Abstract

Alpha-synuclein aggregation is a critical pathological process implicated in neurodegenerative diseases such as Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). This review explores the molecular mechanisms underlying alpha-synuclein aggregation, its role in neurodegeneration, and the clinical implications across various synucleinopathies. By elucidating the complex interplay of protein misfolding, propagation of pathology, and genetic and environmental factors, this review aims to provide insights into current therapeutic strategies and future directions for combating these devastating disorders. Alpha-synuclein, a protein intrinsic to the nervous system, has become a focal point in understanding neurodegenerative diseases, particularly Parkinson's disease (PD). The aggregation of alpha-synuclein is central to the pathophysiology of these conditions, marking a critical intersection between molecular biology and clinical manifestations.