According to Yo-el Ju, MD, and colleagues at Washington University School of Medicine in St. Louis, Missouri, disrupted sleep (as measured by frequency of awakenings or sleep efficiency), is associated with amyloid pathology in a cognitively normal population.
The researchers recruited participants (n=100) aged 45-80 from a cohort half of which has a family history of Alzheimer Disease (AD). Standardized assessments determined that they were cognitively normal (clinical dementia rating 0). Participants wore an ambulatory monitor for 14 days to objectively measure sleep. Additionally, sleep diaries and questionnaires were used to obtain subjective sleep measures. According to Dr. Ju and colleagues, preclinical AD was diagnosed in 25% of participants by abnormal levels of cerebrospinal fluid Ab(42) and/or increased retention of Pittsburgh compound B during amyloid imaging.
The participants’ mean time in bed was approximately 8 hours, similar to subjective report. However mean sleep time was significantly shorter at ∼6.5 hours, due to brief awakenings through the night. The researchers noted that individuals with frequent awakenings (>5/hour) were more likely to have abnormal biomarkers indicating amyloid pathology. A greater proportion of individuals with low sleep efficiency ([sleep time/time in bed] <85%) had preclinical AD, compared to those with high sleep efficiency.
“Further investigation will be required to determine the mechanisms underlying this association and whether sleep changes predict cognitive decline,” the researchers concluded.