, Mark A., Schneider, Stacy, Oliver, Angela, Schneider, Lon S., Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Fleisher, Adam, Marson, Daniel, Griffith, Randall, Clark, David, Geldmacher, David, Brockington, John, Roberson, Erik, Love, Marissa Natelson, Heidebrink, Judith L., Lord, Joanne L., Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Grossman, Hillel, Mitsis, Effie, Shah, Raj C., deToledo-Morrell, Leyla, Doody, Rachelle S., Villanueva-Meyer, Javier, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Duara, Ranjan, Varon, Daniel, Greig, Maria T., Roberts, Peggy, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Albert, Marilyn, Onyike, Chiadi, D’Agostino II, Daniel, Kielb, Stephanie, Galvin, James E., Cerbone, Brittany, Michel, Christina A., Pogorelec, Dana M., Rusinek, Henry, de Leon, Mony J., Glodzik, Lidia, De Santi, Susan, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Doraiswamy, P. Murali, Petrella, Jeffrey R., Borges-Neto, Salvador, Wong, Terence Z., Coleman, Edward, Levey, Allan I., Lah, James J., Cella, Janet S., Burns, Jeffrey M., Swerdlow, Russell H., Brooks, William M., Arnold, Steven E., Karlawish, Jason H., Wolk, David, Clark, Christopher M., Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H.S., Lu, Po H., Bartzokis, George, Smith, Charles D., Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Graff-Radford, Neill R, Parfitt, Francine, Kendall, Tracy, Johnson, Heather, Lopez, Oscar L., Oakley, MaryAnn, Simpson, Donna M., Farlow, Martin R., Hake, Ann Marie, Matthews, Brandy R., Brosch, Jared R., Herring, Scott, Hunt, Cynthia, Porsteinsson, Anton P., Goldstein, Bonnie S., Martin, Kim, Makino, Kelly M., Ismail, M. Saleem, Brand, Connie, Mulnard, Ruth A., Thai, Gaby, Mc-Adams-Ortiz, Catherine, van Dyck, Christopher H., Carson, Richard E., MacAvoy, Martha G., Varma, Pradeep, Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Robin Hsiung, Ging-Yuek, Feldman, Howard, Mudge, Benita, Assaly, Michele, Finger, Elizabeth, Pasternack, Stephen, Rachisky, Irina, Trost, Dick, Kertesz, Andrew, Bernick, Charles, Munic, Donna, Lipowski, Kristine, Weintraub, MASandra, Bonakdarpour, Borna, Kerwin, Diana, Wu, Chuang-Kuo, Johnson, Nancy, Sadowsky, Carl, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Yesavage, Jerome, Taylor, Joy L., Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N., Belden, Christine M., Jacobson, Sandra A., Sirrel, Sherye A., Kowall, Neil, Killiany, Ronald, Budson, Andrew E., Norbash, Alexander, Johnson, Patricia Lynn, Obisesan, Thomas O., Wolday, Saba, Allard, Joanne, Lerner, Alan, Ogrocki, Paula, Tatsuoka, Curtis, Fatica, Parianne, Fletcher, Evan, Maillard, Pauline, Olichney, John, Carmichael, Owen, Kittur, Smita, Borrie, Michael, Lee, T-Y, Bartha, Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Burke, Anna, Trncic, Nadira, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W., Kataki, Maria, Adeli, Anahita, Zimmerman, Earl A., Celmins, Dzintra, Brown, Alice D., Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Flashman, Laura A., Seltzer, Marc, Hynes, Mary L., Santulli, Robert B., Sink, Kaycee M., Gordineer, Leslie, Williamson, Jeff D., Garg, Pradeep, Watkins, Franklin, Ott, Brian R., Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J., Miller, Bruce L., Perry, David, Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Finger, Elizabether, Pasternak, Stephen, Rachinsky, Irina, Rogers, John, Drost, Dick, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Schultz, Susan K., Boles Ponto, Laura L., Shim, Hyungsub, Smith, Karen Ekstam, Relkin, Norman, Chaing, Gloria, Lin, Michael, Ravdin, Lisa, Smith, Amanda, Raj, Balebail Ashok, and Fargher, Kristin

Abstract

Mild cognitive impairment (MCI) is a precursor phase of Alzheimer’s disease (AD). As current treatments may be effective only at the early stages of AD, it is important to track MCI patients who will convert to AD. The aim of this study is to develop a high performance semi-mechanism based approach to predict the conversion from MCI to AD and improve our understanding of MCI-to-AD conversion mechanism. First, analysis of variance (ANOVA) test and lasso regression are employed to identify the markers related to the conversion. Then the Bayesian network based on selected markers is established to predict MCI-to-AD conversion. The structure of Bayesian network suggests that the conversion may start with fibrin clot formation, verbal memory impairment, eating pattern changing and hyperinsulinemia. The Bayesian network achieves a high 10-fold cross-validated prediction performance with 96% accuracy, 95% sensitivity, 65% specificity, area under the receiver operating characteristic curve of 0.82 on data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database. The semi-mechanism based approach provides not only high prediction performance but also clues of mechanism for MCI-to-AD conversion.

Published
2016
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46. The impact of PICALM genetic variations on reserve capacity of posterior cingulate in AD continuum

Author

Xu, Wei, Wang, Hui-Fu, Tan, Lin, Tan, Meng-Shan, Tan, Chen-Chen, Zhu, Xi-Chen, Miao, Dan, Yu, Wan-Jiang, Jiang, Teng, Tan, Lan, Yu, Jin-Tai, Weiner, Michael W., Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Saykin, Andrew J., Morris, John, Shaw, Leslie M., Kaye, Jeffrey, Quinn, Joseph, Silbert, Lisa, Lind, Betty, Carter, Raina, Dolen, Sara, Schneider, Lon S., Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Fleisher, Adam, Heidebrink, Judith L., Lord, Joanne L., Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Doody, Rachelle S., Villanueva-Meyer, Javier, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Ances, Beau, Morris, John C., Carroll, Maria, Creech, Mary L., Franklin, Erin, Mintun, Mark A., Schneider, Stacy, Oliver, Angela, Marson, Daniel, Griffith, Randall, Clark, David, Geldmacher, David, Brockington, John, Roberson, Erik, Natelson Love, Marissa, Grossman, Hillel, Mitsis, Effie, Shah, Raj C., deToledo-Morrell, Leyla, Duara, Ranjan, Varon, Daniel, Greig, Maria T., Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, D’Agostino, Daniel, Kielb, Stephanie, Galvin, James E., Cerbone, Brittany, Michel, Christina A., Pogorelec, Dana M., Rusinek, Henry, de Leon, Mony J., Glodzik, Lidia, De Santi, Susan, Doraiswamy, P. Murali, Petrella, Jeffrey R., Borges-Neto, Salvador, Wong, Terence Z., Coleman, Edward, Smith, Charles D., Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Porsteinsson, Anton P., Goldstein, Bonnie S., Martin, Kim, Makino, Kelly M., Ismail, M. Saleem, Brand, Connie, Mulnard, Ruth A., Thai, Gaby, Mc-Adams-Ortiz, Catherine, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Levey, Allan I., Lah, James J., Cellar, Janet S., Burns, Jeffrey M., Swerdlow, Russell H., Brooks, William M., Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H.S., Lu, Po H., Bartzokis, George, Graff-Radford, Neill R., Parfitt, Francine, Kendall, Tracy, Johnson, Heather, Farlow, Martin R., Hake, Ann Marie, Matthews, Brandy R., Brosch, Jared R., Herring, Scott, Hunt, Cynthia, van Dyck, Christopher H., Carson, Richard E., MacAvoy, Martha G., Varma, Pradeep, Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Robin Hsiung, Ging-Yuek, Feldman, Howard, Mudge, Benita, Assaly, Michele, Finger, Elizabeth, Pasternack, Stephen, Rachisky, Irina, Trost, Dick, Kertesz, Andrew, Bernick, Charles, Munic, Donna, Mesulam, Marek-Marsel, Lipowski, Kristine, Weintraub, Sandra, Bonakdarpour, Borna, Kerwin, Diana, Wu, Chuang-Kuo, Johnson, Nancy, Sadowsky, Carl, Villena, Teresa, Scott Turner, Raymond, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Yesavage, Jerome, Taylor, Joy L., Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N., Belden, Christine M., Jacobson, Sandra A., Sirrel, Sherye A., Kowall, Neil, Killiany, Ronald, Budson, Andrew E., Norbash, Alexander, Lynn Johnson, Patricia, Obisesan, Thomas O., Wolday, Saba, Allard, Joanne, Lerner, Alan, Ogrocki, Paula, Tatsuoka, Curtis, Fatica, Parianne, Fletcher, Evan, Maillard, Pauline, Olichney, John, DeCarli, Charles, Carmichael, Owen, Kittur, Smita, Borrie, Michael, Lee, T-Y, Bartha, Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Potkin, Steven G., Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Burke, Anna, Trncic, Nadira, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W, Kataki, Maria, Adeli, Anahita, Zimmerman, Earl A., Celmins, Dzintra, Brown, Alice D., Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Flashman, Laura A., Seltzer, Marc, Hynes, Mary L., Santulli, Robert B., Sink, Kaycee M., Gordineer, Leslie, Williamson, Jeff D., Garg, Pradeep, Watkins, Franklin, Ott, Brian R., Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J., Miller, Bruce L., Perry, David, Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Relkin, Norman, Chaing, Gloria, Lin, Michael, Ravdin, Lisa, Smith, Amanda, Ashok Raj, Balebail, and Fargher, Kristin

Abstract

Phosphatidylinositolbinding clathrin assembly protein (PICALM) gene is one novel genetic player associated with late-onset Alzheimer’s disease (LOAD), based on recent genome wide association studies (GWAS). However, how it affects AD occurrence is still unknown. Brain reserve hypothesis highlights the tolerant capacities of brain as a passive means to fight against neurodegenerations. Here, we took the baseline volume and/or thickness of LOAD-associated brain regions as proxies of brain reserve capacities and investigated whether PICALM genetic variations can influence the baseline reserve capacities and the longitudinal atrophy rate of these specific regions using data from Alzheimer’s Disease Neuroimaging Initiative (ADNI) dataset. In mixed population, we found that brain region significantly affected by PICALM genetic variations was majorly restricted to posterior cingulate. In sub-population analysis, we found that one PICALM variation (C allele of rs642949) was associated with larger baseline thickness of posterior cingulate in health. We found seven variations in health and two variations (rs543293 and rs592297) in individuals with mild cognitive impairment were associated with slower atrophy rate of posterior cingulate. Our study provided preliminary evidences supporting that PICALM variations render protections by facilitating reserve capacities of posterior cingulate in non-demented elderly.

Published
2016
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47. Effect of CLU genetic variants on cerebrospinal fluid and neuroimaging markers in healthy, mild cognitive impairment and Alzheimer’s disease cohorts

Author

Tan, Lin, Wang, Hui-Fu, Tan, Meng-Shan, Tan, Chen-Chen, Zhu, Xi-Chen, Miao, Dan, Yu, Wan-Jiang, Jiang, Teng, Tan, Lan, Yu, Jin-Tai, Weiner, Michael W., Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Saykin, Andrew J., Morris, John, Shaw, Leslie M., Kaye, Jeffrey, Quinn, Joseph, Silbert, Lisa, Lind, Betty, Carter, Raina, Dolen, Sara, Schneider, Lon S., Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Fleisher, Adam, Heidebrink, Judith L., Lord, Joanne L., Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Doody, Rachelle S., Villanueva-Meyer, Javier, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Ances, Beau, Morris, John C., Carroll, Maria, Creech, Mary L., Franklin, Erin, Mintun, Mark A., Schneider, Stacy, Oliver, Angela, Marson, Daniel, Griffith, Randall, Clark, David, Geldmacher, David, Brockington, John, Roberson, Erik, Love, Marissa Natelson, Grossman, Hillel, Mitsis, Effie, Shah, Raj C., deToledo-Morrell, Leyla, Duara, Ranjan, Varon, Daniel, Greig, Maria T., Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, D’Agostino, Daniel, Kielb, Stephanie, Galvin, James E., Cerbone, Brittany, Michel, Christina A., Pogorelec, Dana M., Rusinek, Henry, de Leon, Mony J., Glodzik, Lidia, De Santi, Susan, Doraiswamy, P. Murali, Petrella, Jeffrey R., Borges-Neto, Salvador, Wong, Terence Z., Coleman, Edward, Smith, Charles D., Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Porsteinsson, Anton P., Goldstein, Bonnie S., Martin, Kim, Makino, Kelly M., Ismail, M. Saleem, Brand, Connie, Mulnard, Ruth A., Thai, Gaby, Mc-Adams-Ortiz, Catherine, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Levey, Allan I., Lah, James J., Cellar, Janet S., Burns, Jeffrey M., Swerdlow, Russell H., Brooks, William M., Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H. S., Lu, Po H., Bartzokis, George, Graff-Radford, Neill R., Parfitt, Francine, Kendall, Tracy, Johnson, Heather, Farlow, Martin R., Hake, Ann Marie, Matthews, Brandy R., Brosch, Jared R., Herring, Scott, Hunt, Cynthia, van Dyck, Christopher H., Carson, Richard E., MacAvoy, Martha G., Varma, Pradeep, Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Hsiung, Ging-Yuek Robin, Feldman, Howard, Mudge, Benita, Assaly, Michele, Finger, Elizabeth, Pasternack, Stephen, Rachisky, Irina, Trost, Dick, Kertesz, Andrew, Bernick, Charles, Munic, Donna, Mesulam, Marek-Marsel, Lipowski, Kristine, Weintraub, Sandra, Bonakdarpour, Borna, Kerwin, Diana, Wu, Chuang-Kuo, Johnson, Nancy, Sadowsky, Carl, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Yesavage, Jerome, Taylor, Joy L., Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N., Belden, Christine M., Jacobson, Sandra A., Sirrel, Sherye A., Kowall, Neil, Killiany, Ronald, Budson, Andrew E., Norbash, Alexander, Johnson, Patricia Lynn, Obisesan, Thomas O., Wolday, Saba, Allard, Joanne, Lerner, Alan, Ogrocki, Paula, Tatsuoka, Curtis, Fatica, Parianne, Fletcher, Evan, Maillard, Pauline, Olichney, John, DeCarli, Charles, Carmichael, Owen, Kittur, Smita, Borrie, Michael, Lee, T -Y, Bartha, Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Potkin, Steven G., Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Burke, Anna, Trncic, Nadira, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W., Kataki, Maria, Adeli, Anahita, Zimmerman, Earl A., Celmins, Dzintra, Brown, Alice D., Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Flashman, Laura A., Seltzer, Marc, Hynes, Mary L., Santulli, Robert B., Sink, Kaycee M., Gordineer, Leslie, Williamson, Jeff D., Garg, Pradeep, Watkins, Franklin, Ott, Brian R., Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J., Miller, Bruce L., Perry, David, Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Relkin, Norman, Chaing, Gloria, Lin, Michael, Ravdin, Lisa, Smith, Amanda, Raj, Balebail Ashok, and Fargher, Kristin

Abstract

The Clusterin (CLU) gene, also known as apolipoprotein J (ApoJ), is currently the third most associated late-onset Alzheimer’s disease (LOAD) risk gene. However, little was known about the possible effect of CLU genetic variants on AD pathology in brain. Here, we evaluated the interaction between 7 CLU SNPs (covering 95% of genetic variations) and the role of CLU in β-amyloid (Aβ) deposition, AD-related structure atrophy, abnormal glucose metabolism on neuroimaging and CSF markers to clarify the possible approach by that CLU impacts AD. Finally, four loci (rs11136000, rs1532278, rs2279590, rs7982) showed significant associations with the Aβ deposition at the baseline level while genotypes of rs9331888 (P = 0.042) increased Aβ deposition. Besides, rs9331888 was significantly associated with baseline volume of left hippocampus (P = 0.014). We then further validated the association with Aβ deposition in the AD, mild cognitive impairment (MCI), normal control (NC) sub-groups. The results in sub-groups confirmed the association between CLU genotypes and Aβ deposition further. Our findings revealed that CLU genotypes could probably modulate the cerebral the Aβ loads on imaging and volume of hippocampus. These findings raise the possibility that the biological effects of CLU may be relatively confined to neuroimaging trait and hence may offer clues to AD.

Published
2016
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48. Early role of vascular dysregulation on late-onset Alzheimer's disease based on multifactorial data-driven analysis

Author

Iturria-Medina, Y., Sotero, R. C., Toussaint, P. J., Mateos-Pérez, J. M., Evans, A. C., Weiner, Michael W., Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Saykin, Andrew J., Morris, John, Shaw, Leslie M., Khachaturian, Zaven, Sorensen, Greg, Kuller, Lew, Raichle, Marc, Paul, Steven, Davies, Peter, Fillit, Howard, Hefti, Franz, Holtzman, Davie, Mesulam, M Marcel, Potter, William, Snyder, Peter, Schwartz, Adam, Montine, Tom, Thomas, Ronald G., Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Jiminez, Gus, Harvey, Danielle, Bernstein, Matthew, Fox, Nick, Thompson, Paul, Schuff, Norbert, Borowski, Bret, Gunter, Jeff, Senjem, Matt, Vemuri, Prashanthi, Jones, David, Kantarci, Kejal, Ward, Chad, Koeppe, Robert A., Foster, Norm, Reiman, Eric M., Chen, Kewei, Mathis, Chet, Landau, Susan, Cairns, Nigel J., Householder, Erin, Taylor-Reinwald, Lisa, Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M., Potkin, Steven, Shen, Li, Faber, Kelley, Kim, Sungeun, Nho, Kwangsik, Thal, Leon, Buckholtz, Neil, Albert, Marylyn, Frank, Richard, Hsiao, John, Kaye, Jeffrey, Quinn, Joseph, Lind, Betty, Carter, Raina, Dolen, Sara, Schneider, Lon S., Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Fleisher, Adam, Heidebrink, Judith L., Lord, Joanne L., Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Doody, Rachelle S., Villanueva-Meyer, Javier, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Ances, Beau, Carroll, Maria, Leon, Sue, Mintun, Mark A., Schneider, Stacy, Oliver, Angela, Marson, Daniel, Griffith, Randall, Clark, David, Geldmacher, David, Brockington, John, Roberson, Erik, Grossman, Hillel, Mitsis, Effie, de Toledo-Morrell, Leyla, Shah, Raj C., Duara, Ranjan, Varon, Daniel, Greig, Maria T., Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, D'Agostino, Daniel, Kielb, Stephanie, Galvin, James E., Cerbone, Brittany, Michel, Christina A., Rusinek, Henry, de Leon, Mony J., Glodzik, Lidia, De Santi, Susan, Doraiswamy, P. Murali, Petrella, Jeffrey R., Wong, Terence Z., Arnold, Steven E., Karlawish, Jason H., Wolk, David, Smith, Charles D., Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Lopez, Oscar L., Oakley, MaryAnn, Simpson, Donna M., Porsteinsson, Anton P., Goldstein, Bonnie S., Martin, Kim, Makino, Kelly M., Ismail, M. Saleem, Brand, Connie, Mulnard, Ruth A., Thai, Gaby, Mc-Adams-Ortiz, Catherine, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Diaz-Arrastia, Ramon, King, Richard, Weiner, Myron, Martin-Cook, Kristen, DeVous, Michael, Levey, Allan I., Lah, James J., Cellar, Janet S., Burns, Jeffrey M., Anderson, Heather S., Swerdlow, Russell H., Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H. S., Lu, Po H., Bartzokis, George, Graff-Radford, Neill R., Parfitt, Francine, Kendall, Tracy, Johnson, Heather, Farlow, Martin R., Hake, AnnMarie, Matthews, Brandy R., Herring, Scott, Hunt, Cynthia, van Dyck, Christopher H., Carson, Richard E., MacAvoy, Martha G., Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Hsiung, Ging-Yuek Robin, Feldman, Howard, Mudge, Benita, Assaly, Michele, Kertesz, Andrew, Rogers, John, Bernick, Charles, Munic, Donna, Kerwin, Diana, Mesulam, Marek-Marsel, Lipowski, Kristine, Wu, Chuang-Kuo, Johnson, Nancy, Sadowsky, Carl, Martinez, Walter, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Frey, Meghan, Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N., Belden, Christine M., Jacobson, Sandra A., Sirrel, Sherye A., Kowall, Neil, Killiany, Ronald, Budson, Andrew E., Norbash, Alexander, Johnson, Patricia Lynn, Allard, Joanne, Lerner, Alan, Ogrocki, Paula, Hudson, Leon, Fletcher, Evan, Carmichael, Owen, Olichney, John, DeCarli, Charles, Kittur, Smita, Borrie, Michael, Lee, T-Y, Bartha, Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Potkin, Steven G., Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W., Kataki, Maria, Adeli, Anahita, Zimmerman, Earl A., Celmins, Dzintra, Brown, Alice D., Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Santulli, Robert B., Kitzmiller, Tamar J., Schwartz, Eben S., Sink, Kaycee M., Williamson, Jeff D., Garg, Pradeep, Watkins, Franklin, Ott, Brian R., Querfurth, Henry, Tremont, Geoffrey, Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J., Miller, Bruce L., Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Finger, Elizabether, Pasternak, Stephen, Rachinsky, Irina, Drost, Dick, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Schultz, Susan K., Ponto, Laura L. Boles, Shim, Hyungsub, Smith, Karen Elizabeth, Relkin, Norman, Chaing, Gloria, Raudin, Lisa, Smith, Amanda, Fargher, Kristin, Raj, Balebail Ashok, Neylan, Thomas, Grafman, Jordan, Davis, Melissa, Morrison, Rosemary, Hayes, Jacqueline, Finley, Shannon, Friedl, Karl, Fleischman, Debra, Arfanakis, Konstantinos, James, Olga, Massoglia, Dino, Fruehling, J. Jay, Harding, Sandra, Peskind, Elaine R., Petrie, Eric C., Li, Gail, Yesavage, Jerome A., Taylor, Joy L., and Furst, Ansgar J.

Abstract

Multifactorial mechanisms underlying late-onset Alzheimer's disease (LOAD) are poorly characterized from an integrative perspective. Here spatiotemporal alterations in brain amyloid-β deposition, metabolism, vascular, functional activity at rest, structural properties, cognitive integrity and peripheral proteins levels are characterized in relation to LOAD progression. We analyse over 7,700 brain images and tens of plasma and cerebrospinal fluid biomarkers from the Alzheimer's Disease Neuroimaging Initiative (ADNI). Through a multifactorial data-driven analysis, we obtain dynamic LOAD–abnormality indices for all biomarkers, and a tentative temporal ordering of disease progression. Imaging results suggest that intra-brain vascular dysregulation is an early pathological event during disease development. Cognitive decline is noticeable from initial LOAD stages, suggesting early memory deficit associated with the primary disease factors. High abnormality levels are also observed for specific proteins associated with the vascular system's integrity. Although still subjected to the sensitivity of the algorithms and biomarkers employed, our results might contribute to the development of preventive therapeutic interventions.

Published
2016
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49. Free the Bun: Prevalence of Alopecia Among Active Duty Service Women, Fiscal Years 2010-2019.

Author

Korona-Bailey, Jessica, Banaag, Amanda, Nguyen, Dana R, Pasieka, Helena, and Koehlmoos, Tracey Pérez

Subjects
*BALDNESS, *WOMEN military personnel, *HAIR diseases, *WOMEN & the military, UNITED States armed forces
Abstract

Introduction Active duty service women (ADSW) constitute 16% of the force. The prevalence of alopecia, a dermatologic condition characterized by hair loss, is understudied in regard to hairstyle regulations across the U.S. military services. Alopecia has several causes; one of which is due to tension on the scalp secondary to tight hairstyles. In the U.S. alopecia has a lifetime prevalence of 1.7-2.1%; no previous studies which evaluated this condition in service women were found. Materials and Methods We used the Military Health System Data Repository to perform a retrospective study to assess the prevalence of alopecia in ADSW from fiscal years (FYs) 2010 to 2019. Statistical analyses included descriptive statistics on patient demographics and trend analysis on the prevalence of alopecia over the 10-year study period. Results A total of 498,219 ADSW were identified over the 10-year study period, of which 2.40% had a diagnosis of alopecia. Overall, the prevalence of alopecia decreases over the 10-year period, with two observed periods of slight increase (FY 2013 to 2014 and FY 2018 to 2019) when comparing prevalence year-to-year. Of those diagnosed, the majority were young, Black, with a senior enlisted rank, and in the U.S. Army. Conclusion The prevalence of alopecia in ADSW is slightly higher than that in civilian populations and is most likely underreported. It is more commonly diagnosed in Black women than would be expected based on ratios of this population in military service. Policy changes to ensure that traction alopecia is a qualifying medical condition for Veterans Affairs disability compensation, mechanisms are in place for more specific coding in the electronic medical record, and treatment options to be covered by TRICARE are recommended. All U.S. military services should consider updating and evaluating regulations to improve the health and quality of life of ADSW. [ABSTRACT FROM AUTHOR]

Published
2023
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50. Ferritin levels in the cerebrospinal fluid predict Alzheimer's disease outcomes and are regulated by APOE

Author

Ayton, Scott, Faux, Noel G., Bush, Ashley I., Weiner, Michael W., Aisen, Paul, Petersen, Ronald, Jack Jr., Clifford R., Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Saykin, Andrew J., Morris, John, Shaw, Leslie M., Khachaturian, Zaven, Sorensen, Greg, Kuller, Lew, Raichle, Marc, Paul, Steven, Davies, Peter, Fillit, Howard, Hefti, Franz, Holtzman, Davie, Marcel Mesulam, M., Potter, William, Snyder, Peter, Schwartz, Adam, Montine, Tom, Thomas, Ronald G., Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Jiminez, Gus, Harvey, Danielle, Bernstein, Matthew, Fox, Nick, Thompson, Paul, Schuff, Norbert, Borowski, Bret, Gunter, Jeff, Senjem, Matt, Vemuri, Prashanthi, Jones, David, Kantarci, Kejal, Ward, Chad, Koeppe, Robert A., Foster, Norm, Reiman, Eric M., Chen, Kewei, Mathis, Chet, Landau, Susan, Cairns, Nigel J., Householder, Erin, Taylor-Reinwald, Lisa, Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M., Potkin, Steven, Shen, Li, Faber, Kelley, Kim, Sungeun, Nho, Kwangsik, Thal, Leon, Buckholtz, Neil, Albert, Marylyn, Frank, Richard, Hsiao, John, Kaye, Jeffrey, Quinn, Joseph, Lind, Betty, Carter, Raina, Dolen, Sara, Schneider, Lon S., Pawluczyk, Sonia, Beccera, Mauricio, Teodoro, Liberty, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Fleisher, Adam, Heidebrink, Judith L., Lord, Joanne L., Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Doody, Rachelle S., Villanueva-Meyer, Javier, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Ances, Beau, Carroll, Maria, Leon, Sue, Mintun, Mark A., Schneider, Stacy, Oliver, Angela, Marson, Daniel, Griffith, Randall, Clark, David, Geldmacher, David, Brockington, John, Roberson, Erik, Grossman, Hillel, Mitsis, Effie, deToledo-Morrell, Leyla, Shah, Raj C., Duara, Ranjan, Varon, Daniel, Greig, Maria T., Roberts, Peggy, Albert, Marilyn, Onyike, Chiadi, 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Abstract

Brain iron elevation is implicated in Alzheimer's disease (AD) pathogenesis, but the impact of iron on disease outcomes has not been previously explored in a longitudinal study. Ferritin is the major iron storage protein of the body; by using cerebrospinal fluid (CSF) levels of ferritin as an index, we explored whether brain iron status impacts longitudinal outcomes in the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. We show that baseline CSF ferritin levels were negatively associated with cognitive performance over 7 years in 91 cognitively normal, 144 mild cognitive impairment (MCI) and 67 AD subjects, and predicted MCI conversion to AD. Ferritin was strongly associated with CSF apolipoprotein E levels and was elevated by the Alzheimer's risk allele, APOE-ɛ4. These findings reveal that elevated brain iron adversely impacts on AD progression, and introduce brain iron elevation as a possible mechanism for APOE-ɛ4 being the major genetic risk factor for AD.

Published
2015
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