4.6 Review

A quantitative meta-analysis of vitamin C in the pathophysiology of Alzheimer's disease

Journal

FRONTIERS IN AGING NEUROSCIENCE
Volume 14, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fnagi.2022.970263

Keywords

vitamin C; Alzheimer's disease; ascorbic acid; amyloid-beta; oxidative stress

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This meta-analysis and systematic review found that AD patients have significantly lower plasma levels of vitamin C, suggesting that vitamin C deficiency is involved in disease progression and supplementation may be an effective strategy for preventing and treating AD.
Purpose: Alzheimer's disease (AD) is a multifaceted neurodegenerative disorder with many complex pathways feeding into its pathogenesis and progression. Vitamin C, an essential dietary antioxidant, is vital for proper neurological development and maintenance. This meta-analysis and systematic review attempted to define the relationship between vitamin C plasma levels and AD while highlighting the importance and involvement of vitamin C in the pathogenesis of AD. Materials and methods: PRISMA guidelines were used to obtain studies quantifying the plasma levels of vitamin C in AD and control subjects. The literature was searched in the online databases PubMed, Google Scholar, and Web of Science. A total of 12 studies were included (n = 1,100) and analyzed using Comprehensive Meta-Analysis 3.0. Results: The results show that there is a significant decrease in the plasma vitamin C levels of AD patients as compared to healthy controls (pooled SMD with random-effect model: -1.164, with 95%CI: -1.720 to -0.608, Z = -4.102, p = 0.00) with significant heterogeneity (I-2 = 93.218). The sensitivity analysis showed directionally similar results. Egger's regression test (p = 0.11) and visual inspection of the funnel plot showed no publication bias. Conclusion: Based on these studies, it can be deduced that the deficiency of vitamin C is involved in disease progression and supplementation is a plausible preventive and treatment strategy. However, clinical studies are warranted to elucidate its exact mechanistic role in AD pathophysiology and prevention.

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