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Cognitive Training Modulates Brain Hypersynchrony in a Population at Risk for Alzheimer’s Disease

疾病 认知 认知储备 阿尔茨海默病 神经科学 认知训练 人口 心理学 痴呆 医学 认知障碍 内科学 环境卫生
作者
Isabel Suárez‐Méndez,Ricardo Bruña,David López‐Sanz,Pedro Montejo Carrasco,Mercedes Montenegro-Peña,María Luisa Delgado‐Losada,Alberto Marcos Dolado,Ramón López-Higes,Fernando Maestú
出处
期刊:Journal of Alzheimer's Disease [IOS Press]
卷期号:86 (3): 1185-1199 被引量:6
标识
DOI:10.3233/jad-215406
摘要

BACKGROUND: Recent studies demonstrated that brain hypersynchrony is an early sign of dysfunction in Alzheimer's disease (AD) that can represent a proxy for clinical progression. Conversely, non-pharmacological interventions, such as cognitive training (COGTR), are associated with cognitive gains that may be underpinned by a neuroprotective effect on brain synchrony. OBJECTIVE: To study the potential of COGTR to modulate brain synchrony and to eventually revert the hypersynchrony phenomenon that characterizes preclinical AD. METHODS: The effect of COGTR was examined in a sample of healthy controls (HC, n = 41, 22 trained) and individuals with subjective cognitive decline (SCD, n = 49, 24 trained). Magnetoencephalographic activity and neuropsychological scores were acquired before and after a ten-week COGTR intervention aimed at improving cognitive function and daily living performance. Functional connectivity (FC) was analyzed using the phase-locking value. A mixed-effects ANOVA model with factors time (pre-intervention/post-intervention), training (trained/non-trained), and diagnosis (HC/SCD) was used to investigate significant changes in FC. RESULTS: We found an average increase in alpha-band FC over time, but the effect was different in each group (trained and non-trained). In the trained group (HC and SCD), we report a reduction in the increase in FC within temporo-parietal and temporo-occipital connections. In the trained SCD group, this reduction was stronger and showed a tentative correlation with improved performance in different cognitive tests. CONCLUSION: COGTR interventions could mitigate aberrant increases in FC in preclinical AD, promoting brain synchrony normalization in groups at a higher risk of developing dementia.
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