Search

Your search keyword '"Dallaire-Théroux, Caroline"' showing total 28 results
Start Over Author "Dallaire-Théroux, Caroline"
28 results on '"Dallaire-Théroux, Caroline"'

1. Recommendations to distinguish behavioural variant frontotemporal dementia from psychiatric disorders

Author

Ducharme, Simon, Dols, Annemiek, Laforce, Robert, Devenney, Emma, Kumfor, Fiona, van den Stock, Jan, Dallaire-Théroux, Caroline, Seelaar, Harro, Gossink, Flora, Vijverberg, Everard, Huey, Edward, Vandenbulcke, Mathieu, Masellis, Mario, Trieu, Calvin, Onyike, Chiadi, Caramelli, Paulo, de Souza, Leonardo Cruz, Santillo, Alexander, Waldö, Maria Landqvist, Landin-Romero, Ramon, Piguet, Olivier, Kelso, Wendy, Eratne, Dhamidhu, Velakoulis, Dennis, Ikeda, Manabu, Perry, David, Pressman, Peter, Boeve, Bradley, Vandenberghe, Rik, Mendez, Mario, Azuar, Carole, Levy, Richard, Le Ber, Isabelle, Baez, Sandra, Lerner, Alan, Ellajosyula, Ratnavalli, Pasquier, Florence, Galimberti, Daniela, Scarpini, Elio, van Swieten, John, Hornberger, Michael, Rosen, Howard, Hodges, John, Diehl-Schmid, Janine, and Pijnenburg, Yolande

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Psychology, Neurosciences, Behavioral and Social Science, Dementia, Alzheimer's Disease Related Dementias (ADRD), Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Frontotemporal Dementia (FTD), Mental Health, Aging, Serious Mental Illness, Neurodegenerative, Acquired Cognitive Impairment, Clinical Research, Genetic Testing, Brain Disorders, Biomedical Imaging, Mental Illness, Genetics, 4.2 Evaluation of markers and technologies, 4.1 Discovery and preclinical testing of markers and technologies, 2.1 Biological and endogenous factors, Mental health, Neurological, Delayed Diagnosis, Diagnosis, Differential, Female, Fluorodeoxyglucose F18, Frontotemporal Dementia, Humans, Magnetic Resonance Imaging, Male, Mental Disorders, Neuroimaging, Neurologic Examination, Neuropsychological Tests, Positron-Emission Tomography, frontotemporal dementia, psychiatry, differential diagnosis, guidelines, biomarkers, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery, Biomedical and clinical sciences, Health sciences
Abstract

The behavioural variant of frontotemporal dementia (bvFTD) is a frequent cause of early-onset dementia. The diagnosis of bvFTD remains challenging because of the limited accuracy of neuroimaging in the early disease stages and the absence of molecular biomarkers, and therefore relies predominantly on clinical assessment. BvFTD shows significant symptomatic overlap with non-degenerative primary psychiatric disorders including major depressive disorder, bipolar disorder, schizophrenia, obsessive-compulsive disorder, autism spectrum disorders and even personality disorders. To date, ∼50% of patients with bvFTD receive a prior psychiatric diagnosis, and average diagnostic delay is up to 5-6 years from symptom onset. It is also not uncommon for patients with primary psychiatric disorders to be wrongly diagnosed with bvFTD. The Neuropsychiatric International Consortium for Frontotemporal Dementia was recently established to determine the current best clinical practice and set up an international collaboration to share a common dataset for future research. The goal of the present paper was to review the existing literature on the diagnosis of bvFTD and its differential diagnosis with primary psychiatric disorders to provide consensus recommendations on the clinical assessment. A systematic literature search with a narrative review was performed to determine all bvFTD-related diagnostic evidence for the following topics: bvFTD history taking, psychiatric assessment, clinical scales, physical and neurological examination, bedside cognitive tests, neuropsychological assessment, social cognition, structural neuroimaging, functional neuroimaging, CSF and genetic testing. For each topic, responsible team members proposed a set of minimal requirements, optimal clinical recommendations, and tools requiring further research or those that should be developed. Recommendations were listed if they reached a ≥ 85% expert consensus based on an online survey among all consortium participants. New recommendations include performing at least one formal social cognition test in the standard neuropsychological battery for bvFTD. We emphasize the importance of 3D-T1 brain MRI with a standardized review protocol including validated visual atrophy rating scales, and to consider volumetric analyses if available. We clarify the role of 18F-fluorodeoxyglucose PET for the exclusion of bvFTD when normal, whereas non-specific regional metabolism abnormalities should not be over-interpreted in the case of a psychiatric differential diagnosis. We highlight the potential role of serum or CSF neurofilament light chain to differentiate bvFTD from primary psychiatric disorders. Finally, based on the increasing literature and clinical experience, the consortium determined that screening for C9orf72 mutation should be performed in all possible/probable bvFTD cases or suspected cases with strong psychiatric features.

Published
2020

2. Tau positron emission tomography, cerebrospinal fluid and plasma biomarkers of neurodegeneration, and neurocognitive testing: an exploratory study of participants with myotonic dystrophy type 1

Author

Laforce, Robert Jr, Dallaire-Théroux, Caroline, Racine, Annie M., Dent, Gersham, Salinas-Valenzuela, Cristian, Poulin, Elizabeth, Cayer, Anne-Marie, Bédard-Tremblay, Daphnée, Rouleau-Bonenfant, Thierry, St-Onge, Frédéric, Schraen-Maschke, Susanna, Beauregard, Jean-Mathieu, Sergeant, Nicolas, and Puymirat, Jack

Published
2022
Full Text
View/download PDF

7. Geriatric dementia care at Ontario Shores: A new model of care

Author

Viau, Katelynn, Yaddaden, Amel, Lussier, Maxime, Bier, Nathalie, Earle, Julie, Duff-Woskosky, Andra, Bartfay, Wally, Desai, Chaitali, Zavitz, Karen, Horsburgh, Sheri, Gamble, Brenda, Lee, Linda, Hillier, Loretta M., Patel, Tejal, Molnar, Frank, Clarke, Jo-Anne, Borrie, Michael, Cammer, Allison, Morgan, Debra, Whiting, Susan, de Vos, Maya, Henri-Bhargava, Alexandre, Votova, Kristine, Delmar, Paul, Kerchner, Geoffrey A, Wang, Guoqiao, Bateman, Randall, Klein, Gregory, Andjelkovic, Mirjana, Abi-Saab, Danielle, Bullain, Szofia, Montoya, Alonso, Fontoura, Paulo, Doody, Rachelle, Tai, Elaine, Harvey, David, Hofmann, Carsten, Ristic, Smiljana, Rehal, Sunita, Voyle, Nicola, Baudler, Monika, Verreault, Phylicia, Rousseau, François, Keller, Evelyn, Simard, Alexandra, Azouaou, Nassima, Jarboui, Manel, Talleria, Lorraine, Duguay, Johanne, Mérette, Chantale, Labbé, Annie, de Arco, Rossana Peredo Nunez, Yous, Marie-Lee, Ploeg, Jenny, Kaasalainen, Sharon, Martin, Lori Schindel, Palumbo, Mary Val, Rambur, Betty, McKenna, Lori, Voyer, Philippe, Allaire, Émilie, Li, Bing, Thaut, Michael, Yogaparan, Thirumagal, Shanmuganathan, Thirunathan, Vickneswaran, Anicha, Sriharan, Sruthy, DeMarco, Mari L., Hsiung, Ging-Yuek Robin, Best, John R., Chertkow, Howard, Gauthier, Serge, Karlawish, Jason, Feldman, Howard, Spaner, Caroline, Christie, Brian, Musteata, Stela, Gawryluk, Jodie, Hofer, Scott, Henri-Bhargava, Alex, Kenny, Rebecca, Elliot, Valerie, Kosteniuk, Julie, Chow, Amanda Froehlich, Bayly, Melanie, O’Connell, Megan E., Kortzman, August, O’Connell, Megan, Kirk, Andrew, Conn, David, Sokoloff, Lisa, Feldman, Sid, Chau, James, Moser, Andrea, Lingum, Navena, Gingrich, Shaen, Shaikh, Salma, Rabheru, Kiran, Cassidy, Keri-Leigh, Checkland, Claire, Parsons, Daria, Massie, Ariane S., Mitchell, Julie Spence, Aksenchuk, Sophia, Lindsay, Barbara, Howard, Maria, Shaw, Courtney, Armitage, Gerrard, Capstick, Andrea, McNeil, Heather, Holyoke, Paul, Vines, Chanile, Giosa, Justine, Khan, Bilal, Shultz, Mary, BEAUCHET, Olivier, Sekhon, Harmehr, Allali, Gilles, Montembeault, Maxime, Brodeur, Catherine, Macoir, Joël, Maxwell, Colleen, Maclagan, Laura, Campitelli, Michael, Yao, Shenzhen, Dharma, Christoffer, Sherin, Tracey, Hogan, David, Bronskill, Susan, Ivo, Jessica, Faisal, Sadaf, McDougall, Aidan, Bauer, Jillian, Pritchard, Sarah, Chang, Feng, Mehta, Deval, Syed, Ali, Carter, Caitlin, Sharma, Shaambhavi, Nagge, Jeff, Naglie, Gary, Stasiulis, Elaine, Yamin, Stephanie, Vrkljan, Brenda, Tuokko, Holly, Sanford, Sarah, Porter, Michelle, Polgar, Jan, Myers, Anita, Moorhouse, Paige, Mazer, Barbara, Marshall, Shawn, Gélinas, Isabelle, Crizzle, Alexander, Byszewski, Anna, Belchior, Patricia, Bédard, Michel, Rapoport, Mark, Minish, Duane, Yetman, Linda, Stephenson, Margaret, McCloskey, Rose, Agbaku, Mansa, Jarrett, Pamela, Cavanagh, Jennifer, Loncar, Adele, Demers, Vickie, Gobessi, Linda, Lodha, Vinay, Scerbe, Andrea, Astell, Arlene, DesRoches, Andrea, Panyavin, Ivan, Feltz, Nick, Wittich, Walter, Aubin, Gabrielle, Hogan, Mariah, Swaminathan, Swathi, Altschuler, Aviva, Murphy, Kelly, Guthrie, Dawn, Williams, Nicole, Campos, Jennifer, Mick, Paul, Orange, Joseph B., Pichora-Fuller, M. Kathleen, Savundranayagam, Marie Y., Phillips, Natalie A., Giroud, Nathalie, Pichora-Fuller, Kathy, Al-Yawer, Faisal, Rehan, Sana, Phillips, Natalie, Beauchet, Olivier, Niculescu, Iulia, Iaboni, Andrea, Quirt, Hannah, Penko, Marion, Tsokas, Mario, Marshall, Cecelia, Flint, Alastair, McGilton, Katherine, O’Connell, Megan E, Stewart, Norma J, Seitz, Dallas, Daku, Jean, Hack, Tracy, Hoium, Faye, Kennett-Russill, Deb, Sauter, Kristen, Holley, Joanna, Wimhurst, Christine, Katchaluba, Janet, Mitchell, Debbie, Severina, Elmira, Dallaire-Théroux, Caroline, Saikali, Stéphan, Duchesne, Simon, Sivananthan, Saskia, Mirza, Saira, Saeed, Usman, Knight, Jo, Ramirez, Joel, Stuss, Donald, Yu, Di, Swardfager, Walter, Keith, Julia, Nestor, Sean, Black, Sandra, Masellis, Mario, Joyal, Marilyne, Kotz, Sonja A., Lenglos, Christophe, Renauld, Emmanuelle, Wilson, Maximiliano A., Fecteau, Shirley, Appel, Lora, Kisonas, Erika, Appel, Eva, Bartlett, Deanna, Klein, Jennifer, Rosenberg, Jarred, Smith, Christopher, Ali, Suad, Narang, Tanya, Wiseman, Micaela, Ein, Natalie, Orchanian-Cheff, Ani, Rylett, Jane, Hogan, David B., Rockwood, Kenneth, Dixon, Roger, Sun, Winnie, Hawkins, Stacey A., Awde, Carolee, Kay, Kelly, Huntsbarger, Deana, Ferrier, Erin, Sourial, Nadia, Arsenault-Lapierre, Genevieve, McAiney, Carrie, Vedel, Isabelle, Ingram, K. Jennifer, Frank, Andrew, Sabra, Iman, Wallace, Bruce, Breau, Michael, Sweet, Lisa, Goubran, Rafiq, Knoefel, Frank, Goubran, Rafik, Stroulia, Eleni, Ault, Laura, Kecskemet, Judith, Guseva, Elena, Lungu, Ovidiu, Goldman, Sondra, Wilchesky, Machelle, Johri, Fozia, Turner, Angelese, Lavoie, Monica, Tang-Wai, David, Leonard, Carol, Graham, Naida L., Rochon, Elizabeth, Middleton, Laura, Herrmann, Nathan, Oh, Paul, Regan, Kayla, Bechard, Lauren, Lanctôt, Krista, Freeman, Shannon, Pettersen, Jacqueline, Tomasone, Jennifer, Dupuis, Sherry, Giangregorio, Lora, Ferris, Rebecca, Stultz, Tim, Mallard, Kirsten, Campbell, Elaine, Chatterjee, Atri, Mackenzie, Ian, Reinshagen, Veronica Hirsh, Ducharme, Blake, Mousavi, Ali, Gill, Sascha, Mouches, Pauline, Wang, Meng, Rajasheskar, Deepthi, MacMaster, Frank, Forkert, Nils, Smith, Eric, Ismail, Zahinoor, Varatharajah, Breni, Camicioli, Richard, Gee, Myrlene, Zwiers, Angela, Sekhon, Ramnik, Charlton, Anna, Arsenault-Lapierre, Geneviève, Ingram, Jennifer, Hawkins, Stacey, Mousavi, SeyedAli, Mackenzie, Ian R. A., Hirsh-Reinshagen, Veronica, Hsiung, Ging-Yuek. R., Gillingham, Susan M.E., Anderson, Nicole D., Alain, Claude, Georgievski, Georgi, Alfaro, Leonardo, McClenaghan, Meridith, Soares, Daniela, Matheson, Maureen, Stanoulis, Krisanne, Boyle, Daniel, Chau, Linh, Pelc, Jordan, Snash, Nadia, Byrne, Joanne, Elalouf, Karine, Alfaro, Andrea Urqueta, Johnson, Aaron, Marinier, Julie-Andrée, Kehayia, Eva, Gagné, Jean-Pierre, Murphy, Caitlin, Ellen, Ruth, Flowers, Brandi, Boulton, Karen Lee, Subotic, Arsenije, McCreary, Cheryl R., Nguyen, Amanda, Saad, Feryal, Alvarez, Ana, Beaudin, Andrew E, Pike, Bruce, Smith, Eric E, Hu, Sophie, Patten, Scott, Fick, Gordon, Sapkota, Shraddha, Mirza, Saira Saeed, Scott, Christopher J., Stuss, Donald T., Black, Sandra E., Le Blanc, Gabriella, Ducharme, Simon, Meilleur-Durand, Synthia, Lévesque, Marianne, St-Onge, Frédéric, Cunnane, Stephen, Villeneuve, Sylvia, Callahan, Brandy, Laforce, Robert, Cetin-Sahin, Deniz, Cummings, Greta G., Schuster, Tibor, Karanofsky, Mark, De Jesus, Belmir J., Cassani, Raymundo, Cecchi, Marco, Fadem, K. C., McGeown, William J., Falk, Tiago H., Chu, Charlene, Zdaniuk, Natalia, Wang, Rosalie, Ouellet, Marie-Christine, Cassivi-Joncas, Alison, Godard-Sebillotte, Claire, Rochette, Louis, Pelletier, Eric, Strumpf, Erin, Margo-Dermer, Eva, Silver, Hilah, Vafaei, Rod, Fok, Alice C, Hsiung, Ging-Yuek R., Ursenbach, Jake, Bethell, Jennifer, Neuman, Mark D, Bateman, Brian T, Hill, Andrea, Wunsch, Hannah, Ritchie, Kim, Cramm, Heidi, Aiken, Alice, Donnelly, Catherine, Goldie, Katie, Delara, Mahin, Ozzoude, Miracle, Varriano, Brenda, McLaughlin, Paula, Troyer, Angela, Bartha, Robert, Symons, Sean, Kwan, Donna, Tan, Brian, Swartz, Richard H., Saposnik, Gustavo, Tartaglia, Maria C., Ahuja, Manan, Siddhpuria, Shailee, Gormley, Jessica, Reppas, Christina, Wong, Eric, Lee, Justin, Patterson, Christopher, Walker, Jennifer, Warry, Wayne, Blind, Melissa, Allaby, Cheryl, Pitawanakwat, Karen, Zhao, Yantao, Lemieux, Andrine, Jacklin, Kristen, Crowshoe, Lindsay, Boehme, Gail, McKenna, Betty, Boyling, Elaine, Webkamigad, Sharlene, Bigeagle, Louise, Akan, Nicole, Wallace, Lindsay, Theou, Olga, Bennett, David, Darvesh, Sultan, Kirkland, Susan, Fisk, John, Andrew, Melissa, Cullen, Stephanie, Carroll, Susan, Mahon, Joel, Sarquis-Adamson, Yanina, Montero-Odasso, Manuel, Sharma, Nabina, Beaton, Derek, Roberts, Angela, Munoz, Doug, Swartz, Richard, Breen, David, Lang, Anthony, Fischer, COrrine, Fischer, Corrine, Kumar, Sanjeeve, Freedman, Morris, Finger, Elizabeth, Zinman, Lorne, Grimes, David A., Sunderland, Kelly M., Binns, Malcolm A., Strother, Stephen C., Mandzia, Jennifer, Orange, JB, Tartaglia, Carmela, El Shatshat, Amna, Rao, Praveen P.N., Teves, Julia, Bodkin, R Jack, Ho, Joanne M-W, Mehdizadeh, Sina, Dolatabadi, Elham, Ng, Kimberley-Dale, Arora, Twinkle, Jizmejian, Melody, Mansfield, Avril, Taati, Babak, Levy, Jake, Savard, Melissa, Pascoal, Tharick, Soucy, Jean-Paul, Rosa-Neto, Pedro, Martins, Felicia, Waller, Shannon, Flora, Parminder, Morland, Chris, Donovan, Steve, Fels, Deborah, Desai, Shital, Boger, Jennifer, Shashtri, Karan, Persaud, Deanna, Marashi, Sheida, Nedlund, Ann-Charlotte, Mäki-Petäjä-Leinonen, Anna, Nygård, Louise, Issakainen, Mervi, ryd, Charlotta, Pan, Yuhan, Joddrell, Phil, Dove, Erica, Owens, Hollis, Park, Elly, Liu, Lili, Kaufman, David, Simonian, Natalie, Chen, Ying, Sunderland, Kelly, Fraser, Julia, Swartz, Rick, Strother, Stephen, Legrand, Diego, Roberge, Pasquale, Vanasse, Alain, Bocti, Christian, Pirrie, Lorraine, Gray, Carolyn Steele, Nippak, Pria, Coughlan, Dave, Teselink, Johannes, Hermann, Nathan, Rasquinha, Fawn, Lanctot, Krista, Webber, Jodi, Woo, Kevin, Chamoun, Elicia, Coulombe, Valérie, Sellami, Leila, Paquette-Raynard, Emmanuelle, Gardner, Sandra, van Zon, Lorraine, Moy, Sally, Sidrak, Mariam, Sternhill, Janis, Feldman, Sidney, Karuza, Jurgis, Berall, Anna, Thomas, Neil, Mattek, Nora, Riley, Thomas, Reynolds, Christina, Marcoe, Jennifer, Sharma, Nicole, Kaye, Jeffrey, Jagtap, Shreya, Rotenberg, Shlomit, Vandermorris, Susan, Anderson, ND, Dawson, DR, Chater, Catherine, Soor, Jaspreet, Ji, Xiang, Koo, Morgan, Compagnone, Jordana, Kertes, Peter, Juby, Angela, Mager, Diana, Davis, Christopher, Jay, David, Blackburn, Toni, Brocks, Dion, Lee, Hyunwoo, Wiggermann, Vanessa, Rauscher, Alexander, Lam, Kevin, Tam, Roger, Popuri, Karteek, Beg, Mirza Faisal, Jacova, Claudia, Sossi, Vesna, Bindra, Jessica, Bouvier, Liziane, Monetta, Laura, Vitali, Paolo, Martel-Sauvageau, Vincent, Godin, Judith, McNeil, Shelly, McElhaney, Janet, Laughton, Thomas, Ho, Joanne, Tung, Jennifer, Dubé, Joseph B., Lin, Tianzhen, Best, Sarah, Truemner, Julia, Sargeant, Patricia L., Borrie, Michael J., Fogarty, Jennifer, Bassi, Nimi, Di Prospero, Cynthia, Whitehead, Victor, Pilon, Randi, Wong, Timothy, Elhayek, Nada, Dasgupta, Monidipa, Davis, Daniel, ORegan, Niamh, Kröger, Edeltraut, Furrer, Daniela, Wilcheski, Machelle, Morin, Michèle, Carmichael, Pierre-Hugues, Champoux, Nathalie, Monette, Johanne, Giguère, Anik, Aubin, Michèle, Durand, Pierre, Whiteside, Jena, Mele, Bria, Merrikh, Daria, Goodarzi, Zahra, Seary, Judith Anne, Bulley, Heather, Diciacca, Allison, Esseltine, Julia, Gaiger, Erin, Jankovic, Ivana, Mackenzie, Stephanie, McBride, Meghan, Knopp-Sihota, Jennifer A., Hoben, Mathias, Poss, Jeffrey W., Rachor, Geoffrey S., Estabrooks, Carole A., and Iroanyah, Ngozi

Subjects
Abstracts: Posters
Published
2020

8. Evaluation of Intensive Versus Standard Blood Pressure Reduction and Association with Cognitive Decline and Dementia: A Systematic Review and Meta-Analysis (S15.007)

Author

Dallaire-Théroux, Caroline, primary, Quesnel-Olivo, Marie-Hélène, additional, Brochu, Karine, additional, Bergeron, Frédéric, additional, O’Connor, Sarah, additional, Turgeon, Alexis, additional, Laforce, Robert, additional, Verreault, Steve, additional, Camden, Marie-Christine, additional, and Duchesne, Simon, additional

Published
2022
Full Text
View/download PDF

9. Evaluation of Intensive vs Standard Blood Pressure Reduction and Association With Cognitive Decline and Dementia

Author

Dallaire-Théroux, Caroline, Quesnel-Olivo, Marie-Hélène, Brochu, Karine, Bergeron, Frédéric, O’Connor, Sarah, Turgeon, Alexis F., Laforce, Robert Jr, Verreault, Steve, Camden, Marie-Christine, and Duchesne, Simon

Subjects
Aged, 80 and over, Male, Research, Incidence, Blood Pressure, Middle Aged, Online Only, Neurology, Hypertension, Humans, Cognitive Dysfunction, Dementia, Female, Original Investigation, Aged
Abstract

Key Points Question Is intensive blood pressure reduction associated with lower rates of cognitive decline and dementia? Findings In this systematic review and meta-analysis of 5 randomized clinical trials with 17 396 participants, there was no significant association of lower blood pressure targets vs standard blood pressure management with the incidence of cognitive decline, dementia, and mild cognitive impairment in middle-aged and older adults with hypertension. Meaning These findings suggest that current evidence does not support intensive blood pressure reduction as a preventive strategy for cognitive decline and dementia., This systematic review and meta-analysis explores the association of intensive blood pressure reduction vs standard blood pressure management with the incidence of cognitive decline and dementia in adults with hypertension., Importance Optimal blood pressure (BP) targets for the prevention of cognitive impairment remain uncertain. Objective To explore the association of intensive (ie, lower than usual) BP reduction vs standard BP management with the incidence of cognitive decline and dementia in adults with hypertension. Data Sources and Study Selection A systematic review and meta-analysis of randomized clinical trials that evaluated the association of intensive systolic BP lowering on cognitive outcomes by searching MEDLINE, Embase, CENTRAL, Web of Science, CINAHL, PsycINFO, the International Clinical Trials Registry Platform, and ClinicalTrials.gov from database inception to October 27, 2020. Data Extraction and Synthesis Data screening and extraction were performed independently by 2 reviewers based on Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines. The risk of bias was assessed using the Cochrane risk of bias 2 tool. Random-effects models with the inverse variance method were used for pooled analyses. The presence of potential heterogeneity was evaluated with the I2 index. Main Outcomes and Measures The primary outcome was cognitive decline. Secondary outcomes included the incidence of dementia, mild cognitive impairment (MCI), cerebrovascular events, serious adverse events, and all-cause mortality. Results From 7755 citations, we identified 16 publications from 5 trials with 17 396 participants (mean age, 65.7 years [range, 63.0-80.5 years]; 10 562 [60.5%] men) and 2 additional ongoing trials. All 5 concluded trials included in quantitative analyses were considered at unclear to high risk of bias. The mean follow-up duration was 3.3 years (range, 2.0 to 4.7 years). Intensive BP reduction was not significantly associated with global cognitive performance (standardized mean difference, 0.01; 95% CI, −0.04 to 0.06; I2 = 0%; 4 trials; 5246 patients), incidence of dementia (risk ratio [RR], 1.09; 95% CI, 0.32 to 3.67; I2 = 27%; 2 trials; 9444 patients) or incidence of MCI (RR, 0.91; 95% CI, 0.73 to 1.14; I2 = 74%; 2 trials; 10 774 patients) when compared with standard treatment. However, a reduction of cerebrovascular events in the intensive group was found (RR, 0.79; 95% CI, 0.67 to 0.93; I2 = 0%; 5 trials; 17 396 patients) without an increased risk of serious adverse events or mortality. Conclusions and Relevance In this study, there was no significant association between BP reduction and lower risk of cognitive decline, dementia, or MCI. The certainty of this evidence was rated low because of the limited sample size, the risk of bias of included trials, and the observed statistical heterogeneity. Therefore, current available evidence does not justify the use of lower BP targets for the prevention of cognitive decline and dementia.

Published
2021

12. Erratum: Recommendations to distinguish behavioural variant frontotemporal dementia from psychiatric disorders (Brain (2020) 143 DOI: 10.1093/brain/awaa018)

Author

Ducharme, Simon, Dols, Annemiek, Laforce, Robert, Devenney, Emma, Kumfor, Fiona, van den Stock, Jan, Dallaire-Théroux, Caroline, Seelaar, Harro, Gossink, Flora, Vijverberg, Everard, Huey, Edward, Vandenbulcke, Mathieu, Masellis, Mario, Trieu, Calvin, Onyike, Chiadi, Caramelli, Paulo, de Souza, Leonardo Cruz, Santillo, Alexander, Waldö, Maria Landqvist, Landin-Romero, Ramon, Piguet, Olivier, Kelso, Wendy, Eratne, Dhamidhu, Velakoulis, Dennis, Ikeda, Manabu, Perry, David, Pressman, Peter, Boeve, Bradley, Vandenberghe, Rik, Mendez, Mario, Azuar, Carole, Levy, Richard, Le Ber, Isabelle, Baez, Sandra, Lerner, Alan, Ellajosyula, Ratnavalli, Pasquier, Florence, Galimberti, Daniela, Scarpini, Elio, van Swieten, John, Hornberger, Michael, Rosen, Howard, Hodges, John, Diehl-Schmid, Janine, Pijnenburg, Yolande, Neurology, Psychiatry, Amsterdam Neuroscience - Neurodegeneration, Human genetics, and APH - Mental Health

Abstract

The authors apologize for misspelling the last name of the author Ratnavalli Ellajosyula. This has now been corrected.

Published
2020
Full Text
View/download PDF

13. Evaluation of intensive versus standard blood pressure reduction and association with cognitive decline and dementia : a systematic review and metaAnalysis

Author

Dallaire-Théroux, Caroline, Quesnel-Olivo, Marie-Hélène, Brochu, Karine, Bergeron, Frédéric, O'Connor, Sarah, Turgeon-Fournier, Alexis, Laforce, Robert, Verreault, Steve, Camden, Marie-Christine, Duchesne, Simon, Dallaire-Théroux, Caroline, Quesnel-Olivo, Marie-Hélène, Brochu, Karine, Bergeron, Frédéric, O'Connor, Sarah, Turgeon-Fournier, Alexis, Laforce, Robert, Verreault, Steve, Camden, Marie-Christine, and Duchesne, Simon

Abstract

Importance: Optimal blood pressure (BP) targets for the prevention of cognitive impairment remain uncertain. Objective: To explore the association of intensive (i.e. lower than usual) BP reduction compared to guidelines on the incidence of cognitive decline and dementia in adults with hypertension. Data Sources and Study Selection: We conducted a systematic review and meta-analysis of randomized controlled trials that evaluated the association of intensive systolic BP lowering on cognitive outcomes by searching MEDLINE, Embase, CENTRAL, Web of Science, CINAHL, PsycINFO, ICTRP and ClinicalTrials.gov for data up to October 27, 2020. Data Extraction and Synthesis: Data screening and extraction were performed independently by two reviewers based on PRISMA guidelines. The risk of bias was assessed using the Cochrane risk-of-bias 2 tool. We used random-effects models using the inverse variance method for our pooled analyses. We evaluated the presence of potential heterogeneity with the I2 index. Main Outcomes and Measures: Our primary outcome was cognitive decline. Secondary outcomes included the incidence of dementia, mild cognitive impairment (MCI), cerebrovascular events, serious adverse events, and all-cause mortality. Results: From 7,755 citations, we identified sixteen publications from five trials (17,396 participants, mean age 65.7 years, 60.5% males) and two additional ongoing trials. All five trials included in quantitative analyses were considered at unclear to high risk of bias. The mean followup duration was 3.3 years (range 2.0 to 4.7 years). Intensive BP reduction was not significantly associated with global cognitive performance (SMD 0.01, 95% CI -0.04 to 0.06, I2 = 0%, four trials, 5,246 patients), incidence of dementia (RR 1.09, 95% CI 0.32 to 3.67, I2 = 27%, two trials, 9,444 patients) or incidence of MCI (RR 0.91, 95% CI 0.73 to 1.14, I2 = 74%, two trials, 10,774 patients) when compared to standard treatment. However, we found a reduction of cerebrovas

Published
2021

14. Evaluation of intensive versus standard blood pressure reduction and association with cognitive decline and dementia : a systematic review and meta-analysis

Author

Verreault, Steve, Turgeon-Fournier, Alexis, Brochu, Karine, Quesnel-Olivo, Marie-Hélène, Duchesne, Simon, O'Connor, Sarah, Laforce, Robert, Dallaire-Théroux, Caroline, Bergeron, Frédéric, Camden, Marie-Christine, Verreault, Steve, Turgeon-Fournier, Alexis, Brochu, Karine, Quesnel-Olivo, Marie-Hélène, Duchesne, Simon, O'Connor, Sarah, Laforce, Robert, Dallaire-Théroux, Caroline, Bergeron, Frédéric, and Camden, Marie-Christine

Abstract

Importance: Optimal blood pressure (BP) targets for the prevention of cognitive impairment remain uncertain. Objective: To explore the association of intensive (i.e. lower than usual) BP reduction compared to guidelines on the incidence of cognitive decline and dementia in adults with hypertension. Data Sources and Study Selection: We conducted a systematic review and meta-analysis of randomized controlled trials that evaluated the association of intensive systolic BP lowering on cognitive outcomes by searching MEDLINE, Embase, CENTRAL, Web of Science, CINAHL, PsycINFO, ICTRP and ClinicalTrials.gov for data up to October 27, 2020. Data Extraction and Synthesis: Data screening and extraction were performed independently by two reviewers based on PRISMA guidelines. The risk of bias was assessed using the Cochrane risk-of-bias 2 tool. We used random-effects models using the inverse variance method for our pooled analyses. We evaluated the presence of potential heterogeneity with the I2 index. Main Outcomes and Measures: Our primary outcome was cognitive decline. Secondary outcomes included the incidence of dementia, mild cognitive impairment (MCI), cerebrovascular events, serious adverse events, and all-cause mortality. Results: From 7,755 citations, we identified sixteen publications from five trials (17,396 participants, mean age 65.7 years, 60.5% males) and two additional ongoing trials. All five trials included in quantitative analyses were considered at unclear to high risk of bias. The mean followup duration was 3.3 years (range 2.0 to 4.7 years). Intensive BP reduction was not significantly associated with global cognitive performance (SMD 0.01, 95% CI -0.04 to 0.06, I2 = 0%, four trials, 5,246 patients), incidence of dementia (RR 1.09, 95% CI 0.32 to 3.67, I2 = 27%, two trials, 9,444 patients) or incidence of MCI (RR 0.91, 95% CI 0.73 to 1.14, I2 = 74%, two trials, 10,774 patients) when compared to standard treatment. However, we found a reduction of cerebrovas

Published
2021

20. Braak neurofibrillary tangle staging prediction from in vivo MRI metrics

Author

Potvin, Olivier, Beheshti, Iman, Dieumegarde, Louis, Duchesne, Simon, Dallaire-Théroux, Caroline, Saikali, Stephan, Potvin, Olivier, Beheshti, Iman, Dieumegarde, Louis, Duchesne, Simon, Dallaire-Théroux, Caroline, and Saikali, Stephan

Abstract

INTRODUCTION: Alzheimer’s disease (AD) diagnosis requires postmortem visualization of amyloid and tau deposits. As brain atrophy can provide assessment of consequent neurodegeneration, our objective was to predict postmortem neurofibrillary tangles (NFT) from in vivo MRI measurements. METHODS: All participants with neuroimaging and neuropathological data from the Alzheimer’s Disease Neuroimaging Initiative, the National Alzheimer’s Coordinating Center and the Rush Memory and Aging Project were selected (n=186). 232 variables were extracted from last MRI before death using FreeSurfer. Nonparametric correlation analysis and multivariable support vector machine classification were performed to provide a predictive model of Braak NFT staging. RESULTS: We demonstrated that 59 of our MRI variables, mostly temporal lobe structures, were significantly associated with Braak NFT stages (p<.005). We obtained a 62.4% correct classification rate for discrimination between transentorhinal, limbic and isocortical groups. DISCUSSION: Structural neuroimaging may therefore be considered as a potential biomarker for early detection of AD-associated neurofibrillary degeneration.

Published
2019

23. Clinical Association of White Matter Hyperintensities Localization in a Mexican Family with Spastic Paraparesis Carrying the PSEN1 A431E Mutation.

Author

Santos-Mandujano, Rosalía A., Ryan, Natalie S., Chávez-Gutiérrez, Lucía, Sánchez-Torres, Carmen, Meraz-Ríos, Marco Antonio, and Dallaire-Théroux, Caroline

Subjects
CEREBRAL small vessel diseases, PARAPARESIS, BRAIN function localization, MILD cognitive impairment, ALZHEIMER'S disease, CEREBRAL atrophy, BRAIN, RESEARCH, PERIPHERAL neuropathy, GENETIC mutation, RESEARCH methodology, MAGNETIC resonance imaging, MEDICAL cooperation, EVALUATION research, COMPARATIVE studies, DISEASE susceptibility, MEMBRANE proteins, GENETIC techniques, PHENOTYPES, GENEALOGY
Abstract

Presenilin 1 gene (PSEN1) mutations are the most common cause of familial Alzheimer's disease (FAD). One of the most abundant FAD mutations, PSEN1 A431E, has been reported to be associated with spastic paraparesis in about half of its carriers, but the determining mechanisms of this phenotype are still unknown. In our study we characterized three A431E mutation carriers, one symptomatic and two asymptomatic, from a Mexican family with a history of spastic paraparesis in all of its affected members. At cognitive assessment and MRI, the symptomatic subject showed an atypical non-amnestic mild cognitive impairment with visuospatial deficits, olfactory dysfunction and significant parieto-occipital brain atrophy. Furthermore, we found several periventricular white matter hyperintensities whose progression pattern and localization correlated with their motor impairment, cognitive profile, and non-motor symptoms. Together, our data suggests that in this family the A431E mutation leads to a divergent neurological disorder in which cognitive deterioration was clinically exceeded by motor impairment and that it involves early glial and vascular pathological changes. [ABSTRACT FROM AUTHOR]

Published
2020
Full Text
View/download PDF

24. Radiological-pathological correlation in Alzheimer's disease : systematic review of antemortem MRI findings

Author

Dallaire-Théroux, Caroline, Callahan, Brandy, Potvin, Olivier, Saikali, Stephan, Dallaire-Théroux, Caroline, Callahan, Brandy, Potvin, Olivier, and Saikali, Stephan

Abstract

Background: The standard method of ascertaining Alzheimer’s disease (AD) remains postmortem assessment of amyloid plaques and neurofibrillary degeneration. Vascular pathology, Lewy bodies, TDP-43, and hippocampal sclerosis are frequent comorbidities. There is therefore a need for biomarkers that can assess these aetiologies and provide a diagnosis in vivo. Objective: We conducted a systematic review of published radiological-pathological correlation studies to determine the relationship between antemortem magnetic resonance imaging (MRI) and neuropathological findings in AD. Methods: We explored PubMed in June-July 2015 using “Alzheimer’s disease” and combinations of radiological and pathological terms. After exclusion following screening and full-text assessment of the 552 extracted manuscripts, three others were added from their reference list. In fine, we report results based on 27 articles. Results: Independently of normal age-related brain atrophy, AD pathology is associated with whole-brain and hippocampal atrophy and ventricular expansion as observed on T1-weighted images. Moreover, cerebral amyloid angiopathy and cortical microinfarcts are also related to brain volume loss in AD. Hippocampal sclerosis and TDP-43 are respectively associated with hippocampal and medial temporal lobe atrophy. Brain volume loss correlates more strongly with tangles than with any other pathological finding. White matter hyperintensities observed on proton density, T2-weighted and FLAIR images are strongly related to vascular pathologies, but are also associated with other histological changes such as gliosis or demyelination. Discussion: Cerebral atrophy and white matter changes in the living brain reflect underlying neuropathology and may be detectable using antemortem MRI. In vivo MRI may therefore be an avenue for AD pathological staging.

Published
2017

25. Radiological-pathological correlation in Alzheimer's disease : systematic review of antemortem MRI findings

Author

Potvin, Olivier, Callahan, Brandy, Dallaire-Théroux, Caroline, Saikali, Stephan, Potvin, Olivier, Callahan, Brandy, Dallaire-Théroux, Caroline, and Saikali, Stephan

Abstract

Background: The standard method of ascertaining Alzheimer’s disease (AD) remains postmortem assessment of amyloid plaques and neurofibrillary degeneration. Vascular pathology, Lewy bodies, TDP-43, and hippocampal sclerosis are frequent comorbidities. There is therefore a need for biomarkers that can assess these aetiologies and provide a diagnosis in vivo. Objective: We conducted a systematic review of published radiological-pathological correlation studies to determine the relationship between antemortem magnetic resonance imaging (MRI) and neuropathological findings in AD. Methods: We explored PubMed in June-July 2015 using “Alzheimer’s disease” and combinations of radiological and pathological terms. After exclusion following screening and full-text assessment of the 552 extracted manuscripts, three others were added from their reference list. In fine, we report results based on 27 articles. Results: Independently of normal age-related brain atrophy, AD pathology is associated with whole-brain and hippocampal atrophy and ventricular expansion as observed on T1-weighted images. Moreover, cerebral amyloid angiopathy and cortical microinfarcts are also related to brain volume loss in AD. Hippocampal sclerosis and TDP-43 are respectively associated with hippocampal and medial temporal lobe atrophy. Brain volume loss correlates more strongly with tangles than with any other pathological finding. White matter hyperintensities observed on proton density, T2-weighted and FLAIR images are strongly related to vascular pathologies, but are also associated with other histological changes such as gliosis or demyelination. Discussion: Cerebral atrophy and white matter changes in the living brain reflect underlying neuropathology and may be detectable using antemortem MRI. In vivo MRI may therefore be an avenue for AD pathological staging.

Published
2017

Catalog

Books, media, physical & digital resources
See catalog results