Oxidative stress and synaptic dysfunction in rodent models of Parkinson's disease.

Neurobiol Dis

Department of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy; IRCCS Mondino Foundation, Pavia, Italy. Electronic address:

Published: October 2022

Parkinson's disease (PD) is a multifactorial disorder involving a complex interplay between a variety of genetic and environmental factors. In this scenario, mitochondrial impairment and oxidative stress are widely accepted as crucial neuropathogenic mechanisms, as also evidenced by the identification of PD-associated genes that are directly involved in mitochondrial function. The concept of mitochondrial dysfunction is closely linked to that of synaptic dysfunction. Indeed, compelling evidence supports the role of mitochondria in synaptic transmission and plasticity, although many aspects have not yet been fully elucidated. Here, we will provide a brief overview of the most relevant evidence obtained in different neurotoxin-based and genetic rodent models of PD, focusing on mitochondrial impairment and synaptopathy, an early central event preceding overt nigrostriatal neurodegeneration. The identification of early deficits occurring in PD pathogenesis is crucial in view of the development of potential disease-modifying therapeutic strategies.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.nbd.2022.105851DOI Listing

Publication Analysis

Top Keywords

oxidative stress
8
synaptic dysfunction
8
rodent models
8
parkinson's disease
8
mitochondrial impairment
8
stress synaptic
4
dysfunction rodent
4
models parkinson's
4
disease parkinson's
4
disease multifactorial
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!