# Extracellular vesicle-based therapies for neurodegenerative diseases

## TL;DR

Extracellular vesicles can both cause and treat neurodegenerative diseases by spreading harmful proteins or delivering therapeutic molecules to the brain.

## Contribution

The paper highlights colostrum-derived EVs as a natural, scalable source for neuroprotective therapies.

## Key findings

- EVs contribute to neurodegeneration by spreading disease-related proteins like beta amyloid and tau.
- EVs can be modified to deliver anti-inflammatory and neuroprotective molecules across the blood-brain barrier.
- Colostrum-derived EVs show promise as a biocompatible and natural therapeutic option for neurodegenerative diseases.

## Abstract

Extracellular vesicles (EVs) are mediators of neurodegeneration and emerging therapeutic tools for central nervous system disorders. On the one hand, they help spread beta amyloid, tau, α-synuclein, TDP-43, and mutant SOD1, contributing to the signs and symptoms of Alzheimer’s, Parkinson’s, Amyotrophic lateral sclerosis, and Huntington’s Diseases. By activating glial cells, they promote chronic neuroinflammation through carrying cytokines, inflammasomes, and chemokines. On the other hand, EVs’ ability to transport neuroregulatory products and cross the blood–brain barrier makes them ideal vehicles for drug delivery. Their function can be surface-modified to deliver targeted therapies, including anti-inflammatory and neuroprotective regulatory RNAs, proteins, and lipids, as well as factors that help maintain neural homeostasis. Notably, we suggest that colostrum-derived EVs, enriched with growth factors and immune-regulatory microRNAs, offer a natural, scalable, and biocompatible source for neuroprotective treatment. Although EVs can act as “Janus-faced” entities – serving both as disease initiators and versatile therapeutic vehicles – controlling their activity can enable immune-based therapeutics for neurodegenerative diseases.