![]() ![]() In addition, we monitored their sleep using a single-channel electroencephalography (EEG) device worn on the forehead. In this study, we analyzed cognitive performance, brain imaging, and cerebrospinal fluid (CSF) AD biomarkers in participants enrolled in longitudinal studies of aging. Previous studies in animal models and humans have associated decreased non-rapid eye movement (NREM) sleep slow wave activity (SWA) with Aβ deposition. Sleep is increasingly recognized as a potential marker for AD pathology and future risk of cognitive impairment. The period in which AD pathology is accumulating in the absence of cognitive symptoms and represents a clinically relevant time window for therapeutic intervention. By the time even the earliest clinical symptoms are detectable, Aβ accumulation is close to reaching its peak and neocortical tau pathology is frequently already present. ![]() In Alzheimer’s disease (AD), deposition of insoluble amyloid-β (Aβ) is followed by intracellular aggregation of tau in the neocortex and subsequent neuronal cell loss, synaptic loss, brain atrophy, and cognitive impairment. ![]()
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