Abstract

BackgroundVitamin D deficiency is associated with an increased risk of Alzheimer’s disease and increased beta-amyloid (Aβ) in animals. Hence we sought to investigate the relationship between plasma 25-hydroxyvitamin D (25(OH)D) and cerebral Aβ in older adults with subjective memory complaints.MethodsThis is a secondary analysis of the Multidomain Alzheimer Preventive Trial. Participants were 178 dementia-free individuals aged 70 years or older with data on plasma 25(OH)D and cerebral Aβ load assessed by [18F]-florbetapir positron emission tomography. Plasma 25(OH)D was measured at study baseline using a commercially available electro-chemiluminescence competitive binding assay. Standard uptake value ratios (SUVRs) were generated using the cerebellum as a reference. Brain regions assessed included the cortex, anterior cingulate, anterior putamen, caudate, hippocampus, medial orbitofrontal cortex, occipital cortex, parietal cortex, pons, posterior cingulate, posterior putamen, precuneus, semioval centre and temporal cortex. Associations were explored using fully adjusted multiple linear regression models.ResultsParticipants had a mean (SD) age of 76.2 years (4.4) and 59.6% were female. The mean (SD) plasma 25(OH)D level was 22.4 ng/ml (10.8) and the mean (SD) cortical SUVR was 1.2 (0.2). We did not find any cross-sectional associations (p > 0.05) between baseline 25(OH)D levels and Aβ in any of the brain regions studied.ConclusionsThese preliminary results suggest that circulating 25(OH)D is not associated with cerebral Aβ in older adults. Further longitudinal studies with the measurement of mid-life vitamin D status are required to explore the relationship between vitamin D and Aβ accrual over time, thereby circumventing the shortfalls of a cross-sectional study.

Highlights

  • Vitamin D deficiency is associated with an increased risk of Alzheimer’s disease and increased beta-amyloid (Aβ) in animals

  • Despite the controversy surrounding the role of vitamin D in cognitive function and Alzheimer’s disease (AD), animal studies suggest that vitamin D hypovitaminosis results in increased brain beta-amyloid (Aβ) [26] and vitamin D promotes a reduction in Aβ brain burden [27, 28]

  • We examined the cross-sectional associations between 25-hydroxyvitamin D (25(OH)D), the major circulating form of vitamin D, and cerebral Aβ in older adults at risk of dementia

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Summary

Introduction

Vitamin D deficiency is associated with an increased risk of Alzheimer’s disease and increased beta-amyloid (Aβ) in animals. Studies have shown that vitamin D insufficiency is associated with a higher risk of Alzheimer’s disease (AD) [9,10,11,12,13,14,15,16] and accelerated cognitive decline [12, 17, 18], some conflicting. Vitamin D has been shown to increase plasma Aβ, in older adults, suggestive of decreased brain Aβ [29]. We examined the cross-sectional associations between 25-hydroxyvitamin D (25(OH)D), the major circulating form of vitamin D, and cerebral Aβ in older adults at risk of dementia. We hypothesized that 25(OH)D would be inversely associated with Aβ

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