神经病学与神经康复学杂志2026，Vol.22Issue(1)：12-20,9.DOI:10.12022/jnnr.2025-0284
α-突触核蛋白寡聚体介导的神经元-胶质细胞交互作用:帕金森病神经退行性变的分子机制研究进展
Advances in the molecular mechanisms of α-synuclein oligomer-mediated neuron-glial cell interactions in Parkinson's disease neurodegeneration
周凡1
作者信息
- 1. 长江大学附属荆州医院神经内科,湖北 荆州 434020
- 折叠
摘要
Abstract
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.关键词
α-突触核蛋白寡聚体/细胞交互作用/帕金森病/神经退行性变/分子机制/炎症反应Key words
Α-synuclein oligomers/Cell-cell interactions/Parkinson's disease/Neurodegeneration/Molecular mechanisms/Inflammatory response引用本文复制引用
周凡..α-突触核蛋白寡聚体介导的神经元-胶质细胞交互作用:帕金森病神经退行性变的分子机制研究进展[J].神经病学与神经康复学杂志,2026,22(1):12-20,9.
