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Your search keyword '"Miranda Tuwaig"' showing total 3 results
Start Over Author "Miranda Tuwaig" Topic 03 medical and health sciences
3 results on '"Miranda Tuwaig"'

1. Amyloid and Tau Pathology Associations With Personality Traits, Neuropsychiatric Symptoms, and Cognitive Lifestyle in the Preclinical Phases of Sporadic and Autosomal Dominant Alzheimer’s Disease

Author

Alexa Pichet Binette, Étienne Vachon-Presseau, John Morris, Randall Bateman, Tammie Benzinger, D. Louis Collins, Judes Poirier, John C.S. Breitner, Sylvia Villeneuve, Ricardo Allegri, Fatima Amtashar, Randy Bateman, Sarah Berman, Courtney Bodge, Susan Brandon, William (Bill) Brooks, Jill Buck, Virginia Buckles, Sochenda Chea, Jasmeer Chhatwal, Patricio Chrem, Helena Chui, Jake Cinco, Jack Clifford, Carlos Cruchaga, Mirelle D‘Mello, Tamara Donahue, Jane Douglas, Noelia Edigo, Nilufer Erekin-Taner, Anne Fagan, Marty Farlow, Angela Farrar, Howard Feldman, Gigi Flynn, Nick Fox, Erin Franklin, Hisako Fujii, Cortaiga Gant, Samantha Gardener, Bernardino Ghetti, Alison Goate, Jill Goldman, Brian Gordon, Neill Graff-Radford, Julia Gray, Jenny Gurney, Jason Hassenstab, Mie Hirohara, David Holtzman, Russ Hornbeck, Siri Houeland DiBari, Takeshi Ikeuchi, Snezana Ikonomovic, Gina Jerome, Mathias Jucker, Celeste Karch, Kensaku Kasuga, Takeshi Kawarabayashi, William (Bill) Klunk, Robert Koeppe, Elke Kuder-Buletta, Christoph Laske, Jae-Hong Lee, Johannes Levin, Daniel Marcus, Ralph Martins, Neal Scott Mason, Colin Masters, Denise Maue-Dreyfus, Eric McDade, Lucy Montoya, Hiroshi Mori, Akem Nagamatsu, Katie Neimeyer, James Noble, Joanne Norton, Richard Perrin, Marc Raichle, John Ringman, Jee Hoon Roh, Stephen Salloway, Peter Schofield, Hiroyuki Shimada, Tomoyo Shiroto, Mikio Shoji, Wendy Sigurdson, Hamid Sohrabi, Paige Sparks, Kazushi Suzuki, Laura Swisher, Kevin Taddei, Jen Wang, Peter Wang, Mike Weiner, Mary Wolfsberger, Chengjie Xiong, Xiong Xu, Angela Tam, Anne Labonté, Anne-Marie Faubert, Axel Mathieu, Cécile Madjar, Charles Edouard Carrier, Christian Dansereau, Christina Kazazian, Claude Lepage, Cynthia Picard, David Maillet, Diane Michaud, Doris Couture, Doris Dea, Claudio Cuello, Alan Barkun, Alan Evans, Blandine Courcot, Christine Tardif, Clément Debacker, Clifford R. Jack, David Fontaine, David S. Knopman, Gerhard Maultaup, Jamie Near, Jeannie-Marie Leoutsakos, Jean-Robert Maltais, Jason Brandt, Jens Pruessner, John C. Morris, Laksanun Cheewakriengkrai, Lisa-Marie Münter, Louis Collins, Mallar Chakravarty, Mark A. Sager, Marina Dauar-Tedeschi, Mark Eisenberg, Natasha Rajah, Paul Aisen, Joanne Toussaint, Pedro Rosa-Neto, Pierre Bellec, Penelope Kostopoulos, Pierre Etienne, Pierre N. Tariot, Pierre Orban, Reisa A. Sperling, Rick Hoge, Ronald G. Thomas, Serge Gauthier, Suzanne Craft, Thomas J. Montine, Vasavan Nair, Véronique Bohbot, Vinod Venugopalan, Vladimir Fonov, Yasser Ituria-Medina, Zaven S. Khachaturian, Eduard Teigner, Elena Anthal, Elsa Yu, Fabiola Ferdinand, Galina Pogossova, Ginette Mayrand, Guerda Duclair, Guylaine Gagné, Holly Newbold-Fox, Illana Leppert, Isabelle Vallée, Jacob W. Vogel, Jennifer Tremblay-Mercier, Joanne Frenette, Josée Frappier, Justin Kat, Justin Miron, Karen Wan, Laura Mahar, Leopoldina Carmo, Louise Théroux, Mahsa Dadar, Marianne Dufour, Marie-Elyse Lafaille-Magnan, Melissa Appleby, Mélissa Savard, Miranda Tuwaig, Mirela Petkova, Pierre Rioux, Pierre-François Meyer, Rana El-Khoury, Renee Gordon, Renuka Giles, Samir Das, Seqian Wang, Shirin Tabrizi, Sulantha Mathotaarachchi, Sylvie Dubuc, Tanya Lee, Thomas Beaudry, Valérie Gervais, Véronique Pagé, Julie Gonneaud, Gülebru Ayranci, Tharick A. Pascoal, René Desautels, Fatiha Benbouhoud, Eunice Farah Saint-Fort, Sander C.J. Verfaillie, Sarah Farzin, Alyssa Salaciak, Stephanie Tullo, Etienne Vachon-Presseau, Leslie-Ann Daoust, Theresa Köbe, Nathan Spreng, Melissa McSweeney, Nathalie Nilsson, Morteza Pishnamazi, and Christophe Bedetti

Subjects
0301 basic medicine, Oncology, medicine.medical_specialty, tau Proteins, Disease, Article, 03 medical and health sciences, Cognition, 0302 clinical medicine, Alzheimer Disease, Internal medicine, mental disorders, medicine, Humans, Dementia, Big Five personality traits, Family history, Life Style, Biological Psychiatry, Aged, Amyloid beta-Peptides, Extraversion and introversion, business.industry, medicine.disease, Neuroticism, 3. Good health, 030104 developmental biology, Positron-Emission Tomography, Cohort, Alzheimer's disease, business, 030217 neurology & neurosurgery
Abstract

Background Major prevention trials for Alzheimer’s disease (AD) are now focusing on multidomain lifestyle interventions. However, the exact combination of behavioral factors related to AD pathology remains unclear. In 2 cohorts of cognitively unimpaired individuals at risk of AD, we examined which combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle (years of education or lifetime cognitive activity) related to the pathological hallmarks of AD, amyloid-β, and tau deposits. Methods A total of 115 older adults with a parental or multiple-sibling family history of sporadic AD (PREVENT-AD [PRe-symptomatic EValuation of Experimental or Novel Treatments for AD] cohort) underwent amyloid and tau positron emission tomography and answered several questionnaires related to behavioral attributes. Separately, we studied 117 mutation carriers from the DIAN (Dominant Inherited Alzheimer Network) study group cohort with amyloid positron emission tomography and behavioral data. Using partial least squares analysis, we identified latent variables relating amyloid or tau pathology with combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle. Results In PREVENT-AD, lower neuroticism, neuropsychiatric burden, and higher education were associated with less amyloid deposition (p = .014). Lower neuroticism and neuropsychiatric features, along with higher measures of openness and extraversion, were related to less tau deposition (p = .006). In DIAN, lower neuropsychiatric burden and higher education were also associated with less amyloid (p = .005). The combination of these factors accounted for up to 14% of AD pathology. Conclusions In the preclinical phase of both sporadic and autosomal dominant AD, multiple behavioral features were associated with AD pathology. These results may suggest potential pathways by which multidomain interventions might help delay AD onset or progression.

Published
2021

2. Deficit in Central Auditory Processing as a Biomarker of Pre-Clinical Alzheimer’s Disease

Author

Judes Poirier, Melissa Savard, Miranda Tuwaig, John C.S. Breitner, Benoît Jutras, David Fontaine, D. Louis Collins, and Pedro Rosa-Neto

Subjects
Male, Central Auditory Processing Disorder, Apolipoprotein E4, Disease, Neuropsychological Tests, Audiology, Cohort Studies, sensorineural assessment, 0302 clinical medicine, prevention, Cerebral Cortex, General Neuroscience, central auditory processing disorder, 05 social sciences, Age Factors, Neuropsychology, Cognition, Organ Size, General Medicine, Middle Aged, Magnetic Resonance Imaging, Cognitive test, Psychiatry and Mental health, Clinical Psychology, pre-clinical Alzheimer’s disease, Auditory Perception, Audiometry, Pure-Tone, Educational Status, Biomarker (medicine), Female, Research Article, medicine.medical_specialty, Prodromal Symptoms, tau Proteins, Prevention of dementia, 050105 experimental psychology, 03 medical and health sciences, Sex Factors, Alzheimer Disease, medicine, Humans, 0501 psychology and cognitive sciences, cognitive function, business.industry, Comprehension, Cross-Sectional Studies, Geriatrics and Gerontology, business, Biomarkers, 030217 neurology & neurosurgery
Abstract

Prevention of dementia due to Alzheimer’s disease (d/AD) requires interventions that slow the disease process prior to symptom onset. To develop such interventions, one needs metrics that assess pre-symptomatic disease progression. Familiar measures of progression include cerebrospinal fluid (CSF) biochemical and imaging analyses, as well as cognitive testing. Changes in the latter can sometimes be difficult to distinguish from effects of “normal” aging. A different approach involves testing of “central auditory processing” (CAP), which enables comprehension of auditory stimuli amidst a distracting background (e.g., conversation in a noisy bar or restaurant). Such comprehension is often impaired in d/AD. Similarly, effortful or diminished auditory comprehension is sometimes reported by cognitively healthy elders, raising the possibility that CAP deficit may be a marker of pre-symptomatic AD. In 187 cognitively and physically healthy members of the aging, AD family history-positive PREVENT-AD cohort, we therefore evaluated whether CAP deficits were associated with known markers of AD neurodegeneration. Such markers included CSF tau concentrations and magnetic resonance imaging volumetric and cortical thickness measures in key AD-related regions. Adjusting for age, sex, education, pure-tone hearing, and APOE ɛ4 status, we observed a persistent relationship between CAP scores and CSF tau levels, entorhinal and hippocampal cortex volumes, cortical thickness, and deficits in cognition (Repeatable Battery for Assessment of Neuropsychological Status total score, and several of its index scales). These cross-sectional observations suggest that CAP may serve as a novel metric for pre-symptomatic AD pathogenesis. They are therefore being followed up longitudinally with larger samples.

Published
2017

3. Subjective Cognitive Decline Is Associated With Altered Default Mode Network Connectivity in Individuals With a Family History of Alzheimer's Disease

Author

Sander C.J. Verfaillie, Alexa Pichet Binette, Etienne Vachon-Presseau, Shirin Tabrizi, Mélissa Savard, Pierre Bellec, Rik Ossenkoppele, Philip Scheltens, Wiesje M. van der Flier, John C.S. Breitner, Sylvia Villeneuve, Paul Aisen, Elena Anthal, Melissa Appleby, Gülebru Ayranci, Alan Barkun, Thomas Beaudry, Fatiha Benbouhoud, Veronique Bohbot, Jason Brandt, John Breitner, Leopoldina Carmo, Edouard Carrier Charles, Mallar Chakravarty, Laksanun Cheewakriengkrai, Louis Collins, Blandine Courcot, Doris Couture, Suzanne Craft, Claudio Cuello, Mahsa Dadar, Christian Dansereau, null DasSamir, Dauar-Tedeschi Marina, Doris Dea, Clement Debacker, Rene Desautels, Sylvie Dubuc, Guerda Duclair, Marianne Dufour, Mark Eisenberg, Rana El-Khoury, Pierre Etienne, Alan Evans, Anne-Marie Faubert, Fabiola Ferdinand, Vladimir Fonov, David Fontaine, Josée Frappier, Frenette Joanne, Guylaine Gagne, Serge Gauthier, Valérie Gervais, Renuka Giles, Julie Gonneaud, Renee Gordon, Rick Hoge, Bradley Hyman, Yasser Ituria-Medina, Clifford Jack, Justin Kat, Christina Kazazian, Zaven Khachaturian, David Knopman, Penelope Kostopoulos, Anne Labonte, Marie-Elyse Lafaille-Magnan, Tanya Lee, Jeannie-Marie Leoutsakos, Claude Lepage, Illana Leppert, Cécile Madjar, Laura Mahar, David Maillet, Jean-Robert Maltais, Axel Mathieu, Sulantha Mathotaarachchi, Gerhard Maultaup, Ginette Mayrand, Pierre-François Meyer, Diane Michaud, Justin Miron, Thomas Montine, John Morris, Lisa-Marie Münter, Vasavan Nair, Jamie Near, Holly Newbold-Fox, Pierre Orban, Véronique Page, Tharick Pascoal, Mirela Petkova, Cynthia Picard, Galina Pogossova, Judes Poirier, Jens Pruessner, Natasha Rajah, Pierre Rioux, Pedro Rosa-Neto, Mark Sager, Eunice Farah Saint-Fort, Reisa Sperling, Angela Tam, Christine Tardif, Pierre Tariot, Eduard Teigner, Louise Theroux, Ronald Thomas, Paule-Joanne Toussaint, Jennifer Tremblay-Mercier, Miranda Tuwaig, Isabelle Vallee, Vinod Venugopalan, Sander Verfaillie, Jacob Vogel, Karen Wan, Seqian Wang, Elsa Yu, Radiology and nuclear medicine, Amsterdam Neuroscience - Neurodegeneration, Neurology, APH - Personalized Medicine, and APH - Methodology

Subjects
0301 basic medicine, Male, medicine.medical_specialty, Cognitive Neuroscience, Audiology, Neuropsychological Tests, Asymptomatic, 03 medical and health sciences, 0302 clinical medicine, Cognition, Alzheimer Disease, Neural Pathways, Medicine, Dementia, Humans, Radiology, Nuclear Medicine and imaging, Cognitive Dysfunction, Effects of sleep deprivation on cognitive performance, Neuropsychological assessment, Cognitive decline, Family history, Biological Psychiatry, Default mode network, Aged, Brain Mapping, medicine.diagnostic_test, business.industry, Middle Aged, medicine.disease, Magnetic Resonance Imaging, 030104 developmental biology, Disease Progression, Female, Neurology (clinical), medicine.symptom, business, 030217 neurology & neurosurgery
Abstract

Background: Both subjective cognitive decline (SCD) and a family history of Alzheimer's disease (AD) portend risk of brain abnormalities and progression to dementia. Posterior default mode network (pDMN) connectivity is altered early in the course of AD. It is unclear whether SCD predicts similar outcomes in cognitively normal individuals with a family history of AD. Methods: We studied 124 asymptomatic individuals with a family history of AD (age 64 ± 5 years). Participants were categorized as having SCD if they reported that their memory was becoming worse (SCD+). We used extensive neuropsychological assessment to investigate five different cognitive domain performances at baseline (n = 124) and 1 year later (n = 59). We assessed interconnectivity among three a priori defined ROIs: pDMN, anterior ventral DMN, medial temporal memory system (MTMS), and the connectivity of each with the rest of brain. Results: Sixty-eight (55%) participants reported SCD. Baseline cognitive performance was comparable between groups (all false discovery rate-adjusted p values >.05). At follow-up, immediate and delayed memory improved across groups, but the improvement in immediate memory was reduced in SCD+ compared with SCD− (all false discovery rate–adjusted p values −, SCD+ subjects showed increased pDMN–MTMS connectivity (false discovery rate–adjusted p

Published
2018

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