604 results on '"Villeneuve, Sylvia"'
Search Results
2. Atypical Brain Aging and Its Association With Working Memory Performance in Major Depressive Disorder
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Adamson, Chris, Adler, Sophie, Alexander-Bloch, Aaron F., Anagnostou, Evdokia, Anderson, Kevin M., Areces-Gonzalez, Ariosky, Astle, Duncan E., Auyeung, Bonnie, Ayub, Muhammad, Bae, Jong Bin, Ball, Gareth, Baron-Cohen, Simon, Beare, Richard, Bedford, Saashi A., Benegal, Vivek, Bethlehem, Richard A.I., Beyer, Frauke, Blangero, John, Cábez, Manuel Blesa, Boardman, James P., Borzage, Matthew, Bosch-Bayard, Jorge F., Bourke, Niall, Bullmore, Edward T., Calhoun, Vince D., Chakravarty, Mallar M., Chen, Christina, Chertavian, Casey, Chetelat, Gaël, Chong, Yap S., Corvin, Aiden, Costantino, Manuela, Courchesne, Eric, Crivello, Fabrice, Cropley, Vanessa L., Crosbie, Jennifer, Crossley, Nicolas, Delarue, Marion, Delorme, Richard, Desrivieres, Sylvane, Devenyi, Gabriel, Di Biase, Maria A., Dolan, Ray, Donald, Kirsten A., Donohoe, Gary, Dorfschmidt, Lena, Dunlop, Katharine, Edwards, Anthony D., Elison, Jed T., Ellis, Cameron T., Elman, Jeremy A., Eyler, Lisa, Fair, Damien A., Fletcher, Paul C., Fonagy, Peter, Franz, Carol E., Galan-Garcia, Lidice, Gholipour, Ali, Giedd, Jay, Gilmore, John H., Glahn, David C., Goodyer, Ian M., Grant, P.E., Groenewold, Nynke A., Gudapati, Shreya, Gunning, Faith M., Gur, Raquel E., Gur, Ruben C., Hammill, Christopher F., Hansson, Oskar, Hedden, Trey, Heinz, Andreas, Henson, Richard N., Heuer, Katja, Hoare, Jacqueline, Holla, Bharath, Holmes, Avram J., Huang, Hao, Ipser, Jonathan, Jack, Clifford R., Jr., Jackowski, Andrea P., Jia, Tianye, Jones, David T., Jones, Peter B., Kahn, Rene S., Karlsson, Hasse, Karlsson, Linnea, Kawashima, Ryuta, Kelley, Elizabeth A., Kern, Silke, Kim, Ki-Woong, Kitzbichler, Manfred G., Kremen, William S., Lalonde, François, Landeau, Brigitte, Lerch, Jason, Lewis, John D., Li, Jiao, Liao, Wei, Liston, Conor, Lombardo, Michael V., Lv, Jinglei, Mallard, Travis T., Marcelis, Machteld, Mathias, Samuel R., Mazoyer, Bernard, McGuire, Philip, Meaney, Michael J., Mechelli, Andrea, Misic, Bratislav, Morgan, Sarah E., Mothersill, David, Ortinau, Cynthia, Ossenkoppele, Rik, Ouyang, Minhui, Palaniyappan, Lena, Paly, Leo, Pan, Pedro M., Pantelis, Christos, Park, Min Tae M., Paus, Tomas, Pausova, Zdenka, Paz-Linares, Deirel, Binette, Alexa Pichet, Pierce, Karen, Qian, Xing, Qiu, Anqi, Raznahan, Armin, Rittman, Timothy, Rodrigue, Amanda, Rollins, Caitlin K., Romero-Garcia, Rafael, Ronan, Lisa, Rosenberg, Monica D., Rowitch, David H., Salum, Giovanni A., Satterthwaite, Theodore D., Schaare, H. Lina, Schabdach, Jenna, Schachar, Russell J., Schöll, Michael, Schultz, Aaron P., Seidlitz, Jakob, Sharp, David, Shinohara, Russell T., Skoog, Ingmar, Smyser, Christopher D., Sperling, Reisa A., Stein, Dan J., Stolicyn, Aleks, Suckling, John, Sullivan, Gemma, Thyreau, Benjamin, Toro, Roberto, Traut, Nicolas, Tsvetanov, Kamen A., Turk-Browne, Nicholas B., Tuulari, Jetro J., Tzourio, Christophe, Vachon-Presseau, Étienne, Valdes-Sosa, Mitchell J., Valdes-Sosa, Pedro A., Valk, Sofie L., van Amelsvoort, Therese, Vandekar, Simon N., Vasung, Lana, Vértes, Petra E., Victoria, Lindsay W., Villeneuve, Sylvia, Villringer, Arno, Vogel, Jacob W., Wagstyl, Konrad, Wang, Yin-Shan S., Warfield, Simon K., Warrier, Varun, Westman, Eric, Westwater, Margaret L., Whalley, Heather C., White, Simon R., Witte, A. Veronica, Yang, Ning, Yeo, B.T. Thomas, Yun, Hyuk Jin, Zalesky, Andrew, Zar, Heather J., Zettergren, Anna, Zhou, Juan H., Ziauddeen, Hisham, Zimmerman, Dabriel, Zugman, Andre, Zuo, Xi-Nian N., Ho, Natalie C.W., Nogovitsyn, Nikita, Metzak, Paul, Ballester, Pedro L., Hassel, Stefanie, Rotzinger, Susan, Poppenk, Jordan, Lam, Raymond W., Taylor, Valerie H., Milev, Roumen, Frey, Benicio N., Harkness, Kate L., Addington, Jean, and Kennedy, Sidney H.
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- 2024
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3. The neurophysiological brain-fingerprint of Parkinson’s disease
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Breitner, John, Poirier, Judes, Baillet, Sylvain, Bellec, Pierre, Bohbot, Véronique, Chakravarty, Mallar, Collins, Louis, Etienne, Pierre, Evans, Alan, Gauthier, Serge, Hoge, Rick, Ituria-Medina, Yasser, Multhaup, Gerhard, Münter, Lisa-Marie, Rajah, Natasha, Rosa-Neto, Pedro, Soucy, Jean-Paul, Vachon-Presseau, Etienne, Villeneuve, Sylvia, Amouyel, Philippe, Appleby, Melissa, Ashton, Nicholas, Auld, Daniel, Ayranci, Gülebru, Bedetti, Christophe, Beland, Marie-Lise, Blennow, Kaj, Westman, Ann Brinkmalm, Cuello, Claudio, Dadar, Mahsa, Daoust, Leslie-Ann, Das, Samir, Dauar-Tedeschi, Marina, De Beaumont, Louis, Dea, Doris, Descoteaux, Maxime, Dufour, Marianne, Farzin, Sarah, Ferdinand, Fabiola, Fonov, Vladimir, Gonneaud, Julie, Kat, Justin, Kazazian, Christina, Labonté, Anne, Lafaille-Magnan, Marie-Elyse, Lalancette, Marc, Lambert, Jean-Charles, Leoutsakos, Jeannie-Marie, Mahar, Laura, Mathieu, Axel, McSweeney, Melissa, Meyer, Pierre-François, Miron, Justin, Near, Jamie, NewboldFox, Holly, Nilsson, Nathalie, Orban, Pierre, Picard, Cynthia, Binette, Alexa Pichet, Poline, Jean-Baptiste, Rabipour, Sheida, Salaciak, Alyssa, Settimi, Matthew, Subramaniapillai, Sivaniya, Tam, Angela, Tardif, Christine, Théroux, Louise, Tremblay-Mercier, Jennifer, Tullo, Stephanie, Ulku, Irem, Vallée, Isabelle, Zetterberg, Henrik, Nair, Vasavan, Pruessner, Jens, Aisen, Paul, Anthal, Elena, Barkun, Alan, Beaudry, Thomas, Benbouhoud, Fatiha, Brandt, Jason, Carmo, Leopoldina, Carrier, Charles Edouard, Cheewakriengkrai, Laksanun, Courcot, Blandine, Couture, Doris, Craft, Suzanne, Dansereau, Christian, Debacker, Clément, Desautels, René, Dubuc, Sylvie, Duclair, Guerda, Eisenberg, Mark, El-Khoury, Rana, Faubert, Anne-Marie, Fontaine, David, Frappier, Josée, Frenette, Joanne, Gagné, Guylaine, Gervais, Valérie, Giles, Renuka, Gordon, Renee, Jack, Clifford, Jutras, Benoit, Khachaturian, Zaven, Knopman, David, Kostopoulos, Penelope, Lapalme, Félix, Lee, Tanya, Lepage, Claude, Leppert, Illana, Madjar, Cécile, Maillet, David, Maltais, Jean-Robert, Mathotaarachchi, Sulantha, Mayrand, Ginette, Michaud, Diane, Montine, Thomas, Morris, John, Pagé, Véronique, Pascoal, Tharick, Peillieux, Sandra, Petkova, Mirela, Pogossova, Galina, Rioux, Pierre, Sager, Mark, Saint-Fort, Eunice Farah, Savard, Mélissa, Sperling, Reisa, Tabrizi, Shirin, Tariot, Pierre, Teigner, Eduard, Thomas, Ronald, Toussaint, Paule-Joanne, Tuwaig, Miranda, Venugopalan, Vinod, Verfaillie, Sander, Vogel, Jacob, Wan, Karen, Wang, Seqian, Yu, Elsa, Beaulieu-Boire, Isabelle, Blanchet, Pierre, Bogard, Sarah, Bouchard, Manon, Chouinard, Sylvain, Cicchetti, Francesca, Cloutier, Martin, Dagher, Alain, Degroot, Clotilde, Desautels, Alex, Dion, Marie Hélène, Drouin-Ouellet, Janelle, Dufresne, Anne-Marie, Dupré, Nicolas, Duquette, Antoine, Durcan, Thomas, Fellows, Lesley K., Fon, Edward, Gagnon, Jean-François, Gan-Or, Ziv, Genge, Angela, Jodoin, Nicolas, Karamchandani, Jason, Lafontaine, Anne-Louise, Langlois, Mélanie, Leveille, Etienne, Lévesque, Martin, Melmed, Calvin, Monchi, Oury, Montplaisir, Jacques, Panisset, Michel, Parent, Martin, Pham-An, Minh-Thy, Postuma, Ronald, Pourcher, Emmanuelle, Rao, Trisha, Rivest, Jean, Rouleau, Guy, Sharp, Madeleine, Soland, Valérie, Sidel, Michael, Wing Sun, Sonia Lai, Thiel, Alexander, Vitali, Paolo, da Silva Castanheira, Jason, Wiesman, Alex I., Hansen, Justine Y., and Misic, Bratislav
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- 2024
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4. A prognostic risk score for development and spread of chronic pain
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Tanguay-Sabourin, Christophe, Fillingim, Matt, Guglietti, Gianluca V., Zare, Azin, Parisien, Marc, Norman, Jax, Sweatman, Hilary, Da-ano, Ronrick, Heikkala, Eveliina, Perez, Jordi, Karppinen, Jaro, Villeneuve, Sylvia, Thompson, Scott J., Martel, Marc O., Roy, Mathieu, Diatchenko, Luda, and Vachon-Presseau, Etienne
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- 2023
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5. How Do Modifiable Risk Factors Affect Alzheimer’s Disease Pathology or Mitigate Its Effect on Clinical Symptom Expression?
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Ourry, Valentin, Binette, Alexa Pichet, St-Onge, Frédéric, Strikwerda-Brown, Cherie, Chagnot, Audrey, Poirier, Judes, Breitner, John, Arenaza-Urquijo, Eider M., Rabin, Jennifer S., Buckley, Rachel, Gonneaud, Julie, Marchant, Natalie L., and Villeneuve, Sylvia
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- 2024
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6. Functional gradients of the medial parietal cortex in a healthy cohort with family history of sporadic Alzheimer’s disease
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Veréb, Dániel, Mijalkov, Mite, Chang, Yu-Wei, Canal-Garcia, Anna, Gomez-Ruis, Emiliano, Maass, Anne, Villeneuve, Sylvia, Volpe, Giovanni, and Pereira, Joana B.
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- 2023
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7. Resting-state MRI functional connectivity as a neural correlate of multidomain lifestyle adherence in older adults at risk for Alzheimer’s disease
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Ai, Meishan, Morris, Timothy P., Zhang, Jiahe, de la Colina, Adrián Noriega, Tremblay-Mercier, Jennifer, Villeneuve, Sylvia, Whitfield-Gabrieli, Susan, Kramer, Arthur F., and Geddes, Maiya R.
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- 2023
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8. Sex-specific relationships between obesity, physical activity, and gray and white matter volume in cognitively unimpaired older adults
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Intzandt, Brittany, Sanami, Safa, Huck, Julia, Villeneuve, Sylvia, Bherer, Louis, and Gauthier, Claudine J.
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- 2023
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9. Midlife physical activity engagement is associated with later-life brain health
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Ai, Meishan, Morris, Timothy P., Noriega de la Colina, Adrián, Thovinakere, Nagashree, Tremblay-Mercier, Jennifer, Villeneuve, Sylvia, H. Hillman, Charles, Kramer, Arthur F., and Geddes, Maiya R.
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- 2024
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10. Accelerated functional brain aging in pre-clinical familial Alzheimer’s disease
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Gonneaud, Julie, Baria, Alex T, Pichet Binette, Alexa, Gordon, Brian A, Chhatwal, Jasmeer P, Cruchaga, Carlos, Jucker, Mathias, Levin, Johannes, Salloway, Stephen, Farlow, Martin, Gauthier, Serge, Benzinger, Tammie LS, Morris, John C, Bateman, Randall J, Breitner, John CS, Poirier, Judes, Vachon-Presseau, Etienne, and Villeneuve, Sylvia
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Biological Psychology ,Psychology ,Clinical Research ,Neurodegenerative ,Aging ,Brain Disorders ,Neurosciences ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Acquired Cognitive Impairment ,Alzheimer's Disease ,Dementia ,Neurological ,Adult ,Aged ,Aged ,80 and over ,Alzheimer Disease ,Amyloid beta-Peptides ,Brain ,Brain Mapping ,Cognitive Dysfunction ,Female ,Genetic Predisposition to Disease ,Humans ,Longitudinal Studies ,Magnetic Resonance Imaging ,Male ,Middle Aged ,Mutation ,Positron-Emission Tomography ,Young Adult ,Alzheimer’s Disease Neuroimaging Initiative ,Dominantly Inherited Alzheimer Network (DIAN) Study Group ,Pre-symptomatic Evaluation of Experimental or Novel Treatments for Alzheimer’s Disease (PREVENT-AD) Research Group - Abstract
Resting state functional connectivity (rs-fMRI) is impaired early in persons who subsequently develop Alzheimer's disease (AD) dementia. This impairment may be leveraged to aid investigation of the pre-clinical phase of AD. We developed a model that predicts brain age from resting state (rs)-fMRI data, and assessed whether genetic determinants of AD, as well as beta-amyloid (Aβ) pathology, can accelerate brain aging. Using data from 1340 cognitively unimpaired participants between 18-94 years of age from multiple sites, we showed that topological properties of graphs constructed from rs-fMRI can predict chronological age across the lifespan. Application of our predictive model to the context of pre-clinical AD revealed that the pre-symptomatic phase of autosomal dominant AD includes acceleration of functional brain aging. This association was stronger in individuals having significant Aβ pathology.
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- 2021
11. The impact of demographic, clinical, genetic, and imaging variables on tau PET status
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Ossenkoppele, Rik, Leuzy, Antoine, Cho, Hanna, Sudre, Carole H, Strandberg, Olof, Smith, Ruben, Palmqvist, Sebastian, Mattsson-Carlgren, Niklas, Olsson, Tomas, Jögi, Jonas, Stormrud, Erik, Ryu, Young Hoon, Choi, Jae Yong, Boxer, Adam L, Gorno-Tempini, Maria L, Miller, Bruce L, Soleimani-Meigooni, David, Iaccarino, Leonardo, La Joie, Renaud, Borroni, Edilio, Klein, Gregory, Pontecorvo, Michael J, Devous, Michael D, Villeneuve, Sylvia, Lyoo, Chul Hyoung, Rabinovici, Gil D, and Hansson, Oskar
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Biomedical and Clinical Sciences ,Clinical Sciences ,Biomedical Imaging ,Aging ,Alzheimer's Disease ,Dementia ,Brain Disorders ,Neurodegenerative ,Clinical Research ,Neurosciences ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Acquired Cognitive Impairment ,Aetiology ,2.1 Biological and endogenous factors ,Neurological ,Alzheimer Disease ,Amyloid beta-Peptides ,Cognitive Dysfunction ,Demography ,Humans ,Positron-Emission Tomography ,tau Proteins ,PET ,Tau ,Aβ ,Alzheimer’ ,s disease ,MCI ,Alzheimer’s Disease Neuroimaging Initiative ,PREVENT-AD research group ,Alzheimer’s disease ,Aβ ,Other Physical Sciences ,Nuclear Medicine & Medical Imaging ,Clinical sciences - Abstract
PurposeA substantial proportion of amyloid-β (Aβ)+ patients with clinically diagnosed Alzheimer's disease (AD) dementia and mild cognitive impairment (MCI) are tau PET-negative, while some clinically diagnosed non-AD neurodegenerative disorder (non-AD) patients or cognitively unimpaired (CU) subjects are tau PET-positive. We investigated which demographic, clinical, genetic, and imaging variables contributed to tau PET status.MethodsWe included 2338 participants (430 Aβ+ AD dementia, 381 Aβ+ MCI, 370 non-AD, and 1157 CU) who underwent [18F]flortaucipir (n = 1944) or [18F]RO948 (n = 719) PET. Tau PET positivity was determined in the entorhinal cortex, temporal meta-ROI, and Braak V-VI regions using previously established cutoffs. We performed bivariate binary logistic regression models with tau PET status (positive/negative) as dependent variable and age, sex, APOEε4, Aβ status (only in CU and non-AD analyses), MMSE, global white matter hyperintensities (WMH), and AD-signature cortical thickness as predictors. Additionally, we performed multivariable binary logistic regression models to account for all other predictors in the same model.ResultsTau PET positivity in the temporal meta-ROI was 88.6% for AD dementia, 46.5% for MCI, 9.5% for non-AD, and 6.1% for CU. Among Aβ+ participants with AD dementia and MCI, lower age, MMSE score, and AD-signature cortical thickness showed the strongest associations with tau PET positivity. In non-AD and CU participants, presence of Aβ was the strongest predictor of a positive tau PET scan.ConclusionWe identified several demographic, clinical, and neurobiological factors that are important to explain the variance in tau PET retention observed across the AD pathological continuum, non-AD neurodegenerative disorders, and cognitively unimpaired persons.
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- 2021
12. White matter hyperintensity load varies depending on subjective cognitive decline criteria
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Morrison, Cassandra, Dadar, Mahsa, Villeneuve, Sylvia, Ducharme, Simon, and Collins, D. Louis
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- 2023
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13. Association of vascular brain injury, neurodegeneration, amyloid and cognitive trajectory
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Han, Ji Won, Maillard, Pauline, Harvey, Danielle, Fletcher, Evan, Martinez, Oliver, Johnson, David K, Olichney, John M, Farias, Sarah T, Villeneuve, Sylvia, Jagust, William, Mungas, Dan, and DeCarli, Charles
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Biomedical and Clinical Sciences ,Neurosciences ,Clinical Sciences ,Clinical Research ,Acquired Cognitive Impairment ,Alzheimer's Disease ,Dementia ,Brain Disorders ,Neurodegenerative ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Behavioral and Social Science ,Prevention ,Aging ,Biomedical Imaging ,Neurological ,Aged ,Aged ,80 and over ,Amyloid beta-Peptides ,Aniline Compounds ,Brain ,Cerebrovascular Disorders ,Cognition ,Cognitive Dysfunction ,Disease Progression ,Executive Function ,Female ,Hippocampus ,Humans ,Independent Living ,Magnetic Resonance Imaging ,Male ,Memory Disorders ,Memory ,Episodic ,Neuropsychological Tests ,Organ Size ,Plaque ,Amyloid ,Positron-Emission Tomography ,Thiazoles ,White Matter ,Cognitive Sciences ,Neurology & Neurosurgery ,Clinical sciences - Abstract
ObjectiveTo determine whether vascular and neurodegenerative factors influence cognition before clinically relevant Alzheimer disease pathology, we analyzed MRI measures and amyloid imaging in an ethnoracially diverse cohort of cognitively normal individuals older than 60 years.MethodsParticipants (n = 154; mean age 74.15 ± 6.94; 50% female; 54% Caucasian, 22.1% Hispanic, 14.9% African American) were recruited from the University of California, Davis Alzheimer's Disease Research Center, who were cognitively normal at baseline, time of PET, and MRI, and received yearly cognitive assessment for 6.23 ± 4.16 years. Mixed model regression with random slope and intercept was calculated for episodic memory and executive function, adjusting for age, sex, education, and ethnicity.ResultsVascular burden score was associated with total white matter hyperintensity (WMH) volume (β, 0.171; 95% confidence interval [CI], 0.024-0.318). WMH volume was associated with low baseline executive function (-0.115; -0.226 to -0.003) and rate of change in memory (-0.029; -0.045 to -0.012). Hippocampal volume was associated with the rate of change in memory (0.040; 0.021-0.059) and executive function (0.024; 0.008-0.039). Continuous measures of amyloid status influenced change in memory (-0.026; -0.044 to -0.008) and executive function (-0.033; -0.046 to -0.021) independently of MRI measures.ConclusionVascular brain injury and neurodegeneration are associated with baseline cognitive performance and the rate of longitudinal change independent of amyloid status among community-dwelling, ethnicity diverse cognitively normal individuals, supporting the role of vascular diseases as risk factors for later-life dementia.
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- 2020
14. Sex differences in longitudinal changes of episodic memory-related brain activity and cognition in cognitively unimpaired older adults with a family history of Alzheimer’s disease
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Samson, Alexandria D., Rajagopal, Sricharana, Pasvanis, Stamatoula, Villeneuve, Sylvia, McIntosh, Anthony R., and Rajah, M. Natasha
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- 2023
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15. Trait Mindfulness Is Associated With Less Amyloid, Tau, and Cognitive Decline in Individuals at Risk for Alzheimer’s Disease
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Strikwerda-Brown, Cherie, Ozlen, Hazal, Pichet Binette, Alexa, Chapleau, Marianne, Marchant, Natalie L., Breitner, John C.S., and Villeneuve, Sylvia
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- 2023
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16. Atypical brain aging and its association with working memory performance in major depressive disorder
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Ho, Natalie C.W., primary, Bethlehem, Richard AI., additional, Seidlitz, Jakob, additional, Nogovitsyn, Nikita, additional, Metzak, Paul, additional, Ballester, Pedro L., additional, Hassel, Stefanie, additional, Rotzinger, Susan, additional, Poppenk, Jordan, additional, Lam, Raymond W., additional, Taylor, Valerie H., additional, Milev, Roumen, additional, Adamson, Chris, additional, Adler, Sophie, additional, Alexander-Bloch, Aaron F., additional, Anagnostou, Evdokia, additional, Anderson, Kevin M., additional, Areces-Gonzalez, Ariosky, additional, Astle, Duncan E., additional, Auyeung, Bonnie, additional, Ayub, Muhammad, additional, Bae, Jong Bin, additional, Ball, Gareth, additional, Baron-Cohen, Simon, additional, Beare, Richard, additional, Bedford, Saashi A., additional, Benegal, Vivek, additional, Bethlehem, Richard A.I., additional, Beyer, Frauke, additional, Blangero, John, additional, Blesa Cábez, Manuel, additional, Boardman, James P., additional, Borzage, Matthew, additional, Bosch-Bayard, Jorge F., additional, Bourke, Niall, additional, Bullmore, Edward T., additional, Calhoun, Vince D., additional, Chakravarty, Mallar M., additional, Chen, Christina, additional, Chertavian, Casey, additional, Chetelat, Gaël, additional, Chong, Yap S., additional, Corvin, Aiden, additional, Costantino, Manuela, additional, Courchesne, Eric, additional, Crivello, Fabrice, additional, Cropley, Vanessa L., additional, Crosbie, Jennifer, additional, Crossley, Nicolas, additional, Delarue, Marion, additional, Delorme, Richard, additional, Desrivieres, Sylvane, additional, Devenyi, Gabriel, additional, Di Biase, Maria A., additional, Dolan, Ray, additional, Donald, Kirsten A., additional, Donohoe, Gary, additional, Dorfschmidt, Lena, additional, Dunlop, Katharine, additional, Edwards, Anthony D., additional, Elison, Jed T., additional, Ellis, Cameron T., additional, Elman, Jeremy A., additional, Eyler, Lisa, additional, Fair, Damien A., additional, Fletcher, Paul C., additional, Fonagy, Peter, additional, Franz, Carol E., additional, Galan-Garcia, Lidice, additional, Gholipour, Ali, additional, Giedd, Jay, additional, Gilmore, John H., additional, Glahn, David C., additional, Goodyer, Ian M., additional, Grant, P.E., additional, Groenewold, Nynke A., additional, Gudapati, Shreya, additional, Gunning, Faith M., additional, Gur, Raquel E., additional, Gur, Ruben C., additional, Hammill, Christopher F., additional, Hansson, Oskar, additional, Hedden, Trey, additional, Heinz, Andreas, additional, Henson, Richard N., additional, Heuer, Katja, additional, Hoare, Jacqueline, additional, Holla, Bharath, additional, Holmes, Avram J., additional, Huang, Hao, additional, Ipser, Jonathan, additional, Jack, Clifford R., additional, Jackowski, Andrea P., additional, Jia, Tianye, additional, Jones, David T., additional, Jones, Peter B., additional, Kahn, Rene S., additional, Karlsson, Hasse, additional, Karlsson, Linnea, additional, Kawashima, Ryuta, additional, Kelley, Elizabeth A., additional, Kern, Silke, additional, Kim, Ki-Woong, additional, Kitzbichler, Manfred G., additional, Kremen, William S., additional, Lalonde, François, additional, Landeau, Brigitte, additional, Lerch, Jason, additional, Lewis, John D., additional, Li, Jiao, additional, Liao, Wei, additional, Liston, Conor, additional, Lombardo, Michael V., additional, Lv, Jinglei, additional, Mallard, Travis T., additional, Marcelis, Machteld, additional, Mathias, Samuel R., additional, Mazoyer, Bernard, additional, McGuire, Philip, additional, Meaney, Michael J., additional, Mechelli, Andrea, additional, Misic, Bratislav, additional, Morgan, Sarah E., additional, Mothersill, David, additional, Ortinau, Cynthia, additional, Ossenkoppele, Rik, additional, Ouyang, Minhui, additional, Palaniyappan, Lena, additional, Paly, Leo, additional, Pan, Pedro M., additional, Pantelis, Christos, additional, Park, Min Tae M., additional, Paus, Tomas, additional, Pausova, Zdenka, additional, Paz-Linares, Deirel, additional, Pichet Binette, Alexa, additional, Pierce, Karen, additional, Qian, Xing, additional, Qiu, Anqi, additional, Raznahan, Armin, additional, Rittman, Timothy, additional, Rodrigue, Amanda, additional, Rollins, Caitlin K., additional, Romero-Garcia, Rafael, additional, Ronan, Lisa, additional, Rosenberg, Monica D., additional, Rowitch, David H., additional, Salum, Giovanni A., additional, Satterthwaite, Theodore D., additional, Schaare, H. Lina, additional, Schabdach, Jenna, additional, Schachar, Russell J., additional, Schöll, Michael, additional, Schultz, Aaron P., additional, Sharp, David, additional, Shinohara, Russell T., additional, Skoog, Ingmar, additional, Smyser, Christopher D., additional, Sperling, Reisa A., additional, Stein, Dan J., additional, Stolicyn, Aleks, additional, Suckling, John, additional, Sullivan, Gemma, additional, Thyreau, Benjamin, additional, Toro, Roberto, additional, Traut, Nicolas, additional, Tsvetanov, Kamen A., additional, Turk-Browne, Nicholas B., additional, Tuulari, Jetro J., additional, Tzourio, Christophe, additional, Vachon-Presseau, Étienne, additional, Valdes-Sosa, Mitchell J., additional, Valdes-Sosa, Pedro A., additional, Valk, Sofie L., additional, van Amelsvoort, Therese, additional, Vandekar, Simon N., additional, Vasung, Lana, additional, Vértes, Petra E., additional, Victoria, Lindsay W., additional, Villeneuve, Sylvia, additional, Villringer, Arno, additional, Vogel, Jacob W., additional, Wagstyl, Konrad, additional, Wang, Yin-Shan S., additional, Warfield, Simon K., additional, Warrier, Varun, additional, Westman, Eric, additional, Westwater, Margaret L., additional, Whalley, Heather C., additional, White, Simon R., additional, Witte, A. Veronica, additional, Yang, Ning, additional, Yeo, B.T. Thomas, additional, Yun, Hyuk Jin, additional, Zalesky, Andrew, additional, Zar, Heather J., additional, Zettergren, Anna, additional, Zhou, Juan H., additional, Ziauddeen, Hisham, additional, Zimmerman, Dabriel, additional, Zugman, Andre, additional, Zuo, Xi-Nian N., additional, Frey, Benicio N., additional, Harkness, Kate L., additional, Addington, Jean, additional, and Kennedy, Sidney H., additional
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- 2024
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17. Vascular Burden Score Impacts Cognition Independent of Amyloid PET and MRI Measures of Alzheimer’s Disease and Vascular Brain Injury
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DeCarli, Charles, Villeneuve, Sylvia, Maillard, Pauline, Harvey, Danielle, Singh, Baljeet, Carmichael, Owen, Fletcher, Evan, Olichney, John, Farias, Sarah, Jagust, William, Reed, Bruce, and Mungas, Dan
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Biological Psychology ,Psychology ,Alzheimer's Disease ,Brain Disorders ,Biomedical Imaging ,Acquired Cognitive Impairment ,Dementia ,Neurosciences ,Basic Behavioral and Social Science ,Neurodegenerative ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Behavioral and Social Science ,Aging ,Clinical Research ,Neurological ,Mental health ,Aged ,Aged ,80 and over ,Alzheimer Disease ,Brain ,Cerebrovascular Trauma ,Cognition ,Cognitive Dysfunction ,Cohort Studies ,Cost of Illness ,Female ,Follow-Up Studies ,Humans ,Magnetic Resonance Imaging ,Male ,Positron-Emission Tomography ,Alzheimer's disease ,cerebrovascular disorders ,cognition ,neuroimaging ,Alzheimer’s disease ,Clinical Sciences ,Cognitive Sciences ,Neurology & Neurosurgery ,Clinical sciences ,Biological psychology - Abstract
Background/objectiveTo determine the impact of vascular burden on rates of decline in episodic memory and executive function. We hypothesize that greater vascular burden will have an additive negative impact on cognition after accounting for baseline cognitive impairment, positron emission tomography (PET) amyloid burden, and magnetic resonance imaging (MRI) measures.MethodsIndividuals were followed an average of 5 years with serial cognitive assessments. Predictor variables include vascular burden score (VBS), quantitative brain MRI assessment, and amyloid imaging. Subjects consisted of 65 individuals, 53% of whom were male, aged 73.2±7.2 years on average with an average of 15.5±3.3 years of educational achievement.ResultsBaseline cognitive impairment was significantly associated poorer episodic memory (p
- Published
- 2019
18. White matter lesions may be an early marker for age-related cognitive decline
- Author
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Morrison, Cassandra, Dadar, Mahsa, Villeneuve, Sylvia, and Collins, D. Louis
- Published
- 2022
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19. White Matter Structure in Older Adults Moderates the Benefit of Sleep Spindles on Motor Memory Consolidation
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Mander, Bryce A, Zhu, Alyssa H, Lindquist, John R, Villeneuve, Sylvia, Rao, Vikram, Lu, Brandon, Saletin, Jared M, Ancoli-Israel, Sonia, Jagust, William J, and Walker, Matthew P
- Subjects
Biomedical and Clinical Sciences ,Neurosciences ,Neurodegenerative ,Behavioral and Social Science ,Clinical Research ,Aging ,Sleep Research ,1.1 Normal biological development and functioning ,Underpinning research ,Neurological ,Adolescent ,Aged ,Aged ,80 and over ,Brain ,Female ,Humans ,Male ,Memory Consolidation ,Motor Skills ,Polysomnography ,Sleep Stages ,White Matter ,Young Adult ,aging ,DTI ,motor memory ,sleep ,sleep spindles ,WMH ,Medical and Health Sciences ,Psychology and Cognitive Sciences ,Neurology & Neurosurgery - Abstract
Sleep spindles promote the consolidation of motor skill memory in young adults. Older adults, however, exhibit impoverished sleep-dependent motor memory consolidation. The underlying pathophysiological mechanism(s) explaining why motor memory consolidation in older adults fails to benefit from sleep remains unclear. Here, we demonstrate that male and female older adults show impoverished overnight motor skill memory consolidation relative to young adults, with the extent of impairment being associated with the degree of reduced frontal fast sleep spindle density. The magnitude of the loss of frontal fast sleep spindles in older adults was predicted by the degree of reduced white matter integrity throughout multiple white matter tracts known to connect subcortical and cortical brain regions. We further demonstrate that the structural integrity of selective white matter fiber tracts, specifically within right posterior corona radiata, right tapetum, and bilateral corpus callosum, statistically moderates whether sleep spindles promoted overnight consolidation of motor skill memory. Therefore, white matter integrity within tracts known to connect cortical sensorimotor control regions dictates the functional influence of sleep spindles on motor skill memory consolidation in the elderly. The deterioration of white matter fiber tracts associated with human brain aging thus appears to be one pathophysiological mechanism influencing subcortical-cortical propagation of sleep spindles and their related memory benefits.SIGNIFICANCE STATEMENT Numerous studies have shown that sleep spindle expression is reduced and sleep-dependent motor memory is impaired in older adults. However, the mechanisms underlying these alterations have remained unknown. The present study reveals that age-related degeneration of white matter within select fiber tracts is associated with reduced sleep spindles in older adults. We further demonstrate that, within these same fiber tracts, the degree of degeneration determines whether sleep spindles can promote motor memory consolidation. Therefore, white matter integrity in the human brain, more than age per se, determines the magnitude of decline in sleep spindles in later life and, with it, the success (or lack thereof) of sleep-dependent motor memory consolidation in older adults.
- Published
- 2017
20. Vascular risk factors are associated with a decline in resting-state functional connectivity in cognitively unimpaired individuals at risk for Alzheimer's disease: Vascular risk factors and functional connectivity changes
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Köbe, Theresa, Binette, Alexa Pichet, Vogel, Jacob W., Meyer, Pierre-François, Breitner, John C.S., Poirier, Judes, and Villeneuve, Sylvia
- Published
- 2021
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21. Regional correlations between [11C]PIB PET and post-mortem burden of amyloid-beta pathology in a diverse neuropathological cohort
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Seo, Sang Won, Ayakta, Nagehan, Grinberg, Lea T, Villeneuve, Sylvia, Lehmann, Manja, Reed, Bruce, DeCarli, Charles, Miller, Bruce L, Rosen, Howard J, Boxer, Adam L, O’Neil, James P, Jin, Lee-Way, Seeley, William W, Jagust, William J, and Rabinovici, Gil D
- Subjects
Biological Psychology ,Biomedical and Clinical Sciences ,Psychology ,Aging ,Alzheimer's Disease Related Dementias (ADRD) ,Neurodegenerative ,Alzheimer's Disease ,Acquired Cognitive Impairment ,Neurosciences ,Dementia ,Biomedical Imaging ,Rare Diseases ,Brain Disorders ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,2.1 Biological and endogenous factors ,Neurological ,Aged ,Aged ,80 and over ,Amyloid beta-Peptides ,Aniline Compounds ,Benzothiazoles ,Cognitive Dysfunction ,Female ,Humans ,Longitudinal Studies ,Male ,Middle Aged ,Positron-Emission Tomography ,Thiazoles ,Imaging ,Pathology ,Amyloid ,Alzheimer's disease ,Alzheimer’s disease ,Biological psychology ,Clinical and health psychology - Abstract
Imaging-pathological correlation studies show that in vivo amyloid-β (Aβ) positron emission tomography (PET) strongly predicts the presence of significant Aβ pathology at autopsy. We sought to determine whether regional PiB-PET uptake would improve sensitivity for amyloid detection in comparison with global measures (experiment 1), and to estimate the relative contributions of different Aβ aggregates to in vivo PET signal (experiment 2). In experiment 1, 54 subjects with [11C] PiB-PET during life and postmortem neuropathologic examination (85.2% with dementia, interval from PET to autopsy 3.1 ± 1.9 years) were included. We assessed Thal amyloid phase (N = 36) and CERAD score (N = 54) versus both global and regional PiB SUVRs. In experiment 2 (N = 42), PiB SUVR and post-mortem amyloid β burden was analyzed in five customized regions of interest matching regions sampled at autopsy. We assessed the relative contribution of neuritic plaques (NPs), diffuse plaques (DPs) and cerebral amyloid angiopathy (CAA) to regional PIB SUVR using multi-linear regression. In experiment 1, there were no differences in Area Under the Curve for amyloid phase ≥ A2 and CERAD score ≥ C2 between global and highest regional PiB SUVR (p = 0.186 and 0.230). In experiment 2, when NPs, DPs, and/or CAA were included in the same model, moderate to severe NPs were independently correlated with PiB SUVR in all regions except for the inferior temporal and calcarine ROI (β = 0.414-0.804, p
- Published
- 2017
22. Longer sleep duration and neuroinflammation in at-risk elderly with a parental history of Alzheimer's disease.
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Baril, Andrée-Ann, Picard, Cynthia, Labonté, Anne, Sanchez, Erlan, Duclos, Catherine, Mohammediyan, Béry, Breitner, John C S, Villeneuve, Sylvia, Poirier, Judes, and Group, PREVENT-AD Research
- Published
- 2024
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- View/download PDF
23. Locus coeruleus integrity is related to an exploitation-based decision-making bias in older adulthood.
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Turner, Gary R., Hewan, Patrick, Wearn, Alfie, van Dooren, Roel, Wyatt, Lindsay, Leppert, Ilana R., Baracchini, Giulia, Hughes, Colleen, Williams, Kayla M., Sylvain, Elisabeth, Tremblay-Mercier, Jennifer, Poirier, Judes, Villeneuve, Sylvia, Tardif, Christine, and Spreng, R. Nathan
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LOCUS coeruleus ,ALZHEIMER'S disease ,ADULTS ,TRANSITION to adulthood ,MAGNETIZATION transfer - Abstract
Optimal decision-making balances exploration for new information against exploitation of known rewards, a process mediated by the locus coeruleus and its norepinephrine projections. We predicted that an exploitation-bias that emerges in older adulthood would be associated with lower microstructural integrity of the locus coeruleus. Leveraging in vivo histological methods from quantitative MRI-magnetic transfer saturation--we provide evidence that older age is associated with lower locus coeruleus integrity. Critically, we demonstrate that an exploitation bias in older adulthood, assessed with a foraging task, is sensitive and specific to lower locus coeruleus integrity. Because the locus coeruleus is uniquely vulnerable to Alzheimer's disease pathology, our findings suggest that aging, and a presymptomatic trajectory of Alzheimer's related decline, may fundamentally alter decision-making abilities in later life. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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24. Iron Deposition and Distribution Across the Hippocampus Is Associated with Pattern Separation and Pattern Completion in Older Adults at Risk for Alzheimer’s Disease.
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Jing Zhou, Wearn, Alfie, Huck, Julia, Hughes, Colleen, Baracchini, Giulia, Tremblay-Mercier, Jennifer, Poirier, Judes, Villeneuve, Sylvia, Tardif, Christine Lucas, Chakravarty, M. Mallar, Daugherty, Ana M., Gauthier, Claudine J., Turner, Gary R., and Spreng, R. Nathan
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DISEASE risk factors ,OLDER people ,IRON ,EPISODIC memory ,ALZHEIMER'S disease - Abstract
Elevated iron deposition in the brain has been observed in older adult humans and persons with Alzheimer’s disease (AD), and has been associated with lower cognitive performance. We investigated the impact of iron deposition, and its topographical distribution across hippocampal subfields and segments (anterior, posterior) measured along its longitudinal axis, on episodic memory in a sample of cognitively unimpaired older adults at elevated familial risk for AD (N= 172, 120 females, 52 males; mean age = 68.8 ± 5.4 years). MRI-based quantitative susceptibility maps were acquired to derive estimates of hippocampal iron deposition. The Mnemonic Similarity Task was used to measure pattern separation and pattern completion, two hippocampally mediated episodic memory processes. Greater hippocampal iron load was associated with lower pattern separation and higher pattern completion scores, both indicators of poorer episodic memory. Examination of iron levels within hippocampal subfields across its long axis revealed topographic specificity. Among the subfields and segments investigated here, iron deposition in the posterior hippocampal CA1 was the most robustly and negatively associated with the fidelity memory representations. This association remained aftercontrolling for hippocampal volume and was observed in the context of normal performance on standard neuropsychological memory measures. These findings reveal that the impact of iron load on episodic memory performance is not uniform across the hippocampus. Both iron deposition levels as well as its spatial distribution, must be taken into account when examining the relationship between hippocampal iron and episodic memory in older adults at elevated risk for AD. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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- View/download PDF
25. Structural white matter properties and cognitive resilience to tau pathology.
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Qiu, Ting, Liu, Zhen‐Qi, Rheault, François, Legarreta, Jon Haitz, Valcourt Caron, Alex, St‐Onge, Frédéric, Strikwerda‐Brown, Cherie, Metz, Amelie, Dadar, Mahsa, Soucy, Jean‐Paul, Pichet Binette, Alexa, Spreng, R. Nathan, Descoteaux, Maxime, and Villeneuve, Sylvia
- Abstract
INTRODUCTION: We assessed whether macro‐ and/or micro‐structural white matter properties are associated with cognitive resilience to Alzheimer's disease pathology years prior to clinical onset. METHODS: We examined whether global efficiency, an indicator of communication efficiency in brain networks, and diffusion measurements within the limbic network and default mode network moderate the association between amyloid‐β/tau pathology and cognitive decline. We also investigated whether demographic and health/risk factors are associated with white matter properties. RESULTS: Higher global efficiency of the limbic network, as well as free‐water corrected diffusion measures within the tracts of both networks, attenuated the impact of tau pathology on memory decline. Education, age, sex, white matter hyperintensities, and vascular risk factors were associated with white matter properties of both networks. DISCUSSION: White matter can influence cognitive resilience against tau pathology, and promoting education and vascular health may enhance optimal white matter properties. Highlights: Aβ and tau were associated with longitudinal memory change over ∼7.5 years.White matter properties attenuated the impact of tau pathology on memory change.Health/risk factors were associated with white matter properties. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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- View/download PDF
26. Insulin-like growth factor binding protein-2 in at-risk adults and autopsy-confirmed Alzheimer brains.
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Quesnel, Marc James, Labonté, Anne, Picard, Cynthia, Zetterberg, Henrik, Blennow, Kaj, Brinkmalm, Ann, Villeneuve, Sylvia, Poirier, Judes, Initiative, for the Alzheimer's Disease Neuroimaging, and Group, the PREVENT-AD Research
- Subjects
SOMATOMEDIN ,ENTORHINAL cortex ,INSULIN-like growth factor-binding proteins ,ALZHEIMER'S disease ,FRONTAL lobe ,MILD cognitive impairment - Abstract
Insulin, insulin-like growth factors (IGF) and their receptors are highly expressed in the adult hippocampus. Thus, disturbances in the insulin-IGF signalling pathway may account for the selective vulnerability of the hippocampus to nascent Alzheimer's disease (AD) pathology. In the present study, we examined the predominant IGF-binding protein in the CSF, IGFBP2. CSF was collected from 109 asymptomatic members of the parental history-positive PREVENT-AD cohort. CSF levels of IGFBP2, core AD and synaptic biomarkers were measured using proximity extension assay, ELISA and mass spectrometry. Cortical amyloid-beta (Aβ) and tau deposition were examined using
18 F-NAV4694 and flortaucipir. Cognitive assessments were performed during up to 8 years of follow-up, using the Repeatable Battery for the Assessment of Neuropsychological Status. T1-weighted structural MRI scans were acquired, and neuroimaging analyses were performed on pre-specified temporal and parietal brain regions. Next, in an independent cohort, we allocated 241 dementia-free ADNI-1 participants into four stages of AD progression based on the biomarkers CSF Aβ42 and total-tau (t-tau). In this analysis, differences in CSF and plasma IGFBP2 levels were examined across the pathological stages. Finally, IGFBP2 mRNA and protein levels were examined in the frontal cortex of 55 autopsy-confirmed AD and 31 control brains from the Quebec Founder Population (QFP) cohort, a unique population isolated from Eastern Canada. CSF IGFBP2 progressively increased over 5 years in asymptomatic PREVENT-AD participants. Baseline CSF IGFBP2 was positively correlated with CSF AD biomarkers and synaptic biomarkers, and negatively correlated with longitudinal changes in delayed memory (P = 0.024) and visuospatial abilities (P = 0.019). CSF IGFBP2 was negatively correlated at a trend-level with entorhinal cortex volume (P = 0.082) and cortical thickness in the piriform (P = 0.039), inferior temporal (P = 0.008), middle temporal (P = 0.014) and precuneus (P = 0.033) regions. In ADNI-1, CSF (P = 0.009) and plasma (P = 0.001) IGFBP2 were significantly elevated in Stage 2 [CSF Aβ(+)/t-tau(+)]. In survival analyses in ADNI-1, elevated plasma IGFBP2 was associated with a greater rate of AD conversion (hazard ratio = 1.62, P = 0.021). In the QFP cohort, IGFBP2 mRNA was reduced (P = 0.049); however, IGFBP2 protein levels did not differ in the frontal cortex of autopsy-confirmed AD brains (P = 0.462). Nascent AD pathology may induce an upregulation in IGFBP2 in asymptomatic individuals. CSF and plasma IGFBP2 may be valuable markers for identifying CSF Aβ(+)/t-tau(+) individuals and those with a greater risk of AD conversion. [ABSTRACT FROM AUTHOR]- Published
- 2024
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27. Contactin 5 and Apolipoproteins Interplay in Alzheimer's Disease.
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Dauar, Marina Tedeschi, Picard, Cynthia, Labonté, Anne, Breitner, John, Rosa-Neto, Pedro, Villeneuve, Sylvia, and Poirier, Judes
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ALZHEIMER'S disease ,APOLIPOPROTEINS ,LIQUID chromatography-mass spectrometry ,MEMBRANE proteins ,ENTORHINAL cortex ,IMMOBILIZATION stress - Abstract
Background: Apolipoproteins and contactin 5 are proteins associated with Alzheimer's disease (AD) pathophysiology. Apolipoproteins act on transport and clearance of cholesterol and phospholipids during synaptic turnover and terminal proliferation. Contactin 5 is a neuronal membrane protein involved in key processes of neurodevelopment. Objective: To investigate the interactions between contactin 5 and apolipoproteins in AD, and the role of these proteins in response to neuronal damage. Methods: Apolipoproteins (measured by Luminex), contactin 5 (measured by Olink's proximity extension assay), and cholesterol (measured by liquid chromatography mass spectrometry) were assessed in the cerebrospinal fluid (CSF) and plasma of cognitively unimpaired participants (n = 93). Gene expression was measured using polymerase chain reaction in the frontal cortex of autopsied-confirmed AD (n = 57) and control subjects (n = 31) and in the hippocampi of mice following entorhinal cortex lesions. Results: Contactin 5 positively correlated with apolipoproteins B (p = 5.4×10
–8 ), D (p = 1.86×10–4 ), E (p = 2.92×10–9 ), J (p = 2.65×10–9 ), and with cholesterol (p = 0.0096) in the CSF, and with cholesterol (p = 0.02), HDL (p = 0.0143), and LDL (p = 0.0121) in the plasma. Negative correlations were seen between CNTN5, APOB (p = 0.034) and APOE (p = 0.015) mRNA levels in the brains of control subjects. In the mouse model, apoe and apoj gene expression increased during the reinnervation phase (p < 0.05), while apob (p = 0.023) and apod (p = 0.006) increased in the deafferentation stage. Conclusions: Extensive interactions were observed between contactin 5 and apolipoproteins and cholesterol, possibly due to neuronal damage. The alterations in gene expression of apolipoproteins suggest a role in axonal, terminal, and synaptic remodeling in response to entorhinal cortex damage. [ABSTRACT FROM AUTHOR]- Published
- 2024
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28. β-amyloid, hippocampal atrophy and their relation to longitudinal brain change in cognitively normal individuals
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Fletcher, Evan, Villeneuve, Sylvia, Maillard, Pauline, Harvey, Danielle, Reed, Bruce, Jagust, William, and DeCarli, Charles
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Biological Psychology ,Psychology ,Alzheimer's Disease ,Aging ,Neurodegenerative ,Brain Disorders ,Dementia ,Neurosciences ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Acquired Cognitive Impairment ,2.1 Biological and endogenous factors ,Neurological ,Aged ,Aged ,80 and over ,Alzheimer Disease ,Amyloid beta-Peptides ,Atrophy ,Cerebral Amyloid Angiopathy ,Cognition ,Cohort Studies ,Female ,Hippocampus ,Humans ,Magnetic Resonance Imaging ,Male ,Regression Analysis ,Alzheimer's ,Longitudinal ,beta-amyloid ,Neurodegeneration ,Normals ,β-amyloid ,Clinical Sciences ,Neurology & Neurosurgery ,Biological psychology - Abstract
Recent literature has examined baseline hippocampal volume and extent of brain amyloidosis to test potential synergistic effects on worsening cognition and extent of brain atrophy. Use of hippocampal volume in prior studies was based on the notion that limbic circuit degeneration is an early manifestation of the Alzheimer's Disease (AD) pathophysiology. To clarify these interactions early in the AD process, we tested the effects of amyloid and baseline normalized hippocampal volume on longitudinal brain atrophy rates in a group of cognitively normal individuals. Results showed that the combination of elevated β-amyloid and baseline hippocampal atrophy is associated with increased rates specific to the limbic circuit and splenium. Importantly, this atrophy pattern emerged from a voxelwise analysis, corroborated by regression models over region of interests in native space. The results are broadly consistent with previous studies of the effects of amyloid and baseline hippocampal atrophy in normals, while pointing to accelerated atrophy of AD-vulnerable regions detectable at the preclinical stage.
- Published
- 2016
29. Tau accumulation and its spatial progression across the Alzheimer’s disease spectrum
- Author
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St-Onge, Frédéric, primary, Chapleau, Marianne, additional, Breitner, John C S, additional, Villeneuve, Sylvia, additional, and Pichet Binette, Alexa, additional
- Published
- 2023
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30. Amyloid and tau pathology are associated with white matter properties in cognitively unimpaired older adults at risk of AD dementia
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Qiu, Ting, primary, Rheault, François, additional, Soucy, Jean‐Paul, additional, Spreng, R. Nathan, additional, Binette, Alexa Pichet, additional, Descoteaux, Maxime, additional, and Villeneuve, Sylvia, additional
- Published
- 2023
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31. Tracing the spatial extent of cortical tau over time in Alzheimer’s disease
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St‐Onge, Frederic, primary, Binette, Alexa Pichet, additional, Chapleau, Marianne, additional, Breitner, John C.S., additional, and Villeneuve, Sylvia, additional
- Published
- 2023
- Full Text
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32. The role of biofluid markers in predicting near‐term cognitive impairment
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Yakoub, Yara, primary, Ashton, Nicholas J., additional, Karikari, Thomas K, additional, Montoliu‐Gaya, Laia, additional, Schöll, Michael, additional, Spreng, R. Nathan, additional, Rosa‐Neto, Pedro, additional, Soucy, Jean‐Paul, additional, Breitner, John C.S., additional, Zetterberg, Henrik, additional, Blennow, Kaj, additional, Poirier, Judes, additional, and Villeneuve, Sylvia, additional
- Published
- 2023
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- View/download PDF
33. Domain‐specific cognitive decline associates with differential regional tau burden in the Alzheimer’s disease spectrum
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St‐Onge, Frederic, primary, Binette, Alexa Pichet, additional, Chapleau, Marianne, additional, Breitner, John C.S., additional, and Villeneuve, Sylvia, additional
- Published
- 2023
- Full Text
- View/download PDF
34. Dissociable influences of maternal vs paternal Alzheimer’s risk on neurocognitive and cardiovascular health in men and women
- Author
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Savignac, Chloé, primary, St‐Onge, Frederic, additional, Villeneuve, Sylvia, additional, Badhwar, AmanPreet, additional, Taliun, Sarah A Gagliano, additional, Farhan, Sali, additional, Geddes, Maiya R., additional, Medina, Yasser Iturria, additional, Poirier, Judes, additional, Spreng, R. Nathan, additional, and Bzdok, Danilo, additional
- Published
- 2023
- Full Text
- View/download PDF
35. Multivariate white matter differences links to cognition in individuals with family history of Alzheimer’s disease and APOE4 genetic risk
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Tremblay, Stefanie A, primary, Spreng, R. Nathan, additional, Alasmar, Zaki, additional, Pirhadi, Amir, additional, Tardif, Christine L, additional, Chakravarty, M. Mallar, additional, Villeneuve, Sylvia, additional, Leppert, Ilana R, additional, Carbonell, Felix, additional, Medina, Yasser Iturria, additional, Steele, Christopher J, additional, and Gauthier, Claudine J, additional
- Published
- 2023
- Full Text
- View/download PDF
36. Sex and family history differences in Aβ and tau vulnerability in preclinical Alzheimer’s disease
- Author
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Ourry, Valentin, primary, St‐Onge, Frederic, additional, Mohammediyan, Bery, additional, Yakoub, Yara, additional, Soucy, Jean‐Paul, additional, Poirier, Judes, additional, Breitner, John C.S., additional, and Villeneuve, Sylvia, additional
- Published
- 2023
- Full Text
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37. The Influence of Prior Head Injury on Late‐Life Cognition and White Matter Microstructure in Older Adults At‐Risk of Alzheimer’s disease
- Author
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Chiu, Larissa Kristi, primary, Ai, Meishan, additional, Tremblay‐Mercier, Jennifer, additional, Villeneuve, Sylvia, additional, and Geddes, Maiya R., additional
- Published
- 2023
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38. Sleep Quality and Day‐to‐Day Variability: Relation to Alzheimer’s pathology in Cognitively Unimpaired Older Adults At‐Risk of AD Dementia
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Mohammediyan, Bery, primary, Baril, Andree‐Ann, additional, St‐Onge, Frederic, additional, Ourry, Valentin, additional, Carrier, Julie, additional, Breitner, John C.S., additional, Poirier, Judes, additional, and Villeneuve, Sylvia, additional
- Published
- 2023
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39. Neurophysiological activity linked to Alzheimer’s disease pathology relates to longitudinal cognition and progression to mild cognitive impairment
- Author
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Rudolf, Jonathan E Gallego, primary, Wiesman, Alex I, additional, Baillet, Sylvain, additional, and Villeneuve, Sylvia, additional
- Published
- 2023
- Full Text
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40. Memory retrieval activation moderates the effect of Alzheimer’s disease pathology on memory performance
- Author
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Vockert, Niklas, primary, Molloy, Eóin N., additional, Pilar, Andrea Pacha, additional, Binette, Alexa Pichet, additional, Remz, Jordana, additional, Rajah, Natasha, additional, Villeneuve, Sylvia, additional, and Maass, Anne, additional
- Published
- 2023
- Full Text
- View/download PDF
41. Midlife Physical Activity Engagement is Associated With Later-life Brain Health
- Author
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Ai, Meishan, primary, Morris, Timothy P., additional, Colina, Adrián Noriega de la, additional, Thovinakere, Nagashree, additional, Tremblay-Mercier, Jennifer, additional, Villeneuve, Sylvia, additional, Hillman, Charles, additional, Kramer, Arthur F., additional, and Geddes, Maiya R., additional
- Published
- 2023
- Full Text
- View/download PDF
42. Existing Pittsburgh Compound-B positron emission tomography thresholds are too high: statistical and pathological evaluation
- Author
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Villeneuve, Sylvia, Rabinovici, Gil D, Cohn-Sheehy, Brendan I, Madison, Cindee, Ayakta, Nagehan, Ghosh, Pia M, La Joie, Renaud, Arthur-Bentil, Samia Kate, Vogel, Jacob W, Marks, Shawn M, Lehmann, Manja, Rosen, Howard J, Reed, Bruce, Olichney, John, Boxer, Adam L, Miller, Bruce L, Borys, Ewa, Jin, Lee-Way, Huang, Eric J, Grinberg, Lea T, DeCarli, Charles, Seeley, William W, and Jagust, William
- Subjects
Biological Psychology ,Psychology ,Neurodegenerative ,Biomedical Imaging ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Aging ,Alzheimer's Disease ,Brain Disorders ,Acquired Cognitive Impairment ,Dementia ,Neurosciences ,4.2 Evaluation of markers and technologies ,Detection ,screening and diagnosis ,Neurological ,Aged ,Alzheimer Disease ,Amyloid beta-Peptides ,Aniline Compounds ,Female ,Humans ,Image Interpretation ,Computer-Assisted ,Male ,Positron-Emission Tomography ,Radiopharmaceuticals ,Reference Values ,Thiazoles ,Young Adult ,Alzheimer's disease ,dementia ,biomarkers ,neurodegeneration ,beta-amyloid ,Medical and Health Sciences ,Psychology and Cognitive Sciences ,Neurology & Neurosurgery ,Biomedical and clinical sciences ,Health sciences - Abstract
Amyloid-β, a hallmark of Alzheimer's disease, begins accumulating up to two decades before the onset of dementia, and can be detected in vivo applying amyloid-β positron emission tomography tracers such as carbon-11-labelled Pittsburgh compound-B. A variety of thresholds have been applied in the literature to define Pittsburgh compound-B positron emission tomography positivity, but the ability of these thresholds to detect early amyloid-β deposition is unknown, and validation studies comparing Pittsburgh compound-B thresholds to post-mortem amyloid burden are lacking. In this study we first derived thresholds for amyloid positron emission tomography positivity using Pittsburgh compound-B positron emission tomography in 154 cognitively normal older adults with four complementary approaches: (i) reference values from a young control group aged between 20 and 30 years; (ii) a Gaussian mixture model that assigned each subject a probability of being amyloid-β-positive or amyloid-β-negative based on Pittsburgh compound-B index uptake; (iii) a k-means cluster approach that clustered subjects into amyloid-β-positive or amyloid-β-negative based on Pittsburgh compound-B uptake in different brain regions (features); and (iv) an iterative voxel-based analysis that further explored the spatial pattern of early amyloid-β positron emission tomography signal. Next, we tested the sensitivity and specificity of the derived thresholds in 50 individuals who underwent Pittsburgh compound-B positron emission tomography during life and brain autopsy (mean time positron emission tomography to autopsy 3.1 ± 1.8 years). Amyloid at autopsy was classified using Consortium to Establish a Registry for Alzheimer's Disease (CERAD) criteria, unadjusted for age. The analytic approaches yielded low thresholds (standard uptake value ratiolow = 1.21, distribution volume ratiolow = 1.08) that represent the earliest detectable Pittsburgh compound-B signal, as well as high thresholds (standard uptake value ratiohigh = 1.40, distribution volume ratiohigh = 1.20) that are more conservative in defining Pittsburgh compound-B positron emission tomography positivity. In voxel-wise contrasts, elevated Pittsburgh compound-B retention was first noted in the medial frontal cortex, then the precuneus, lateral frontal and parietal lobes, and finally the lateral temporal lobe. When compared to post-mortem amyloid burden, low proposed thresholds were more sensitive than high thresholds (sensitivities: distribution volume ratiolow 81.0%, standard uptake value ratiolow 83.3%; distribution volume ratiohigh 61.9%, standard uptake value ratiohigh 62.5%) for CERAD moderate-to-frequent neuritic plaques, with similar specificity (distribution volume ratiolow 95.8%; standard uptake value ratiolow, distribution volume ratiohigh and standard uptake value ratiohigh 100.0%). A receiver operator characteristic analysis identified optimal distribution volume ratio (1.06) and standard uptake value ratio (1.20) thresholds that were nearly identical to the a priori distribution volume ratiolow and standard uptake value ratiolow. In summary, we found that frequently applied thresholds for Pittsburgh compound-B positivity (typically at or above distribution volume ratiohigh and standard uptake value ratiohigh) are overly stringent in defining amyloid positivity. Lower thresholds in this study resulted in higher sensitivity while not compromising specificity.
- Published
- 2015
43. Imaging Vascular Disease and Amyloid in the Aging Brain: Implications for Treatment.
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Villeneuve, Sylvia and Jagust, William J
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Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Patient Safety ,Brain Disorders ,Alzheimer's Disease ,Neurosciences ,Aging ,Neurodegenerative ,Clinical Research ,Dementia ,Vascular Cognitive Impairment/Dementia ,Behavioral and Social Science ,Biomedical Imaging ,Acquired Cognitive Impairment ,Prevention ,Aetiology ,2.1 Biological and endogenous factors ,Neurological ,Cardiovascular ,Alzheimer’ disease ,amyloid ,treatment ,vascular brain injuries ,vascular risk factors - Abstract
Vascular risk factors (e.g. hypertension, dyslipidemia and diabetes) are well known risk factors for Alzheimer' disease. These vascular risk factors lead to vascular brain injuries, which also increase the likelihood of dementia. The advent of amyloid PET imaging has helped establish that vascular risk factors also lead to Alzheimer's disease via pathways that are independent from vascular brain injuries, at least, when vascular brain injuries are measured as white matter lesions and infarcts. While vascular brain injuries (white matter lesions and infarcts) do not seem to influence amyloid pathology, some evidence from amyloid imaging suggests that increased vascular risk is related to increased amyloid burden. Furthermore, while vascular brain injuries and amyloid have an additive and independent impact on brain integrity, vascular risk factors might potentiate the impact of amyloid on cortical thickness on brain regions vulnerable to Alzheimer's disease. New research should further explore and confirm, or refute, possible interactions between amyloid and vascular risk factors on brain integrity and cognition. Neuroimaging tools used to assess vascular brain integrity should also be expanded. Measuring cortical blood flow or damage to the capillary system might, for instance, give insight about how vascular risk factors can be associated to amyloid burden and impact. These findings also stress the need for monitoring vascular risk factors in midlife as a strategy for Alzheimer's disease prevention.
- Published
- 2015
44. Neuroprotective pathways: lifestyle activity, brain pathology, and cognition in cognitively normal older adults
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Wirth, Miranka, Haase, Claudia M, Villeneuve, Sylvia, Vogel, Jacob, and Jagust, William J
- Subjects
Brain Disorders ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Acquired Cognitive Impairment ,Neurosciences ,Dementia ,Behavioral and Social Science ,Alzheimer's Disease ,Basic Behavioral and Social Science ,Neurodegenerative ,Aging ,Aetiology ,2.1 Biological and endogenous factors ,Neurological ,Mental health ,Aged ,Aged ,80 and over ,Alzheimer Disease ,Amyloid beta-Peptides ,Brain ,Cognition ,Female ,Humans ,Life Style ,Magnetic Resonance Imaging ,Male ,Motor Activity ,Positron-Emission Tomography ,Surveys and Questionnaires ,Cognitive activity ,Physical activity ,Cognitive aging ,Beta-amyloid ,PIB-PET ,White matter lesion ,Clinical Sciences ,Neurology & Neurosurgery - Abstract
This study used path analysis to examine effects of cognitive activity and physical activity on cognitive functioning in older adults, through pathways involving beta-amyloid (Aβ) burden, cerebrovascular lesions, and neural injury within the brain regions affected in Alzheimer's disease (AD). Ninety-two cognitively normal older adults (75.2 ± 5.6 years) reported lifetime cognitive activity and current physical activity using validated questionnaires. For each participant, we evaluated cortical Aβ burden (using [(11)C] labeled Pittsburgh-Compound-B positron emission tomography), cerebrovascular lesions (using magnetic resonance imaging-defined white matter lesion [WML]), and neural integrity within AD regions (using a multimodal neuroimaging biomarker). Path models (adjusted for age, gender, and education) indicated that higher lifetime cognitive activity and higher current physical activity was associated with fewer WMLs. Lower WML volumes were in turn related to higher neural integrity and higher global cognitive functioning. As shown previously, higher lifetime cognitive activity was associated with lower [(11)C] labeled Pittsburgh-Compound-B retention, which itself moderated the impact of neural integrity on cognitive functioning. Lifestyle activity may thus promote cognitive health in aging by protecting against cerebrovascular pathology and Aβ pathology thought to be relevant to AD development.
- Published
- 2014
45. Vascular risk and A&bgr; interact to reduce cortical thickness in AD vulnerable brain regions
- Author
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Villeneuve, Sylvia, Reed, Bruce R, Madison, Cindee M, Wirth, Miranka, Marchant, Natalie L, Kriger, Stephen, Mack, Wendy J, Sanossian, Nerses, DeCarli, Charles, Chui, Helena C, Weiner, Michael W, and Jagust, William J
- Subjects
Biomedical and Clinical Sciences ,Neurosciences ,Clinical Sciences ,Prevention ,Biomedical Imaging ,Aging ,Clinical Research ,Alzheimer's Disease ,Brain Disorders ,Acquired Cognitive Impairment ,Neurodegenerative ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Dementia ,2.1 Biological and endogenous factors ,Aetiology ,Neurological ,Aged ,Aged ,80 and over ,Alzheimer Disease ,Amyloid beta-Peptides ,Aniline Compounds ,Brain ,Chi-Square Distribution ,Female ,Humans ,Longitudinal Studies ,Magnetic Resonance Imaging ,Male ,Neuropsychological Tests ,Positron-Emission Tomography ,Risk Factors ,Thiazoles ,Vascular Diseases ,Cognitive Sciences ,Neurology & Neurosurgery ,Clinical sciences - Abstract
ObjectiveThe objective of this study was to define whether vascular risk factors interact with β-amyloid (Aβ) in producing changes in brain structure that could underlie the increased risk of Alzheimer disease (AD).MethodsSixty-six cognitively normal and mildly impaired older individuals with a wide range of vascular risk factors were included in this study. The presence of Aβ was assessed using [(11)C]Pittsburgh compound B-PET imaging, and cortical thickness was measured using 3-tesla MRI. Vascular risk was measured with the Framingham Coronary Risk Profile Index.ResultsIndividuals with high levels of vascular risk factors have thinner frontotemporal cortex independent of Aβ. These frontotemporal regions are also affected in individuals with Aβ deposition, but the latter show additional thinning in parietal cortices. Aβ and vascular risk were found to interact in posterior (especially in parietal) brain regions, where Aβ has its greatest effect. In this way, the negative effect of Aβ in posterior regions is increased by the presence of vascular risk.ConclusionAβ and vascular risk interact to enhance cortical thinning in posterior brain regions that are particularly vulnerable to AD. These findings give insight concerning the mechanisms whereby vascular risk increases the likelihood of developing AD and supports the therapeutic intervention of controlling vascular risk for the prevention of AD.
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- 2014
46. Gene–Environment Interactions: Lifetime Cognitive Activity, APOE Genotype, and Beta-Amyloid Burden
- Author
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Wirth, Miranka, Villeneuve, Sylvia, La Joie, Renaud, Marks, Shawn M, and Jagust, William J
- Subjects
Alzheimer's Disease ,Aging ,Dementia ,Neurodegenerative ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Acquired Cognitive Impairment ,Brain Disorders ,Neurosciences ,Genetics ,Clinical Research ,2.1 Biological and endogenous factors ,Aetiology ,Neurological ,Quality Education ,Aged ,Aged ,80 and over ,Amyloid beta-Peptides ,Apolipoprotein E4 ,Brain Chemistry ,Cognition ,Female ,Gene-Environment Interaction ,Genetic Carrier Screening ,Genotype ,Humans ,Longevity ,Longitudinal Studies ,Male ,Middle Aged ,Positron-Emission Tomography ,aging ,Alzheimer's disease ,APOE ,beta-amyloid ,lifestyle activity ,PIB-PET ,β-amyloid ,Medical and Health Sciences ,Psychology and Cognitive Sciences ,Neurology & Neurosurgery - Abstract
Carriers of the apolipoprotein E (APOE) ε4 allele, the major genetic risk for Alzheimer's disease (AD), harbor an increased load of β-amyloid (Aβ) plaque burden that is felt to be a major instigator of AD development. Data has suggested that lifestyle factors may reduce AD risk by directly mitigating Aβ pathology, which could be particularly beneficial in APOE ε4 carriers. We therefore examined the interaction between lifetime cognitive activity and the APOE ε4 allele in relation to brain Aβ burden. We obtained measures of lifetime cognitive activity in 118 cognitively normal human individuals (mean age: 76.13 ± 5.56 years, 70 women) using a validated questionnaire that included measures over early, middle, and current age epochs. Hierarchical regression models (adjusted for age, gender, and years of education) were conducted to examine effects of APOE ε4 carrier status, lifetime cognitive activity, and the interaction of the two factors with cortical Aβ deposition, quantified using [11C] Pittsburgh-compound-B (PIB)-PET. As expected, the ε4 carriers exhibited higher PIB retention compared with noncarriers. Lifetime cognitive activity moderated the APOE genotype effect such that cortical PIB retention was diminished in ε4 carriers that reported higher cognitive activity over the life course. The findings suggest that greater lifetime cognitive activity may forestall AD pathology, specifically in genetically susceptible individuals. The effect could imply that cognitive training promotes increased neural efficiency that might retard the lifelong neurally mediated deposition of Aβ.
- Published
- 2014
47. Gene-environment interactions: lifetime cognitive activity, APOE genotype, and β-amyloid burden.
- Author
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Wirth, Miranka, Villeneuve, Sylvia, La Joie, Renaud, Marks, Shawn M, and Jagust, William J
- Subjects
Humans ,Positron-Emission Tomography ,Longitudinal Studies ,Heterozygote Detection ,Cognition ,Brain Chemistry ,Longevity ,Genotype ,Aged ,Aged ,80 and over ,Middle Aged ,Female ,Male ,Apolipoprotein E4 ,Amyloid beta-Peptides ,Gene-Environment Interaction ,APOE ,Alzheimer's disease ,PIB-PET ,aging ,lifestyle activity ,β-amyloid ,Genetic Carrier Screening ,beta-amyloid ,and over ,Neurology & Neurosurgery ,Medical and Health Sciences ,Psychology and Cognitive Sciences - Abstract
Carriers of the apolipoprotein E (APOE) ε4 allele, the major genetic risk for Alzheimer's disease (AD), harbor an increased load of β-amyloid (Aβ) plaque burden that is felt to be a major instigator of AD development. Data has suggested that lifestyle factors may reduce AD risk by directly mitigating Aβ pathology, which could be particularly beneficial in APOE ε4 carriers. We therefore examined the interaction between lifetime cognitive activity and the APOE ε4 allele in relation to brain Aβ burden. We obtained measures of lifetime cognitive activity in 118 cognitively normal human individuals (mean age: 76.13 ± 5.56 years, 70 women) using a validated questionnaire that included measures over early, middle, and current age epochs. Hierarchical regression models (adjusted for age, gender, and years of education) were conducted to examine effects of APOE ε4 carrier status, lifetime cognitive activity, and the interaction of the two factors with cortical Aβ deposition, quantified using [11C] Pittsburgh-compound-B (PIB)-PET. As expected, the ε4 carriers exhibited higher PIB retention compared with noncarriers. Lifetime cognitive activity moderated the APOE genotype effect such that cortical PIB retention was diminished in ε4 carriers that reported higher cognitive activity over the life course. The findings suggest that greater lifetime cognitive activity may forestall AD pathology, specifically in genetically susceptible individuals. The effect could imply that cognitive training promotes increased neural efficiency that might retard the lifelong neurally mediated deposition of Aβ.
- Published
- 2014
48. Cortical thickness mediates the effect of &bgr;-amyloid on episodic memory
- Author
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Villeneuve, Sylvia, Reed, Bruce R, Wirth, Miranka, Haase, Claudia M, Madison, Cindee M, Ayakta, Nagehan, Mack, Wendy, Mungas, Dan, Chui, Helena C, DeCarli, Charles, Weiner, Michael W, and Jagust, William J
- Subjects
Biomedical and Clinical Sciences ,Neurosciences ,Clinical Sciences ,Acquired Cognitive Impairment ,Alzheimer's Disease ,Clinical Research ,Dementia ,Neurodegenerative ,Aging ,Brain Disorders ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Prevention ,Aetiology ,2.1 Biological and endogenous factors ,Neurological ,Aged ,Aged ,80 and over ,Amyloid beta-Peptides ,Cerebral Cortex ,Cognition Disorders ,Cognitive Dysfunction ,Female ,Humans ,Male ,Memory ,Episodic ,Neuropsychological Tests ,Radionuclide Imaging ,Cognitive Sciences ,Neurology & Neurosurgery ,Clinical sciences - Abstract
ObjectiveTo investigate the associations among β-amyloid (Aβ), cortical thickness, and episodic memory in a cohort of cognitively normal to mildly impaired individuals at increased risk of vascular disease.MethodsIn 67 subjects specifically recruited to span a continuum of cognitive function and vascular risk, we measured brain Aβ deposition using [(11)C] Pittsburgh compound B-PET imaging and cortical thickness using MRI. Episodic memory was tested using a standardized composite score of verbal memory, and vascular risk was quantified using the Framingham Coronary Risk Profile index.ResultsIncreased Aβ was associated with cortical thinning, notably in frontoparietal regions. This relationship was strongest in persons with high Aβ deposition. Increased Aβ was also associated with lower episodic memory performance. Cortical thickness was found to mediate the relationship between Aβ and memory performance. While age had a marginal effect on these associations, the relationship between Aβ and cortical thickness was eliminated after controlling for vascular risk except when examined in only Pittsburgh compound B-positive subjects, in whom Aβ remained associated with thinner cortex in precuneus and occipital lobe. In addition, only the precuneus was found to mediate the relationship between Aβ and memory after controlling for vascular risk.ConclusionThese results suggest strong links among Aβ, cortical thickness, and memory. They highlight that, in individuals without dementia, vascular risk also contributes to cortical thickness and influences the relationships among Aβ, cortical thickness, and memory.
- Published
- 2014
49. Associations Between Serum Cholesterol Levels and Cerebral Amyloidosis
- Author
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Reed, Bruce, Villeneuve, Sylvia, Mack, Wendy, DeCarli, Charles, Chui, Helena C, and Jagust, William
- Subjects
Biomedical and Clinical Sciences ,Neurosciences ,Clinical Sciences ,Dementia ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Alzheimer's Disease ,Neurodegenerative ,Aging ,Cardiovascular ,Clinical Research ,Acquired Cognitive Impairment ,Brain Disorders ,Atherosclerosis ,Aetiology ,2.1 Biological and endogenous factors ,Neurological ,Aged ,Aged ,80 and over ,Alzheimer Disease ,Amyloid beta-Peptides ,Amyloidosis ,Cerebral Cortex ,Cholesterol ,Cohort Studies ,Cross-Sectional Studies ,Female ,Humans ,Male ,Radionuclide Imaging - Abstract
ImportanceBecause deposition of cerebral β-amyloid (Aβ) seems to be a key initiating event in Alzheimer disease (AD), factors associated with increased deposition are of great interest. Whether elevated serum cholesterol levels act as such a factor is unknown.ObjectiveTo investigate the association between serum cholesterol levels and cerebral Aβ during life early in the AD process.Design, setting, and participantsA multisite, university medical center-based, cross-sectional analysis of potential associations between contemporaneously assayed total serum cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and cerebral Aβ, measured with carbon C11-labeled Pittsburgh Compound B (PIB) positron emission tomography. Seventy-four persons (mean age, 78 years) were recruited via direct outreach in stroke clinics and community senior facilities following a protocol designed to obtain a cohort enriched for cerebrovascular disease and elevated vascular risk. Three patients had mild dementia. All others were clinically normal (n = 33) or had mild cognitive impairment (n = 38).ResultsCerebral Aβ was quantified using a Global PIB Index, which averages PIB retention in cortical areas prone to amyloidosis. Statistical models that controlled for age and the apolipoprotein E ε4 allele revealed independent associations among the levels of LDL-C, HDL-C, and PIB index. Higher LDL-C and lower HDL-C levels were both associated with a higher PIB index. No association was found between the total cholesterol level and PIB index. No association was found between statin use and PIB index, and controlling for cholesterol treatment in the statistical models did not alter the basic findings.Conclusions and relevanceElevated cerebral Aβ level was associated with cholesterol fractions in a pattern analogous to that found in coronary artery disease. This finding, in living humans, is consistent with prior autopsy reports, epidemiologic findings, and animal and in vitro work, suggesting an important role for cholesterol in Aβ processing. Because cholesterol levels are modifiable, understanding their link to Aβ deposition could potentially and eventually have an effect on retarding the pathologic cascade of AD. These findings suggest that understanding the mechanisms through which serum lipids modulate Aβ could offer new approaches to slowing Aβ deposition and thus to reducing the incidence of AD.
- Published
- 2014
50. Tau accumulation and its spatial progression across the Alzheimer's disease spectrum.
- Author
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St-Onge, Frédéric, Chapleau, Marianne, Breitner, John C S, Villeneuve, Sylvia, and Binette, Alexa Pichet
- Published
- 2024
- Full Text
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