Life Extension Newsletter
Life Extension Newsletter
Higher Vitamin D in Middle Age Linked with Lower Alzheimer’s Marker Later in Life
A recently published study revealed an association between higher vitamin D levels during midlife and less tau (a protein that accumulates in the brains of individuals with Alzheimer's disease) 16 years later.1
"Mid-life is a time where risk factor modification can have a greater impact," coauthor Martin David Mulligan, MB, BCh, BAO, of the University of Galway noted. "These results suggest that higher vitamin D levels in midlife may offer protection against developing these tau deposits in the brain and that low vitamin D levels could potentially be a risk factor that could be modified and treated to reduce the risk of dementia. Of course, these results need to be further tested with additional studies."
The study included 793 dementia-free men and women who participated in the Framingham Heart Study Generation 3. Participants' age averaged 39 years at the beginning of the study when 25-hydroxyvitamin D levels were measured in the blood. Scans were conducted an average of 16 years later to measure brain levels of tau and amyloid beta proteins, which are elevated in people with Alzheimer's disease.
Thirty-four percent of the participants had low vitamin D levels of less than 30 nanograms per milliliter (ng/mL) at the beginning of the study. Those who had higher vitamin D levels had less tau protein 16 years later than participants whose vitamin D levels were low.
No association between vitamin D and amyloid, another brain protein associated with Alzheimer's disease, was observed. "Our finding of an association between serum 25-hydroxyvitamin D and tau but not amyloid in younger cohorts may indeed reflect the temporal progression of Alzheimer's disease pathology," Mulligan and associates wrote. "Medial entorhinal cortex tau accumulates earlier than cortical amyloid beta. Therefore, in younger or preclinical populations, associations with tau may be more readily detectable than those with amyloid, which accumulates significantly later."
"Low vitamin D in midlife may represent a potentially modifiable target to mitigate the risk of neuroimaging signs of preclinical dementia," they concluded.
The findings were reported in the June 2026 issue of the journal Neurology Open Access.
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Apply What You’ve Learned: Alzheimer's disease
- Alzheimer's disease is characterized by cognitive decline that leads to dementia and death. Its causes appear to be multifactorial. Age, inflammation, oxidative stress, genetics, infections, vascular disease, mitochondrial dysfunction and other risk factors play a role in the disease's development.
- Neurofibrillary tangles that occur within brain cells known as neurons are formed when tau proteins clump together, causing cell dysfunction and cell death in the brains of people with Alzheimer's disease.
- As with most diseases, healthy eating patterns like the Mediterranean diet have been associated with a lower risk of Alzheimer's disease.2 The diet emphasizes plant‑based meals, vegetables, fruit, whole grain, legumes, nuts and olive oil, with regular intake of fish and seafood, moderate amounts of lean meat and chicken, and limited consumption of sweets and red meat.3 Adherence to a Mediterranean diet, as well as to a pattern known as the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND, a combination of Mediterranean and DASH diets), has been associated with a reduced risk of Alzheimer's disease pathology at autopsy.4
- Although a combinatorial lifestyle approach including healthy eating patterns, exercise and guidance from a health care professional is needed, specific nutrients have shown promise against aspects of the disease when added to the diet. A fat-soluble form of thiamin (vitamin B1) known as benfotiamine, the plant compound huperzine A, Panax ginseng, Ginkgo biloba and other nutrients have been associated with benefits in human studies.5-8
References
- Mulligan MD, Scott MR, Yang Q, et al. Association of circulating vitamin D in midlife with increased tau-PET burden in dementia-free adults. Neurol Open Access. 2026 Jun;2(2):e000057.
- Fekete M, Varga P, Ungvari Z, et al. The role of the Mediterranean diet in reducing the risk of cognitive impairement, dementia, and Alzheimer's disease: a meta-analysis. Geroscience. 2025 Jun;47(3):3111-3130.
- Mediterranean diet. Medline Plus. National Library of Medicine. 2024 Jul 24. https://medlineplus.gov/ency/patientinstructions/000110.htm Accessed 2026 Apr 16.
- Agarwal P, Leurgans SE, Agrawal S, et al. Association of Mediterranean-DASH Intervention for Neurodegenerative Delay and Mediterranean diets With Alzheimer disease pathology. Neurology. 2023 May 30;100(22):e2259-e2268.
- Gibson GE, Luchsinger JA, Cirio R, et al. Benfotiamine and cognitive decline in Alzheimer's disease: results of a randomized placebo-controlled phase iia clinical trial. J Alzheimers Dis. 2020;78(3):989-1010.
- Wang GS, Wang HW, Wei AH, et al. Efficacy and safety of natural acetylcholinesterase inhibitor huperzine A in the treatment of Alzheimer’s disease: an updated meta-analysis. J Neural Transm (Vienna). 2009 Apr;116(4):457-65.
- Lee ST, Chu K, Sim JY, et al. Panax ginseng enhances cognitive performance in Alzheimer disease. Alzheimer Dis Assoc Disord. 2008 Jul-Sep;22(3):222-6.
- Kandiah N, Ong PA, Yuda T, et al. Treatment of dementia and mild cognitive impairment with or without cerebrovascular disease: Expert consensus on the use of Ginkgo biloba extract, EGb 761®. CNS Neurosci Ther. 2019 Feb;25(2):288-298.
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