Alzheimers relationship vitamin and

VITAMIN D AND DEMENTIA • The Journal of Prevention of Alzheimer's Disease

alzheimers relationship vitamin and

Alzheimer's disease, for example, is a neurodegenerative disease that They concluded instead that "the link between vitamin D and brain. New research suggests that vitamin D may prevent Alzheimer's disease and other types of dementia, but more study is needed to understand this link. Keywords: vitamin E, oxidative stress, Alzheimer's disease, SNPs, A concrete connection between vitamin E and AD is the significant.

At the molecular level, previous work supports the connection. Collectively, these insights suggest that the effectiveness of vitamin E therapy may relate to the SNPs in vitamin E-related genes.

Vitamin E may be an effective agent in pre-emptively slowing the progression of AD, but it is not likely to be efficacious in reversing disease symptoms in advanced phases.

The debate regarding safe supplementation dosing of alpha-tocopherol seems to be eternal [ 4665 ]. No AD trials—even at IU alpha-tocopherol—demonstrated an increased risk of mortality. However, we cannot ignore that there have been several clinical trials that have shown increased all-cause mortality of high-dose vitamin E treatment. Regarding toxicity, it should be noted that there have been no reports of adverse effects of high levels of vitamin E from food products [ 35 ].

alzheimers relationship vitamin and

This observation speaks to our earlier point that a large proportion of individuals may have a sub-clinical deficiency of vitamin E that over time contributes to an increased risk of developing AD. Additionally, this underscores the idea that vitamin E status should be routinely monitored, especially in specific populations.

alzheimers relationship vitamin and

Advancements in genetic technologies allow for continued and focused research to stratify and explain the present inconclusive evidence and design future trials addressing vitamin E as an effective therapy in AD treatment. Definitely, the significant amount of positive findings justifies more extensive research in order to find cures to combat this devastating progressive neurological disease that physically and mentally transforms individuals.

Acknowledgments Ursuline College Department of Biology supported the publication costs associated with this paper. The authors thank Stefanie Rhine for the careful reading of the paper.

Author Contributions All authors contributed meaningfully to the writing and editing of the paper. Conflicts of Interest The authors declare no conflict of interest.

VITAMIN D AND DEMENTIA

Ataxia with isolated vitamin E deficiency: Heterogeneity of mutations and phenotypic variability in a large number of families. Affinity for alpha-tocopherol transfer protein as a determinant of the biological activities of vitamin E analogs. Influence of major structural features of tocopherols and tocotrienols on their omega-oxidation by tocopherol-omega-hydroxylase.

Can Vitamin D deficiency lead to Alzheimer’s?

Metabolism, biological activity and significance in human vitamin E nutrition. Intracellular trafficking of vitamin E in hepatocytes: The role of tocopherol transfer protein.

Vitamin D: Can it prevent Alzheimer's & dementia? - Mayo Clinic

Vitamin E status in cholestasis. Prospective, long-term study of fat-soluble vitamin status in children with cystic fibrosis identified by newborn screen. Altered vitamin E status in Niemann-Pick type C disease. First proof that vitamin E is major lipid-soluble, chain-breaking antioxidant in human blood plasma. Prevention and treatment of Alzheimer disease and aging: The cohort consisted of 5, adults recruited in — and an additional African-American participants recruited in — Of these 5, participants, 4, ambulatory participants had complete exam data in — the baseline assessment for the current study.

Serum hydroxyvitamin D 25 OH D concentrations were not measured in 1, participants who had prevalent cardiovascular disease or stroke one or more of the following: This resulted in a final sample of 1, participants for the main prospective analyses and 1, participants for the secondary baseline analyses. Those lost to follow-up defined as participants with serum 25 OH D measured but no diagnostic assessment of incident dementia were older mean [SD], Standard protocol approvals, registrations, and patient consents.

The institutional review boards at each participating institution approved the research protocols, and all participants provided written informed consent.

Vitamin D and the risk of dementia and Alzheimer disease

Serum 25 OH D measurement. Dementia and AD status was assessed in — by a committee of neurologists and psychiatrists on the basis of annual cognitive assessments, repeat MRI scans, medical records, questionnaires, and proxy interviews.

Diagnosis of dementia was based on a progressive or static cognitive deficit with impairment in at least 2 cognitive domains and a history of normal cognitive function before the onset of abnormalities. Further details can be found elsewhere. We adjusted for covariates identified as potential confounders 1— 3 Cox proportional hazards models were used to assess the associations between baseline serum 25 OH D and the risk of incident all-cause dementia and AD. Participants were considered at risk for dementia from baseline — and were censored at death or the end of follow-up in June The proportionality of hazards assumption was assessed using the Schoenfeld residuals technique.

In basic adjusted models, we controlled for age and season of blood collection. In fully adjusted models, we controlled for education, sex, BMI, smoking, alcohol consumption, and depressive symptoms.

To investigate any threshold, we used multivariate adjusted penalized smoothing spline plots.