The Role of α-Synuclein in Etiology of Neurodegenerative Diseases

Author:

Krawczuk Daria1ORCID,Groblewska Magdalena2,Mroczko Jan1,Winkel Izabela3,Mroczko Barbara12ORCID

Affiliation:

1. Department of Neurodegeneration Diagnostics, Medical University of Białystok, 15-089 Białystok, Poland

2. Department of Biochemical Diagnostics, University Hospital in Białystok, 15-269 Białystok, Poland

3. Dementia Disorders Centre, Medical University of Wroclaw, 50-425 Ścinawa, Poland

Abstract

A presynaptic protein called α-synuclein plays a crucial role in synaptic function and neurotransmitter release. However, its misfolding and aggregation have been implicated in a variety of neurodegenerative diseases, particularly Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy. Emerging evidence suggests that α-synuclein interacts with various cellular pathways, including mitochondrial dysfunction, oxidative stress, and neuroinflammation, which contributes to neuronal cell death. Moreover, α-synuclein has been involved in the propagation of neurodegenerative processes through prion-like mechanisms, where misfolded proteins induce similar conformational changes in neighboring neurons. Understanding the multifaced roles of α-synuclein in neurodegeneration not only aids in acquiring more knowledge about the pathophysiology of these diseases but also highlights potential biomarkers and therapeutic targets for intervention in alpha-synucleinopathies. In this review, we provide a summary of the mechanisms by which α-synuclein contributes to neurodegenerative processes, focusing on its misfolding, oligomerization, and the formation of insoluble fibrils that form characteristic Lewy bodies. Furthermore, we compare the potential value of α-synuclein species in diagnosing and differentiating selected neurodegenerative diseases.

Funder

Medical University of Białystok

Publisher

MDPI AG

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