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<p>Parkinson’s disease (PD), a prevalent age-related neurodegenerative movement disorder, is fundamentally driven by the accumulation of abnormal alpha-synuclein (α-Syn) within dopaminergic neurons of the substantia nigra pars compacta (SNpc). While astrocytes normally protect neurons through antioxidant release, anti-inflammatory actions influenced by microglia, and dopaminergic receptor signaling, a critical shift occurs as α-Syn progressively accumulates within astrocytes themselves. This intracellular α-Syn buildup is central to transforming astrocytes from a protective state into a detrimental one. Genetic mutations linked to PD further impair astrocytic functions like antioxidant defense. The precise mechanisms by which α-Syn accumulation drives this harmful phenotypic shift in astrocytes remain unclear, but it significantly worsens PD pathology. This review examines the dual roles of astrocytes in PD pathogenesis, emphasizing α-Syn’s pivotal role in their functional transformation.</p>

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Astrocytic dysfunction in Parkinson’s disease pathogenesis: focusing on alpha-synuclein

  • 期刊论文

  • 发表日期：

    2026年3月27日

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  • Zainah Al-Qahtani,
  • Hayder M. Al-kuraishy,
  • Ali I. Al-Gareeb,
  • Ali K. Albuhadily,
  • Ahmed M. Abdelaziz,
  • Mubarak Alruwaili,
  • Gaber El-Saber Batiha

摘要

Parkinson’s disease (PD), a prevalent age-related neurodegenerative movement disorder, is fundamentally driven by the accumulation of abnormal alpha-synuclein (α-Syn) within dopaminergic neurons of the substantia nigra pars compacta (SNpc). While astrocytes normally protect neurons through antioxidant release, anti-inflammatory actions influenced by microglia, and dopaminergic receptor signaling, a critical shift occurs as α-Syn progressively accumulates within astrocytes themselves. This intracellular α-Syn buildup is central to transforming astrocytes from a protective state into a detrimental one. Genetic mutations linked to PD further impair astrocytic functions like antioxidant defense. The precise mechanisms by which α-Syn accumulation drives this harmful phenotypic shift in astrocytes remain unclear, but it significantly worsens PD pathology. This review examines the dual roles of astrocytes in PD pathogenesis, emphasizing α-Syn’s pivotal role in their functional transformation.