Association of Modifiable Lifestyle Factors With Cortical Amyloid Burden and Cerebral Glucose Metabolism in Older Adults With Mild Cognitive Impairment

IMPORTANCE: Understanding the association of lifestyle factors with mild cognitive impairment enables the development of evidence-based interventions for delaying cognitive impairment. OBJECTIVE: To explore whether objectively measured lifestyle factors, such as physical activity, conversation, and sleep, are associated with cortical amyloid burden and cerebral glucose metabolism in older adults with mild cognitive impairment. DESIGN, SETTING, AND PARTICIPANTS: This cohort study included 855 community-dwelling adults in Usuki, Oita Prefecture, Japan, aged 65 years or older. Data were collected from August 2015 to December 2017. Participants were reviewed to examine risk and protective lifestyle factors for dementia. Data analysis was conducted in June 2019. EXPOSURES: Wearable sensors, carbon-11 labeled Pittsburgh compound B positron emission tomography images, and fluorine-18 fluorodeoxyglucose positron emission tomography images. MAIN OUTCOMES AND MEASURES: Wearable sensor data, such as walking steps, conversation time, and sleep, were collected from August 2015 to October 2017, and positron emission tomography images were collected from October 2015 to December 2017. A multiple regression model and change-point regression model were used to examine the association of lifestyle factors with mean amyloid or fluorodeoxyglucose uptake, assessed on the basis of a standardized uptake value ratio of the frontal lobes, temporoparietal lobes, and posterior cingulate gyrus with the cerebellar cortex as the reference region. The bootstrap method was used to obtain nonparametric 95% CIs on the associations of lifestyle factors with cognitive decline. RESULTS: Of the 855 adults in the study, 118 (13.8%) were diagnosed with mild cognitive impairment, with a mean (SD) age of 75.7 (5.8) years and 66 (55.9%) women. Total sleep time was inversely associated with fluorodeoxyglucose uptake after adjusting for covariates (β = −0.287; 95% CI, −0.452 to −0.121, P < .001). Change-point regression showed an inverse association between total sleep time and mean amyloid uptake when sleep duration was longer than 325 minutes (B = −0.0018; 95% CI, −0.0031 to −0.0007). CONCLUSIONS AND RELEVANCE: To our knowledge, this is the first study to demonstrate that total sleep time was associated with brain function in older adults with mild cognitive impairment. Sleep duration is a potentially modifiable risk factor for dementia at the mild cognitive impairment stage.