Sander C J Verfaillie1, Alexa Pichet Binette2, Etienne Vachon-Presseau3, Shirin Tabrizi4, Mélissa Savard4, Pierre Bellec5, Rik Ossenkoppele6, Philip Scheltens6, Wiesje M van der Flier7, John C S Breitner8, Sylvia Villeneuve9. 1. Montreal Neurological Institute, Montreal, Quebec, Canada; Centre for the Studies on Prevention of Alzheimer's Disease, Douglas Mental Health University Institute Research Centre, Montreal, Quebec, Canada; Department of Psychiatry, McGill University, Montreal, Quebec, Canada; Alzheimer Center and Department of Neurology, Vrije Universiteit Medical Centre, Amsterdam, The Netherlands; Amsterdam Neuroscience, Amsterdam, The Netherlands. 2. Centre for the Studies on Prevention of Alzheimer's Disease, Douglas Mental Health University Institute Research Centre, Montreal, Quebec, Canada; Integrated Program in Neuroscience, McGill University, Montreal, Quebec, Canada. 3. Department of Physiology, Northwestern University, Chicago, Illinois. 4. Centre for the Studies on Prevention of Alzheimer's Disease, Douglas Mental Health University Institute Research Centre, Montreal, Quebec, Canada. 5. Centre de recherche de l'Institut universitaire de gériatrie de Montréal, Montreal, Quebec, Canada; Department of Computer Science and Operations Research, University of Montreal, Montreal, Quebec, Canada. 6. Alzheimer Center and Department of Neurology, Vrije Universiteit Medical Centre, Amsterdam, The Netherlands; Amsterdam Neuroscience, Amsterdam, The Netherlands. 7. Alzheimer Center and Department of Neurology, Vrije Universiteit Medical Centre, Amsterdam, The Netherlands; Department of Epidemiology and Biostatistics, Vrije Universiteit Medical Centre, Amsterdam, The Netherlands; Amsterdam Neuroscience, Amsterdam, The Netherlands. 8. Montreal Neurological Institute, Montreal, Quebec, Canada; Centre for the Studies on Prevention of Alzheimer's Disease, Douglas Mental Health University Institute Research Centre, Montreal, Quebec, Canada; Department of Psychiatry, McGill University, Montreal, Quebec, Canada. 9. Montreal Neurological Institute, Montreal, Quebec, Canada; Centre for the Studies on Prevention of Alzheimer's Disease, Douglas Mental Health University Institute Research Centre, Montreal, Quebec, Canada; Department of Psychiatry, McGill University, Montreal, Quebec, Canada. Electronic address: sylvia.villeneuve@mcgill.ca.
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 < .05). When compared with SCD-, SCD+ subjects showed increased pDMN-MTMS connectivity (false discovery rate-adjusted p < .05). Higher connectivity between the MTMS and the rest of the brain was associated with better baseline immediate memory, attention, and global cognition, whereas higher MTMS and pDMN-MTMS connectivity were associated with lower immediate memory over time (all false discovery rate-adjusted p values < .05). CONCLUSIONS: SCD in cognitively normal individuals is associated with diminished immediate memory practice effects and a brain connectivity pattern that mirrors early AD-related connectivity failure.
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 < .05). When compared with SCD-, SCD+ subjects showed increased pDMN-MTMS connectivity (false discovery rate-adjusted p < .05). Higher connectivity between the MTMS and the rest of the brain was associated with better baseline immediate memory, attention, and global cognition, whereas higher MTMS and pDMN-MTMS connectivity were associated with lower immediate memory over time (all false discovery rate-adjusted p values < .05). CONCLUSIONS: SCD in cognitively normal individuals is associated with diminished immediate memory practice effects and a brain connectivity pattern that mirrors early AD-related connectivity failure.
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