Skip to content
Preprint · OA via OpenAlex

[Aggregation and spread of synuclein in Parkinson's disease].

Erwan Bézard, Benjamin Dehay

PubMed · 2022 · ▲ 5 citations

Abstract

The vast majority of neurodegenerative diseases are associated with an accumulation of undegraded and aggregated proteins. Hence the word proteinopathies is now used to refer to these neurodegenerative diseases. The synucleinopathies are one component of them, in particular in Parkinson's disease. The neuropathological features of Parkinson's disease are the progressive loss of dopamine neurons in the midbrain and the formation of aggregates composed mainly of a-synuclein protein. Experimental evidence suggests that under pathological conditions, normal soluble a-synuclein protein adopts an abnormal folding and subsequently aggregates, with a propensity to spread throughout the central nervous system. This review article discusses the specifics of a-synuclein aggregation and emerging mechanisms for understanding its spread and aims at providing a molecular explanation for the progression of the disease in humans.

◌ CITATION ONLY
Full text is not openly licensed for redistribution here. Read it at the source:

Read at source →

Provenance

Source
OpenAlex
DOI
10.1051/medsci/2021241
Canonical
link ↗
Fetched
2026-10-21 MST

Cite this

APA
Bézard, E., &amp; Dehay, B. (2022). [Aggregation and spread of synuclein in Parkinson's disease]. <em>PubMed</em>. https://doi.org/10.1051/medsci/2021241
Vancouver
Bézard E, Dehay B. [Aggregation and spread of synuclein in Parkinson's disease]. PubMed. 2022. doi:10.1051/medsci/2021241.
BibTeX
@unpublished{erwan2022Aggreg, title = {[Aggregation and spread of synuclein in Parkinson's disease].}, author = {Erwan Bézard and Benjamin Dehay}, journal = {PubMed}, year = {2022}, doi = {10.1051/medsci/2021241}, }

Research neighborhood

References, citing works, and semantically nearest findings. Click a node to open it.

Related findings