# Mechanism of Exercise-Regulated Intestinal Flora for Alzheimer’s Disease Based on Gut–Brain Axis

**Authors:** Huiying Zhao, Wei Wu, Xiaofan Men

PMC · DOI: 10.3390/nu18020254 · 2026-01-13

## TL;DR

This review explains how exercise can help treat Alzheimer’s by improving gut health and brain communication through the gut–brain axis.

## Contribution

The paper systematically summarizes how exercise modulates gut flora to alleviate Alzheimer’s disease via the gut–brain axis.

## Key findings

- Exercise improves gut flora diversity, which may slow Alzheimer’s progression.
- Exercise strengthens the blood–brain barrier and upregulates BDNF, supporting brain health.
- Different types of exercise have varying effects on gut flora and Alzheimer’s improvement.

## Abstract

Alzheimer’s disease (AD) is a chronic neurodegenerative disorder characterized by progressive loss of cognitive function. Its main pathological features include accumulation of Amyloid-beta (Aβ) plaques, excessive phosphorylation of microtubule-associated protein tau (tau protein), and neuroinflammation. In recent years, studies have confirmed intestinal flora is closely connected to AD. Gut–brain axis has an important part in AD. Intestinal flora can achieve signal communication between gut and brain through metabolic, immune, neural, and endocrine pathways, thereby slowing down AD. It has been discovered that exercise is not only beneficial to physical health but also has a positive impact on the brain function. In recent years, more and more studies have found exercise can alleviate AD through the following four major pathways: regulating the diversity of intestinal flora, strengthening the blood–brain barrier (BBB), regulating immune homeostasis, and upregulating the brain-derived neurotrophic factor (BDNF). In this review, we have summarized intestinal flora in AD and systematically expounded potential regulatory pathways of exercise in modulating intestinal flora for AD. This provides a more theoretical basis for subsequent research targeting “gut–brain axis” to regulate AD. At the same time, this review also summarizes differences in different exercise types on improving intestinal flora for alleviating AD, providing new ideas and strategies for AD.

## Linked entities

- **Diseases:** Alzheimer’s disease (MONDO:0004975), neuroinflammation (MONDO:0004466)

## Full-text entities

- **Genes:** MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}
- **Diseases:** AD (MESH:D000544), loss of cognitive function (MESH:D003072), neuroinflammation (MESH:D000090862), neurodegenerative disorder (MESH:D019636)

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12845132/full.md

---
Source: https://tomesphere.com/paper/PMC12845132