# Dual role of exosomes in neurodegenerative diseases: a molecular bridge between neuroinflammation and transmission of pathological proteins

**Authors:** Wei An, Ze Jin, Yan Li

PMC · DOI: 10.3389/fneur.2025.1708655 · Frontiers in Neurology · 2026-01-14

## TL;DR

This review explores how exosomes contribute to neurodegenerative diseases by linking inflammation and the spread of harmful proteins.

## Contribution

The paper highlights the dual role of exosomes in neuroinflammation and pathological protein transmission in NDDs.

## Key findings

- Exosomes mediate neuroinflammation in diseases like Alzheimer’s and Parkinson’s.
- They act as carriers for spreading misfolded proteins between cells.
- Exosomes influence disease progression through intercellular signaling.

## Abstract

Neurodegenerative diseases (NDDs) are complex disorders characterized by the progressive loss of neuronal function. Their pathological mechanisms involve multiple levels, including neuroinflammation, abnormal protein aggregation, and disrupted cell signaling. Diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Amyotrophic Lateral Sclerosis (ALS), multiple sclerosis (MS), and prion diseases not only severely impact patients’ quality of life but also pose significant challenges for medical research due to their complex pathogenesis and the lack of effective treatments. In recent years, extracellular vesicles (EVs), particularly exosomes, have garnered increasing attention for their critical role in cell-to-cell communication. Exosomes are membrane-enclosed nanovesicles approximately 30–150 nm in diameter that can carry proteins, lipids, nucleic acids, and other bioactive molecules, influencing recipient cells through paracrine or distant signaling. This review aims to summarize the roles of exosomes as mediators of neuroinflammation and as vehicles for intercellular transmission of pathogenic proteins in neurodegenerative diseases.

## Linked entities

- **Diseases:** Alzheimer’s disease (MONDO:0004975), Parkinson’s disease (MONDO:0005180), Amyotrophic Lateral Sclerosis (MONDO:0004976), multiple sclerosis (MONDO:0005301)

## Full-text entities

- **Diseases:** neuroinflammation (MESH:D000090862), NDDs (MESH:D019636), loss (MESH:D016388), prion diseases (MESH:D017096), AD (MESH:D000544), function (MESH:D003291), MS (MESH:D009103), PD (MESH:D010300), ALS (MESH:D000690)
- **Chemicals:** lipids (MESH:D008055)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12847281/full.md

## References

125 references — full list in the complete paper: https://tomesphere.com/paper/PMC12847281/full.md

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Source: https://tomesphere.com/paper/PMC12847281