A recent paper in the New England Journal of Medicine reported on a number of biomarker and behavior changes in dominantly inherited Alzheimer’s disease, and proposed that treatment and prevention trials could incorporate these pathophysiological changes to gauge the likelihood of future clinical success.1 Some of the changes noted were reduced glucose metabolism in the brain, amyloid-beta deposition in the brain, and increased cognitive impairment.
Colleagues and I suggested in a published commentary on this paper that raising serum 25-hydroxyvitamin D [25(OH)D] concentrations might be able to prevent or slow the development of Alzheimer’s disease.2 The evidence is outlined here.
Two studies found vitamin D reduced amyloid-beta in the brain.3, 4 One paper found a beneficial role of vitamin D for glucose transport and utilization in the brain.5 A recent longitudinal study found a significant increase in global cognitive impairment for women with low vs. high serum 25(OH)D concentrations.6 A recent review discussed the evidence that vitamin D reduces the risk of cognitive impairment.7
Additional evidence that vitamin D reduces the risk of Alzheimer’s disease is given in several other papers.8, 9
Thus, higher serum 25(OH)D concentrations may reduce the risk of Alzheimer’s disease. Based on results from other studies, serum 25-hydroxyvitamin D concentrations should be above 40 ng/ml (100 nmol/l) for optimal health.10
1.Bateman RJ, Xiong C, Benzinger TL, et al. Clinical and Biomarker Changes in Dominantly Inherited Alzheimer’s Disease. N Engl J Med. 2012; DOI: 10.1056/NEJMoa1202753
2. Grant WB, Mascitelli L, Goldstein MR. Vitamin D may reduce the risk of dominantly inherited Alzheimer’s disease. NEJM. http://www.nejm.org/doi/full/10.1056/NEJMoa1202753#t=comments
3. Yu J, Gattoni-Celli M, Zhu H, et al. Vitamin D3-enriched diet correlates with a decrease of amyloid plaques in the brain of AβPP transgenic mice. J Alzheimers Dis. 2011;25:295-307.
4. Mizwicki MT, Menegaz D, Zhang J, et al. Genomic and nongenomic signaling induced by 1α,25(OH)2-vitamin D3 promotes the recovery of amyloid-β phagocytosis by Alzheimer’s disease macrophages. J Alzheimers Dis. 2012;29:51-62.
5. Kumar PT, Antony S, Nandhu MS, et al. Vitamin D3 restores altered cholinergic and insulin receptor expression in the cerebral cortex and muscarinic M3 receptor expression in pancreatic islets of streptozotocin induced diabetic rats. J Nutr Biochem. 2011;22:418-25.
6. Slinin Y, Paudel M, Taylor BC, et al. Association Between Serum 25(OH) Vitamin D and the Risk of Cognitive Decline in Older Women. J Gerontol A Biol Sci Med Sci. 2012 Mar 27. [Epub ahead of print]
7. Soni M, Kos K, Lang IA, et al. Vitamin D and cognitive function. Scand J Clin Lab Invest Suppl. 2012 Apr;243:79-82.
8. Wang L, Hara K, Van Baaren JM, et al. Vitamin D receptor and Alzheimer’s disease: a genetic and functional study. Neurobiol Aging. 2012 Aug;33(8):1844.e1-9.
9. Annweiler C, Rolland Y, Schott AM, et al. Higher Vitamin D Dietary Intake Is Associated With Lower Risk of Alzheimer’s Disease: A 7-Year Follow-up. J Gerontol A Biol Sci Med Sci. 2012 Apr 13. [Epub ahead of print]
10. Cannell JJ, Hollis BW, Zasloff M, Heaney RP. Diagnosis and treatment of vitamin D deficiency. Expert Opin Pharmacother. 2008 Jan;9(1):107-18.