Date Published: April 25, 2018
Publisher: BioMed Central
Author(s): Fati Nourhashemi, Claudie Hooper, Christelle Cantet, Catherine Féart, Isabelle Gennero, Pierre Payoux, Anne Sophie Salabert, Sophie Guyonnet, Philipe De Souto Barreto, Bruno Vellas.
Vitamin 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.
This 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.
Participants 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.
These 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.
Vitamin D is a fat-soluble steroid hormone that seems crucial for brain health in humans [1–5]. Low vitamin D status is common amongst the elderly and is considered a major health problem [6–8]. Studies have shown that vitamin D insufficiency is associated with a higher risk of Alzheimer’s disease (AD) [9–16] and accelerated cognitive decline [12, 17, 18], although some conflicting results are reported [19–21]. Randomized controlled trials (RCTs) investigating the effects of vitamin D supplementation (alone or in combination with other drugs) on cognitive decline and AD onset are limited [22–25] and have largely proven unsuccessful to date [22, 23, 25].
We have shown that vitamin D measured as 25(OH)D was not associated with cerebral Aβ independently or as a function of ApoE ε4 status. To the best of our knowledge, this is the first study to explore the associations between circulating plasma vitamin D (measured biochemically) and cerebral Aβ.
We have shown here that circulating 25(OH)D was not associated with cerebral Aβ in older adults at risk of dementia cross-sectionally. However, a longitudinal observational study including mid-life vitamin D measurements is warranted to examine the relationship between plasma 25(OH)D and cerebral Aβ accrual over time.