| Sumario: | α-Synucleinopathies are a group of neurodegenerative diseases characterized by the abnormal aggregation of α-synuclein (α-Syn), including Parkinson's disease (PD), multiple system atrophy (MSA), dementia with Lewy bodies (DLB), and pure autonomic failure (PAF). Autonomic dysfunction is one of the most common non-motor symptoms in α-synucleinopathies, yet its underlying mechanisms remain unclear. α-Synucleinopathies exhibit the significant heterogeneity, and progress in developing novel therapeutic strategies remains limited. This review systemly explores the pathogenesis of autonomic dysfunction in α-synucleinopathies, with a focus on α-Syn conformational abnormalities, the peripheralcentral prion-like spread model, and the mechanisms by which α-Syn aggregates damage peripheral autonomic nerves. Furthermore, it summarizes recent advancements in drug therapies, non-pharmacological therapies, and α-Syn-targeted therapies, aiming to provide new insights for clinical practice and future research on α-synucleinopathies.
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