Vitamin D deficiency has been previously associated with a higher Alzheimer’s disease (AD) risk, a condition marked by dependent living and severe cognitive impairment. AD is histologically defined by the presence of brain amyloid beta (Aβ) plaques and neurofibrillary tangles. Ways to enhance Aβ clearance have been examined in order to sustain cognition and delay AD onset. In vitro and in vivo studies suggest that vitamin D might enhance brain Aβ transportation to the periphery by up-regulating P-glycoprotein production. The purpose of this study was to examine the effect of vitamin D supplementation on plasma Aβ in an older population.
This study was a parallel-arm, double-blinded, randomized control trial. Participants consumed either a vitamin D supplement or placebo once a week for eight weeks (n=23). Only vitamin D insufficient (serum total 25-OH, D < 30 ng/mL) people were included in the study, and all participants were considered to be cognitively normal (MMSE scores > 27). Serum total 25-OH, D and plasma Aβ1-40 measurements were recorded before and after the eight-week trial. The plasma Aβ1-40 change was compared between the vitamin D group and control group.
The vitamin D group experienced a 45% greater change in plasma Aβ1-40 than the control group. The effect size was 0.228 when controlling for baseline plasma Aβ1-40 (p=0.045), 0.197 when controlling for baseline plasma Aβ1-40 and baseline physical activity (p=0.085), and 0.179 when controlling for baseline plasma Aβ1-40, baseline physical activity, and age (p=0.116). In conclusion, vitamin D supplementation might increase brain Aβ clearance in humans, but physical activity and age also appear to modulate Aβ metabolism.