帕金森病（Parkinson’s disease，PD）作为一种常见的神经退行性疾病，其发病机制复杂且尚未完全阐明。α-突触核蛋白（alpha-synuclein，α-syn）异常聚集形成的寡聚体被认为是PD病理的核心因素之一，这些寡聚体不仅在神经元内积累，还通过介导神经元与胶质细胞之间的交互作用，推动病理进程。当前研究表明，α-syn寡聚体通过诱导胶质细胞激活和炎症反应，加剧神经元损伤，进而促进神经退行性变。然而，关于α-syn寡聚体在神经元-胶质细胞信号传导中的具体分子机制仍存在诸多未解之谜。本文系统综述了α-syn寡聚体的形成过程及其毒性机制，胶质细胞的激活状态及相关炎症通路，以及二者间的交互信号传递最新进展，旨在揭示其在PD病理中的关键作用。通过综合分析这些分子机制，期望为PD的早期诊断和治疗提供新的理论支持和研究方向，推动相关疾病干预策略的发展。

Parkinson's disease (PD) is a common neurodegenerative disorder whose pathogenesis is complex and remains incompletely understood. Oligomers formed by the abnormal aggregation of α‍-synuclein (α‍-syn) are considered one of the central culprits of PD pathology. These oligomers accumulate not only within neurons but also propagate pathological changes by mediating neuron-glia crosstalk. Accumulating evidence indicates that α‍-syn oligomers exacerbate neuronal injury and accelerate neurodegeneration by triggering glial activation and inflammatory responses. Nevertheless, the precise molecular mechanisms through which α-syn oligomers transduce signals between neurons and glia are still largely unresolved. Here we systematically review the biogenesis and toxic mechanisms of α-syn oligomers, the activation states of glial cells and their associated inflammatory pathways, and the latest advances in intercellular signaling between the two compartments, with the goal of illuminating the pivotal roles of these processes in PD pathobiology. By integrating these molecular insights, we aim to provide new theoretical frameworks and research directions for the early diagnosis and treatment of Parkinson's disease, thereby fostering the development of innovative therapeutic strategies.