![]() ![]() We then provide evidence that these tools are crucial for modelling Parkinson’s disease pathogenesis, causing protein misfolding and aggregation, synaptic dysfunction, brain plasticity impairment and cell-to-cell spreading of alpha-synuclein species. In this review, we first describe the cellular and animal models developed over recent years to study the physiological and pathological roles of this protein, including transgenic techniques, use of viral vectors and intracerebral injections of alpha-synuclein fibrils. Thus, a deep understanding of alpha-synuclein physiological and pathophysiological functions is crucial. The pathogenesis of Parkinson’s disease is complex and not yet fully clarified and the heterogeneity of the disease, with diverse genetic susceptibility and risk factors and different clinical courses, adds further complexity. Several explanations exist for this issue. However, these treatments have not yet shown clear efficacy in slowing the progression of this disease. Some progress has been made over recent years in identifying disease-modifying therapies for Parkinson’s disease that target alpha-synuclein. The critical role of alpha-synuclein in Parkinson’s disease represents a pivotal discovery. ![]()
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