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- W3130333669 abstract "Abstract BackgroundRecent neuroimaging studies in humans and animal models of Alzheimer’s disease (AD) demonstrated brain hyper-synchrony under amyloid burden, which is being identified as a proxy for conversion to dementia. The potential of non-pharmacological interventions to reverse this neurophysiological phenomenon in the early stages of the disease is still an open question. MethodBrain synchrony modulation by cognitive training (CogTr) was examined in a cohort of healthy controls (HC, n = 41, 22 trained) and individuals with subjective cognitive decline (SCD, n = 49, 24 trained). Magnetoencephalographic (MEG) activity and comprehensive neuropsychological scores were acquired before and after completion of a ten-week CogTr program aimed at improving cognitive function and daily living performance. Functional connectivity (FC) analyses were carried out using the phase-locking value. A mixed-effects ANOVA with factors stage (pre-intervention or post-intervention), CogTr (trained or non-trained), and cognitive status (HC or SCD) was used to estimate significant FC changes across MEG recordings.ResultsAlpha-band FC increases were observed for the whole sample (both trained and non-trained), but the effect was different in each group. For the trained group (both HC and SCD), we report a reduction in the FC increase within temporo-parietal and temporo-occipital connections. This effect was particularly manifest in trained participants with SCD, for whom the reduction in the FC increase also correlated with enhanced cognitive performance in different neuropsychological domains (memory, language, and executive function).ConclusionsCogTr programs could mitigate the increase in FC observed in preclinical AD, promoting brain synchrony normalization in groups at increased risk for developing the disease." @default.
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- W3130333669 date "2021-02-16" @default.
- W3130333669 modified "2023-10-02" @default.
- W3130333669 title "Cognitive Training Modulates Brain Hypersynchrony in a Population at Risk for Alzheimer’s Disease" @default.
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- W3130333669 doi "https://doi.org/10.21203/rs.3.rs-201673/v1" @default.
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