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<p>Parkinson’s disease (PD) is the second most common neurodegenerative disorder worldwide, characterized primarily by motor symptoms such as resting tremor, rigidity, and bradykinesia, accompanied by non-motor symptoms (NMS) including constipation and depression. The underlying mechanisms of PD are multifaceted, driven by a complex interaction between genetic and environmental factors that remain to be entirely understood. In recent years, an increasing body of evidence has confirmed that the abnormal aggregation of α-synuclein (α-Syn), mitochondrial dysfunction, and neuroinflammatory activation are not isolated pathological events; rather, they constitute the core driving mechanism of PD pathogenesis and progression through complex networked interactions. This narrative review examines the independent mechanisms of these three pathological components, provides an in-depth analysis of their regulatory interaction networks, and summarizes therapeutic targets and synergistic treatment strategies for the pathological axes, aiming to provide theoretical support for disease-modifying therapy and early intervention in PD.</p>

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The vicious cycle: unraveling the interplay between α-synuclein, mitochondrial dysfunction, and neuroinflammation in Parkinson’s disease

  • 期刊论文

  • 发表日期：

    2026年5月30日

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  • Yu-lin Liang,
  • Feng-ge Yang,
  • Qiang Tang

摘要

Parkinson’s disease (PD) is the second most common neurodegenerative disorder worldwide, characterized primarily by motor symptoms such as resting tremor, rigidity, and bradykinesia, accompanied by non-motor symptoms (NMS) including constipation and depression. The underlying mechanisms of PD are multifaceted, driven by a complex interaction between genetic and environmental factors that remain to be entirely understood. In recent years, an increasing body of evidence has confirmed that the abnormal aggregation of α-synuclein (α-Syn), mitochondrial dysfunction, and neuroinflammatory activation are not isolated pathological events; rather, they constitute the core driving mechanism of PD pathogenesis and progression through complex networked interactions. This narrative review examines the independent mechanisms of these three pathological components, provides an in-depth analysis of their regulatory interaction networks, and summarizes therapeutic targets and synergistic treatment strategies for the pathological axes, aiming to provide theoretical support for disease-modifying therapy and early intervention in PD.