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101. 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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108. Refractive change and photorefractive keratectomy treatment for a late traumatic flap loss.

Author

Meng-Yin Lin, Chang, David C. K., Hsiao, John C. J., and I.-Jong Wang

Subjects
CASE studies, LASIK, VISION, EYE care, QUALITATIVE research
Abstract

The article presents a case study of 28-year-old woman who suffered a flap loss caused by a scratch from a cat's paw. She undergone laser-assisted situ in keratomileusis (LASIK) and received a photorefractive keratectomy (PRK) re-treatment. After six months of LASIK, her vision was normal in both eyes. The article discusses flap loss related problems of LASIK.

Published
2010
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110. Metabolic Changes Associated With Second-Generation Antipsychotic Use in Alzheimer's Disease Patients: The CATIE-AD Study.

Author

Ling Zheng, Mack, Wendy J., Dagerman, Karen S., Hsiao, John K., Lebowitz, Barry O., Lyketsos, Constantine G., Stroup, Scott, Sultzer, David L., Tariot, Pierre N., Vigen, Cheryl, and Schneider, Lon S.

Subjects
ANTIPSYCHOTIC agents, DRUG side effects, ALZHEIMER'S patients, PATHOLOGICAL psychology, DISEASE complications, SCHIZOPHRENIA, METABOLIC disorders, PRESENILE dementia, OLANZAPINE, LOW-cholesterol diet
Abstract

Objective: The second-generation antipsychotics are associated with metabolic abnormalities in patients with schizophrenia. Elderly patients with Alzheimer's disease are frequently treated with these antipsychotics, but limited data are available on their metabolic effects. Method: The authors assessed 186 male and 235 female Alzheimer's disease outpatients from the Clinical Antipsychotic Trials of Intervention Effectiveness—Alzheimer's Disease (CATIE-AD) for changes in weight, waist circumference, blood pressure, fasting glucose, and lipids in relation to duration of second-generation antipsychotic use (i.e., olanzapine, quetiapine, and risperidone) throughout the 36-week trial, using logistic regression and mixedeffects models. Results: Women showed significant weight gain (0.14 Ib/week of use) while change was nonsignificant in men. Clinically significant weight gain (i,e., ≥7% of body weight) was seen among patients with antipsychotic use ≤12. weeks (odds ratio [OR]=1.56, 95% Cl=0.53 to 4.58), between 12 and 24 weeks (0R=2.89, 95% C1=0.97 to 8.64), and >24 weeks (OR= 3.38, 95% Cl-1.24 to 9.23) relative to patients who did not use antipsychotics during the trial. Olanzapine and quetiapine treatments were significantly associated with weight gain (0.12 and 0.14 Ib/week, respectively), in addition, olanzapine was significantly associated with decreases in HDL cholesterol (-0.19 mg/dl/week) and increased girth (0.07 inches/week) relative to the placebo group. No treatment effects were noted for changes in blood pressure, glucose, and triglycerides. Conclusion: Second-generation antipsychotic use was associated with weight gain in women, with olanzapine and quetiapine in particulan and with unfavorable change in HDL cholesterol and girth with oianzapine. The potential consequences of these effects suggest that patients with Alzheimer's disease treated with second-generation antipsychotics should be monitored closely. [ABSTRACT FROM AUTHOR]

Published
2009
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117. 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, D'Agostino II, Daniel, Kielb, Stephanie, Galvin, James E., Cerbone, Brittany, Michel, Christina A., Rusinek, Henry, de Leon, Mony J, Glodzik, Lidia, De Santi, Susan, Murali Doraiswamy, P., 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., Saleem Ismail, M., 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, Ann Marie, 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, Scott Turner, Raymond, 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, Elizabeth Smith, Karen, Relkin, Norman, Chaing, Gloria, Raudin, Lisa, Smith, Amanda, Fargher, Kristin, Ashok Raj, Balebail, Neylan, Thomas, Grafman, Jordan, Davis, Melissa, Morrison, Rosemary, Hayes, Jacqueline, Finley, Shannon, Friedl, Karl, Fleischman, Debra, Arfanakis, Konstantinos, James, Olga, Massoglia, Dino, Jay Fruehling, J., Harding, Sandra, Peskind, Elaine R., Petrie, Eric C., Li, Gail, Yesavage, Jerome A., Taylor, Joy L., and Furst, Ansgar J.

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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118. Large-scale genomics unveil polygenic architecture of human cortical surface area

Author

Chen, Chi-Hua, Peng, Qian, Schork, Andrew J., Lo, Min-Tzu, Fan, Chun-Chieh, Wang, Yunpeng, Desikan, Rahul S., Bettella, Francesco, Hagler, Donald J., McCabe, Connor, Chang, Linda, Akshoomoff, Natacha, Newman, Erik, Ernst, Thomas, Van Zijl, Peter, Kuperman, Joshua, Murray, Sarah, Bloss, Cinnamon, Appelbaum, Mark, Gamst, Anthony, Thompson, Wesley, Bartsch, Hauke, Weiner, Michael, 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, Carrillo, Maria, Kuller, Lew, Raichle, Marc, Paul, Steven, Davies, Peter, Fillit, Howard, Hefti, Franz, Holtzman, Davie, Mesulman, M. Marcel, Potter, William, Snyder, Peter J., 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, 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 M.Y., Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M., Potkin, Steven, Shen, Li, Faber, Kelley, Kim, Sungeun, Nho, Kwangsik, Thal, Leon, Frank, Richard, Buckholtz, Neil, Albert, Marilyn, Hsiao, John, Westlye, Lars T., Kremen, William S., Jernigan, Terry L., Hellard, Stephanie Le, Steen, Vidar M., Espeseth, Thomas, Huentelman, Matt, Håberg, Asta K., Agartz, Ingrid, Djurovic, Srdjan, Andreassen, Ole A., Schork, Nicholas, and Dale, Anders M.

Abstract

Little is known about how genetic variation contributes to neuroanatomical variability, and whether particular genomic regions comprising genes or evolutionarily conserved elements are enriched for effects that influence brain morphology. Here, we examine brain imaging and single-nucleotide polymorphisms (SNPs) data from ∼2,700 individuals. We show that a substantial proportion of variation in cortical surface area is explained by additive effects of SNPs dispersed throughout the genome, with a larger heritable effect for visual and auditory sensory and insular cortices (h2∼0.45). Genome-wide SNPs collectively account for, on average, about half of twin heritability across cortical regions (N=466 twins). We find enriched genetic effects in or near genes. We also observe that SNPs in evolutionarily more conserved regions contributed significantly to the heritability of cortical surface area, particularly, for medial and temporal cortical regions. SNPs in less conserved regions contributed more to occipital and dorsolateral prefrontal cortices.

Published
2015
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122. The Mechanisms of Action of Lithium: II. Effects on Adenylate Cyclase Activity and β-Adrenergic Receptor Binding in Normal Subjects

Author

Risby, Emile D., Hsiao, John K., Manji, Husseini K., Bitran, Jose, Moses, Frances, Zhou, Dong Feng, and Potter, William Z.

Abstract

• As part of a study of the effects of lithium carbonate on neurochemical function in man, platelet and lymphocyte adenylate cyclase activity and lymphocyte β-adrenergic receptor binding characteristics were determined before and after 2 weeks of lithium treatment in 10 normal volunteers. Lithium had differential effects on platelet and lymphocyte adenylate cyclase activity. In platelets, basal and stimulated (guanyl imidodiphosphate [Gpp[NH]p] or cesium fluoride) adenylate cyclase activity was significantly augmented by lithium treatment. By contrast, in lymphocytes, Gpp(NH)p- and cesium fluoride—stimulated adenylate cyclase activity was unaffected, while basal activity was decreased modestly after lithium. These results are consistent with preclinical studies that suggest that lithium's effects on adenylate cyclase activity are specific with respect to tissue and brain region and that lithium may interfere with guanine nucleotide binding (G) protein function. Lithium treatment significantly increased the ratio of low- to high-affinity dissociation constants for agonist displacement of antagonist binding to lymphocyte β-adrenergic receptors (thought to reflect coupling between the β-adrenergic receptor and stimulatory G protein). Lithium had significant effects on measures associated with signal transduction that might be contrasted to its more subtle effects on neuronal function (norepinephrine release) and neuroendocrine systems (responses to serotoninergic challenge) in these same subjects (reported in a companion article). Lithium's primary site of action may be on signal transduction mechanisms. These effects subsequently may be manifested in changes in neurotransmitter function that may be important to lithium's mood-stabilizing actions.

Published
1991
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123. The Mechanisms of Action of Lithium: I. Effects on Serotoninergic and Noradrenergic Systems in Normal Subjects

Author

Manji, Husseini K., Hsiao, John K., Risby, Emile D., Oliver, Jerry, Rudorfer, Matthew V., and Potter, William Z.

Abstract

• The effects of 2 weeks of lithium carbonate administration at therapeutic plasma levels were examined in 11 normal volunteers. Serotoninergic function before and after lithium administration was assessed using low-dose intravenous clomipramine hydrochloride challenge, while urinary and plasma metabolites of norepinephrine (NE) were used to assess noradrenergic systems. Long-term lithium administration in normal subjects did not significantly or consistently enhance serotonin-mediated neuroendocrine responses but did increase measures related to neuronal release of NE. No statistically significant effects of lithium on prolactin, corticotropin, or cortisol responses to serotoninergic challenge could be detected. The probability of a type II error was assessed, and a doubling of prolactin level was unlikely to have been missed, although more modest increases (<75%) could have been overlooked. After 2 weeks of lithium administration, there were significant increases in 24-hour urinary excretion of NE, normetanephrine, and fractional NE release, compatible with increased neuronal release of NE and a lithium-induced subsensitivity in α2-adrenergic receptor function. These changes were not statistically significant after 1 week of administration, suggesting that increased NE release is characteristic of long rather than short-term lithium administration. Since previous reports have demonstrated enhanced prolactin responses after short but not long-term lithium use, the present study points to temporal specificity in lithium's effects on both serotoninergic and noradrenergic function. Lithium's effects on NE release were consistent but small (a 16% increase), while its effects on serotoninergic responses were larger (a 50% increase in prolactin responses) but quite inconsistent, suggesting that neither of these systems is the primary site of action of lithium.

Published
1991
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124. Cerebrospinal Fluid and Plasma Monoamine Metabolites and Their Relation to Psychosis: Implications for Regional Brain Dysfunction in Schizophrenia

Author

Pickar, David, Breier, Alan, Hsiao, John K., Doran, Allen R., Wolkowitz, Owen M., Pato, Carlos N., Konicki, P. Eric, and Potter, William Z.

Abstract

• The relationship between central (cerebrospinal fluid [CSF]) and peripheral (plasma) monoaminergic metabolites and psychotic symptoms was examined in 22 drug-free schizophrenic inpatients. The CSF homovanillic acid levels did not differ significantly between patients and normal controls (n = 33). The CSF homovanillic acid levels, however, were negatively correlated with ratings of psychosis and positive symptoms, and the CSF homovanillic acid and 5-hydroxyindoleacetic acid levels correlated negatively with individual deficit symptoms. Stepwise and hierarchical multiple-regression analysis revealed that among monoaminergic measures, only the CSF and plasma homovanillic acid levels contributed significantly to the total Brief Psychiatric Rating Scale and positive symptom variance with negative and positive partial correlations, respectively. Levels of CSF 3-methoxy-4-hydroxyphenylglycol, but not of CSF norepinephrine, were significantly elevated in the schizophrenic patients compared with controls, and plasma 3-methoxy-4-hydroxyphenylglycol levels were positively correlated with negative symptoms. We discuss the potential implications of these findings for a model of dopaminergic dysfunction in schizophrenia involving distinct cortical and subcortical contributions.

Published
1990
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125. Effects of Renal Clearance on Plasma Concentrations of Homovanillic Acid: Methodologic Cautions

Author

Potter, William Z., Hsiao, John K., and Goldman, Samuel M.

Abstract

• Recently, there has been considerable interest in plasma concentrations of homovanillic acid (HVA) in various psychiatric disorders. Homovanillic acid is a weak organic acid, and its excretion probably resembles that of other organic acids (eg, paminohippuric acid) that are actively secreted by the kidney. Alterations in renal plasma flow can affect clearance of organic acids, resulting in changes in plasma concentrations. In our study, concentrations of plasma HVA and urinary HVA (from 24hour urine collections) were measured in 20 prepubescent boys who received 3 weeks of placebo, dextroamphetamine sulfate, and fenfluramine hydrochloride in a randomized, double-blind, counterbalanced study of the treatment of attention-deficit disorder. Plasma HVA concentrations were significantly lower during fenfluramine treatment than during amphetamine treatment. This difference, however, seemed to be caused by alterations in renal clearance of HVA rather than changes in production. Whole-body production of HVA, as indexed by total urinary HVA excretion, was unaffected by the different treatments, while renal clearance of HVA did differ significantly between amphetamine and fenfluramine treatment. It seems that alterations in renal clearance can affect plasma HVA concentrations, which should be taken into account when plasma HVA is studied.

Published
1989
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126. Diagnosing Diagnoses: Receiver Operating Characteristic Methods and Psychiatry

Author

Hsiao, John K., Bartko, John J., and Potter, William Z.

Abstract

With every issue of the Archives, the reader is inundated with psychiatric research: new treatments, new biological abnormalities, new diagnostic methods, new diagnoses—the list seems endless. It is difficult to conceive of anyone, except, of course, our dedicated Editor, who bothers to read every article in every issue. Indeed, it would be a rare individual who had the time to read every abstract. In the current issue of the Archives, Mossman and Somoza1 reexamine the dexamethasone suppression test (DST) using a statistical method that is new to psychiatry, namely, receiver operating characteristic (ROC). Using this method, they are able to demonstrate that there is significant variability in the performance of the DST among different psychiatric centers. As with any statistical method, ROC involves more than a little mathematics, and the natural question as one leafs through the See also p 653. Archives is "Why should I bother with this?"

Published
1989
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127. Monoamine Neurotransmitter Interactions and the Prediction of Antidepressant Response

Author

Hsiao, John K., Agren, Hans, Bartko, John J., Rudorfer, Matthew V., Linnoila, Markku, and Potter, William Z.

Abstract

• Clinical studies of monoamine neurotransmitter function in depression have concentrated on individual monoamines without focusing on interactions between monoamine systems. Virtually all modern studies have found significant correlations between monoamine metabolite concentrations in cerebrospinal fluid (CSF). These correlations should in part reflect interactions between central monoamine systems. In the present analysis, CSF had been obtained from depressed patients before (n = 40) and after (n =36) antidepressant treatment. The patients were grouped based on their response to treatment. Absolute concentrations of CSF monoamine metabolites (homovanillic acid, 5-hydroxyindoleacetic acid, and 3-methoxy-4-hydroxyphenylethyleneglycol) did not differ between the two groups before or after treatment. However, when correlations between metabolites were compared, nonresponders to treatment differed considerably from responders. In responders, as in previously described normal populations, all three metabolites correlated with one another before and after treatment, and treatment-induced changes in metabolite concentrations also correlated with one another. In contrast, metabolites in nonresponders did not correlate with one another before treatment, nor did treatment-induced changes correlate with one another in this group. Furthermore, correlations between treatment-induced changes in metabolites differed significantly between responders and nonresponders, and there was a trend for pretreatment correlations to differ as well. The lack of correlation between monoamine metabolites in nonresponders suggests that interactions between monoamine systems may be disrupted in these individuals. Using CSF metabolite correlations to study neurotransmitter interactions may have clinical relevance and yields information not available from examining neurotransmitters in isolation.

Published
1987
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134. International Contact Lens Prescribing in 2009.

Author

Morgan, Philip B., Woods, Craig A., Tranoudis, Ioannis G., Helland, Magne, Efron, Nathan, Knajian, Razmig, Grupcheva, Christina N., Jones, Deborah, Tan, Kah-Ooi, Pesinova, Alice, Ravn, Ole, Santodomingo, Jacinto, Vodnyanszky, Edit, Erdinest, Nir, Hreinsson, Hreinn Ingi, Montani, Giancarlo, Itoi, Motozumi, Bendoriene, Jolanta, Van der Worp, Eef, and Hsiao, John

Subjects
CONTACT lenses, CONSUMERS, DEMOGRAPHIC surveys, SOFT contact lenses, OPHTHALMIC lenses
Abstract

The article reports on more than 25,000 contact lens prescriptions globally in 2009. Wearer demographics were reportedly stable with female patients accounting for two-thirds of users and the oldest and youngest patients being 95 years old and 6 months old, respectively. It is stated that rigid, soft and extended wear contact lenses respectively accounted for 8 percent, more than 90 percent and less than 10 percent of new fits. The widely varying frequency of lens replacements is also noted.

Published
2010

135. Dr. Lieberman and Colleagues Reply.

Author

Lieberman, Jeffrey A., Stroup, T. Scott, McEvoy, Joseph P., Swartz, Marvin S., Rosenheck, Roberta A., Perkins, Diana O., Keefe, Richard S. E., Davis, Sonia M., Davis, Clarence E., Hsiao, John, Severe, Joanne, and Lebowitz, Barry D.

Subjects
LETTERS to the editor, DRUGS
Abstract

A reply to a letter to the editor is presented with regards to the misconceptions of Clinical Antipsychotic Trials of Intervention Effectiveness on doses of medication, published in the March 2006 issue.

Published
2006
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136. Clinical Response to Clozapine in Patients With Schizophrenia

Author

Pickar, David, Litman, Robert E., Hong, Walter W., Su, Tom P., Weissman, Ellen M., Hsiao, John K., and Potter, William Z.

Abstract

One of the take-home messages from our recent report regarding the clinical and biological effects of the atypical neuroleptic, clozapine, was that the admixture of clozapine's effects on dopaminergic, serotonergic, and noradrenergic systems may underlie its unique efficacy in otherwise poorly responsive patients with schizophrenia.1 We agree with a suggestion by R. W. Pies, MD, (unpublished communication to the Archives, May 1992) that clozapine's diverse pharmacologic properties indicate strategies for augmentation of neuroleptic drugs in treatment-resistant patients and that thioridazine or mesoridazine besylate may be particularly useful, given their relatively low incidence of extrapyramidal side effects.Whereas much attention has been given to the 5-hydroxytryptamine2 (5-HT2) antagonism of clozapine, including the ratio of 5-HT2 to D2 affinities as a predictor of neuroleptic atypicality,2 we have noted that clozapine's relatively potent α2-antagonism (putatively contributing to observed increases in norepinephrine turnover) is distinct among

Published
1994
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138. Lithium Treatment Increases Norepinephrine Turnover in the Plasma of Healthy Subjects-Reply

Author

Manji, HUSSEINI K., Hsiao, John K., Potter, William Z., and Risby, Emile D.

Abstract

IN REPLY.— We read with interest the letter substantiating our finding that subchronic treatment of normal subjects with lithium is associated with enhanced release of NE. We demonstrated that 2 weeks' (but not 1 week's) lithium administration significantly increased levels of urinary NE, NMN, and a derived measure of NE release ([NE +NMN]/ [NE+NMN+VMA + MHPG], in which VMA indicates vanillylmandelic acid, and MHPG, 3-methoxy-4-hydroxyphenylglycol). Interestingly, lithium produced a nearsignificant 20% increase in levels of NE in plasma but did not affect levels of MHPG in plasma.In their study of seven healthy volunteers, Poirier-Littre et al observe that 3-week treatment with lithium results in significant increases in levels of total DOPEG (66%) and sulfate-conjugated DOPEG (71%) in plasma. These findings are of considerable interest because Goldstein et al1 have recently demonstrated that DOPEG in plasma (DHPG) is derived primarily from sympathetic nerves and that procedures activating the sympathetic nervous system (eg,

Published
1993
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141. Use of Antipsychotics Pre- and Post-Dissemination of CATIE Data.

Author

Cascade EF, Kalali AH, Lieberman J, Hsiao J, Keefe R, and Stroup S

Abstract

We investigated the share of branded and generic antipsychotics before and after the publication of the CATIE results in September, 2005. According to our data, the publication of the CATIE results has had very little impact on new patient starts. To determine the impact of CATIE on use of olanzapine (Zyprexa((R))) subsequent to first line therapy, we also examined product share for switch/add patients. We found that since the publication of the CATIE results, the use of olanzapine has stabilized, following a decline subsequent to first line therapy, and may potentially be growing very slowly. An expert commentary is provided on the data.

Published
2007

142. Disparate Biochemical Actions of Electroconvulsive Therapy and Antidepressant Drugs.

Author

Rudorfer MV, Risby ED, Hsiao JK, Linnoila M, and Potter WZ

Abstract

Electroconvulsive therapy (ECT) effects on monoamine transmitter metabolites in the cerebrospinal fluid (CSF) were evaluated in three patients after completion of a course of bilateral or unilateral ECT. Each patient had earlier undergone an unsuccessful trial with an antidepressant drug. Despite the disparate nature of the basic pharmacology of the antidepressant drugs used, common chronic effects were observed in the CSF, with reductions in 3-methoxy-4-hydroxyphenylglycol (MHPG) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations in all patients despite lack of therapeutic response. Homovanillic acid (HVA) changes were inconsistent. After ECT, however, no CSF changes were observed in the one nonresponder to that treatment. The two ECT responders showed marked increases in CSF 5-HIAA and HVA over their respective baselines, with an elevation in MHPG in one patient only. Further study of the mechanisms of action of ECT should focus on the serotonin and dopamine systems and on the differences between responders and nonresponders.

Published
1988

143. ECT and Neurological Disorders.

Author

Hsiao JK, Messenheimer JA, and Evans DL

Abstract

Clinicians become concerned when ECT is contemplated in an individual with a neurological disorder. In this review, the authors summarize the reports on the use of ECT in the presence of neurological disease. Because blood pressure, cerebral blood flow, and intracranial pressure rise with ECT, space-occupying lesions with increased intracranial pressure, cerebral aneurysm, recent head trauma, or active CNS infection pose special concerns for ECT treatment. In this review, we conclude that epilepsy and states with lowered seizure threshold may predispose to prolonged seizures. A history of head injury or stroke probably does not increase risk. Toxic/metabolic disorders are not contraindications to ECT, although correction of the underlying imbalance is a first priority. Extrapyramidal, demyelinating, and neuromuscular disorders pose little increased risk. Indeed, in Parkinson's Disease, ECT may be beneficial for the motor symptoms. As a general rule, it seems advisable to treat the underlying disorder prior to beginning ECT.

Published
1987

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