# Axonopathy: mechanisms and potential therapeutic targets for neurodegenerative diseases

**Authors:** Ruinan Shen, Kijung Sung, Jianqing Ding, Chengbiao Wu

PMC · DOI: 10.1186/s40035-026-00543-7 · Translational Neurodegeneration · 2026-03-24

## TL;DR

This review discusses how axon dysfunction contributes to neurodegenerative diseases and highlights axons as a potential target for new therapies.

## Contribution

The paper emphasizes axons as a novel therapeutic target for treating neurodegenerative diseases.

## Key findings

- Axonopathy is an early and significant factor in diseases like Alzheimer’s and Parkinson’s.
- Recent advances show axons play a key role in neuronal health and disease progression.
- Targeting axons could lead to new treatments for neurodegenerative conditions.

## Abstract

Axons are unique structural and functional features of nerve cells, which play a critical role in regulating neuronal homeostasis. Dysfunction and degeneration of axons (axonopathy) has been established as an early and prominent contributing mechanism to the pathogenesis of neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. In this review, we briefly summarize the structure and function of axons, and highlight recent advances in the understanding of the role of axons in health and disease. We argue that axons are a potential target for developing novel therapies for neurodegenerative diseases.

## Linked entities

- **Diseases:** Alzheimer’s disease (MONDO:0004975), Parkinson’s disease (MONDO:0005180), Huntington’s disease (MONDO:0007739), amyotrophic lateral sclerosis (MONDO:0004976)

## Full-text entities

- **Diseases:** neurodegenerative diseases (MESH:D019636), Huntington's disease (MESH:D006816), Axonopathy (MESH:D016472), amyotrophic lateral sclerosis (MESH:D000690), Dysfunction and degeneration of axons (MESH:D009410), Alzheimer's disease (MESH:D000544), Parkinson's disease (MESH:D010300)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC13011709/full.md

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13011709/full.md

## References

6 references — full list in the complete paper: https://tomesphere.com/paper/PMC13011709/full.md

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Source: https://tomesphere.com/paper/PMC13011709