AAN: Low Sleep Efficiency Tied to Preclinical Alzheimer's

Frequent awakenings linked to amyloid pathology in cognitively normal adults

TUESDAY, Feb. 14 (HealthDay News) -- Disrupted sleep is associated with amyloid pathology in cognitively normal individuals, according to a study being released in advance of its presentation at the annual meeting of the American Academy of Neurology, which will be held from April 21 to 28 in New Orleans.

To investigate the relationship between sleep disruption and preclinical Alzheimer's disease, Yo-el Ju, M.D., from the Washington University School of Medicine in St. Louis, and colleagues measured sleep with actigraphy in cognitively normal individuals. One hundred participants, aged 45 to 80 years, underwent objective sleep measures using an actigraph for 14 days. In 25 percent of the participants, preclinical Alzheimer's disease was diagnosed based on abnormal levels of cerebrospinal fluid amyloid-beta-42 and/or elevated retention of Pittsburgh compound B during amyloid imaging.

The investigators found that the mean time in bed was approximately eight hours, and the mean sleep time was approximately 6.5 hours. Individuals who awoke frequently (more than five times per hour) were more likely to have abnormal biomarkers indicative of amyloid pathology. Compared with individuals with high sleep efficiency (sleep time/time in bed), a greater proportion of individuals with low sleep efficiency (<85 percent) had preclinical Alzheimer's disease.

"The association between disrupted sleep and amyloid plaques is intriguing, but the information from this study can't determine a cause-effect relationship or the direction of this relationship. We need longer-term studies, following individuals' sleep over years, to determine whether disrupted sleep leads to amyloid plaques, or whether brain changes in early Alzheimer's disease lead to changes in sleep," Ju said in a statement. "Our study lays the groundwork for investigating whether manipulating sleep is a possible strategy in the prevention or slowing of Alzheimer disease."

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