# Clathrin-mediated endocytosis as an axis for the etiopathogenesis of Parkinson's disease

## TL;DR

This paper explores how clathrin-mediated endocytosis may play a role in Parkinson's disease, offering new insights into its causes and potential treatments.

## Contribution

The paper highlights new genetic and functional evidence linking clathrin-mediated endocytosis to Parkinson's disease etiology.

## Key findings

- Genetic and functional data support a role for clathrin-mediated endocytosis in Parkinson's disease risk.
- CME dysfunction may contribute to the development of Parkinson's disease and related disorders.
- Targeting CME could offer therapeutic potential for Parkinson's disease.

## Abstract

Clathrin-mediated endocytosis (CME) is a core process in eukaryotic cells, providing a mechanism to selectively take up cargo from the extracellular space into the cytoplasm. Emerging data from both Mendelian and idiopathic forms of Parkinson's disease and parkinsonism syndromes supports a role for key players in CME in determining the risk of developing these neurodegenerative disorders. This Perspective summarizes the current genetic and functional evidence supporting a role for CME in Parkinson's disease, suggesting routes through which CME dysfunction could contribute to the etiopathogenesis of this disorder, and discussing the therapeutic potential for targeting CME in the context of neurodegeneration linked to Parkinson's disease and parkinsonism.

Summary: New insights into the genetics of Parkinson's disease reveal a potential role for clathrin-mediated endocytosis, opening up new avenues for investigating the pathobiology of Parkinson's disease and developing novel drugs.