Folic Acid as a Potential Therapeutic Agent for Alzheimer's Disease: Effects on Inflammatory Cytokines, Amyloid Deposition, and Neurotransmitter Metabolism
Abstract
Objective: Alzheimer's disease (AD) is a degenerative disease of the central nervous system characterized by neuroinflammation and amyloid deposition. Folic acid (FA), a B vitamin, may improve the course of AD by modulating inflammation and neuroprotection. The aim of this study was to investigate the effects of FA supplementation on serum inflammatory cytokines (IL-1β, IL-6, TNF-α), amyloid (Aβ1-42), Tau proteins, and neurotransmitters (GABA, 5-HT, Ach) in AD patients.
Methods: 114 AD patients were included and randomly divided into control group (donepezil treatment) and experimental group (donepezil + folic acid treatment) for 3 months. Inflammatory factors, Aβ1-42, Tau, neurotransmitter levels and nutritional status were assessed before and after treatment.
Results: The total effective rate of the experimental group (89.47%) was significantly higher than that of the control group (75.44%), and the levels of inflammatory factors (IL-1β, IL-6, and TNF-α), Aβ1-42, and Tau were significantly lower (P<0.05), and neurotransmitters (GABA, 5-HT, and Ach) and nutritional indexes (albumin and hemoglobin) were significantly higher.
Conclusion: FA supplementation can effectively delay AD progression by inhibiting neuroinflammation, reducing amyloid deposition, regulating neurotransmitter metabolism and improving nutritional status.
Copyright (c) 2025 Shaowei Jing, Yanqiu Wang, Yang Liu, Yi Luo, Xiaoqing Wen, Yao Ma, Haoxuan Zhu, Gongcai Chen, Xiaochun Ouyang
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