Associations between physical activity and markers of brain pathology in autosomal dominant Alzheimer's disease: A preliminary report: Prevention (nonpharmacological) / Exercise.

Background: Physical activity is a promising lifestyle factor that could protect against memory decline in preclinical Alzheimer's disease (AD). Greater physical activity has been shown to attenuate the relationship between amyloid‐b and cognitive decline and neurodegeneration in individuals at risk for dementia. Yet, little is known about the relation of physical activity with tau pathology, a strong predictor of cognitive decline. Autosomal dominant Alzheimer's disease (ADAD) provides a unique opportunity to study preclinical AD since carriers of ADAD mutations are destined to develop dementia at early age, have a well‐characterized disease trajectory, and do not present age‐related comorbidities. We examined physical activity levels in young mutation carriers and non‐carriers from a Colombian kindred with ADAD, and explored the associations among physical activity, brain pathology (amyloid and tau), hippocampus volume, and memory performance. Methods: Ten Presenilin‐1 E280A cognitively unimpaired mutation carriers and 23 matched non‐carriers (ages: μ=37.46, σ:6.01) traveled from Colombia to Boston for 11C Pittsburgh compound B‐PET (amyloid), Flortaucipir‐PET (tau), MRI and cognitive testing. All completed the 7‐day Physical Activity Recall questionnaire, which provides a measure of metabolic equivalents (METS) based on an estimate of the energy expenditure for common physical activities. Group differences were tested using the Mann Whitney U test. Linear regressions were used to examine associations between METS, imaging markers, and memory. Results: Compared to non‐carriers, mutation carriers had greater cortical amyloid (non‐carriers: μ=1.05, σ=0.03, carriers: μ=1.26, σ=0.20, p<.001), and performed worse on the CERAD word list recall test (non‐carriers: μ=7.96, σ=1.24, carriers: μ=5.83, σ=2.75, p=.012). Groups did not differ in age, sex, education or METS (non‐carriers: μ=248.89, σ:27.53; carriers: μ=249., σ:20.81). Further, METS were not significantly associated with pathology levels, age, hippocampus volume or memory. However, those carriers (n=4) with the highest entorhinal and inferior temporal tau burden also had the lowest METS. Conclusion: Preliminary findings of this ongoing study suggest that physical activity levels may not be associated with markers of neurodegeneration or memory performance in early preclinical ADAD. Future studies with larger samples and longitudinal follow‐up are needed to better understand the role of physical activity in the risk and progression of AD. [ABSTRACT FROM AUTHOR]
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