# Folic acid as a potential therapeutic agent for Alzheimer's disease: Effects on inflammatory cytokines, amyloid deposition, and neurotransmitter metabolism

## TL;DR

This study shows that folic acid, when added to standard treatment, can slow Alzheimer's progression by reducing inflammation and improving brain chemicals.

## Contribution

The study demonstrates folic acid's novel therapeutic potential in Alzheimer's by targeting inflammation, amyloid, and neurotransmitters.

## Key findings

- Folic acid reduced inflammatory cytokines IL-1b, IL-6, and TNF-a in Alzheimer's patients.
- Folic acid lowered amyloid (Ab1-42) and Tau protein levels, key markers of Alzheimer's pathology.
- Folic acid increased neurotransmitters GABA, 5-HT, and Ach, and improved nutritional status.

## Abstract

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. This study aimed to investigate the effects of FA supplementation on serum inflammatory cytokines (IL-1b, IL-6, TNF-a), amyloid (Ab1-42), Tau proteins, and neurotransmitters (GABA, 5-HT, Ach) in AD patients.

We conducted a follow-up-controlled trial; 114 AD patients were included and randomly divided into a control group (donepezil treatment) and an experimental group (donepezil + FA treatment) for 3 months. Inflammatory factors, Ab1-42, Tau, neurotransmitter levels and nutritional status were assessed before and after treatment.

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-1b, IL-6, and TNF-a), Ab1-42, and Tau were significantly lower (P<0.05), and neurotransmitters (GABA, 5-HT, and Ach) and nutritional indexes (albumin and hemoglobin) were substantially higher.

FA supplementation can effectively delay AD progression by inhibiting neuroinflammation, reducing amyloid deposition, regulating neurotransmitter metabolism and improving nutritional status.