# Crosstalk between exosomes and cellular senescence: A core vicious loop promoting α-synuclein pathology in Parkinson's disease

Article · Mao W, Song W, Zhang Y, Feng W, Wang H, Cheng B

- Archive id: doi:10.4103/nrr.nrronline-d-26-00800
- Published: 2026-09-30
- Venue: Neural regeneration research
- DOI: https://doi.org/10.4103/nrr.nrronline-d-26-00800
- PMID: 42821418
- Citations: 0
- Source URL: https://doi.org/10.4103/nrr.nrronline-d-26-00800
- Provenance: europepmc

## Abstract

Abstract Parkinson's disease is characterized by α-synuclein aggregation, dopaminergic neuron loss, and neuroinflammation. Emerging evidence reveals complex crosstalk between exosomes and cellular senescence in Parkinson's disease pathogenesis. Exosomes mediate α-synuclein transmission and neuroinflammation, while delivering protective factors such as miRNAs that inhibit cellular senescence. Senescent cells secrete pro-inflammatory factors via mitochondrial dysfunction and the senescence-associated secretory phenotype, linking to Parkinson's disease mitophagy defects. This forms a vicious "senescence-protein deposition-inflammation" cycle, with senescent cell-derived exosomes exacerbating α-synuclein aggregation and inflammation. Therapeutically, exosomes are ideal drug carriers due to blood-brain barrier penetrability and low immunogenicity for targeted antioxidant delivery. Future perspectives highlight exosome-based biomarkers and brain-gut axis intervention as promising directions. We propose integrating exosome engineering and senolytic strategies to lay the foundation for early diagnosis and precision therapy of Parkinson's disease, promoting diagnosis-intervention translational research and bridging bench-tobedside translation.

_Abstract reproduced under CC-BY (article license as recorded by Europe PMC; abstract reproduced unmodified apart from markup removal)._

Topics: [Biology of Aging & Longevity](https://space-kitty.com/topics/aging-longevity)

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