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<p>Parkinson’s disease (PD) is a&#xa0;progressive neurological disorder characterized by stiffness, tremors, and walking difficulties, caused by the degeneration of dopaminergic neurons. The main pathological features of PD include the accumulation of α‑synuclein (α-syn), which leads to the formation of Lewy bodies (LBs), and the death of dopaminergic neurons in the substantia nigra. TFEB (transcription factor EB) is a&#xa0;key regulator of autophagy and lysosomal biogenesis, which are essential for breaking down protein aggregates. TFEB and autophagy-lysosome pathways contribute to the development of major neurodegenerative diseases by promoting neuroinflammation, disrupting synaptic plasticity, increasing oxidative stress, and causing neuronal apoptosis. TFEB exhibits neuroprotective functions that can be enhanced through increased expression via treatments like adeno-associated virus-mediated overexpression, trehalose, and others. TFEB plays several protective roles, especially in diseases involving α‑syn production, autophagy-lysosomal pathways, neuroinflammation, and mitochondrial dysfunction. This review focuses on the molecular role of TFEB in autolysosomal regulation, as well as the pathophysiology of PD, including its connections to α‑syn, mitochondrial dysfunction, and neuroinflammation. It also explores potential strategies for modulating TFEB expression as novel therapeutic approaches, highlighting the importance of developing such treatments to prevent disease progression.</p>

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Role of TFEB in parkinson’s disease: pathophysiological insights and therapeutic approaches

  • 期刊论文

  • 发表日期：

    2024年12月1日

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  • Royal Patel,
  • Ajeet Singh,
  • Sowjanya Pulipati,
  • Priyanka Tyagi,
  • Divyang Patel,
  • Beena Goyal,
  • Shashi Prabha,
  • Bipin Bihari,
  • Vikash Kumar Chaudhary

摘要

Parkinson’s disease (PD) is a progressive neurological disorder characterized by stiffness, tremors, and walking difficulties, caused by the degeneration of dopaminergic neurons. The main pathological features of PD include the accumulation of α‑synuclein (α-syn), which leads to the formation of Lewy bodies (LBs), and the death of dopaminergic neurons in the substantia nigra. TFEB (transcription factor EB) is a key regulator of autophagy and lysosomal biogenesis, which are essential for breaking down protein aggregates. TFEB and autophagy-lysosome pathways contribute to the development of major neurodegenerative diseases by promoting neuroinflammation, disrupting synaptic plasticity, increasing oxidative stress, and causing neuronal apoptosis. TFEB exhibits neuroprotective functions that can be enhanced through increased expression via treatments like adeno-associated virus-mediated overexpression, trehalose, and others. TFEB plays several protective roles, especially in diseases involving α‑syn production, autophagy-lysosomal pathways, neuroinflammation, and mitochondrial dysfunction. This review focuses on the molecular role of TFEB in autolysosomal regulation, as well as the pathophysiology of PD, including its connections to α‑syn, mitochondrial dysfunction, and neuroinflammation. It also explores potential strategies for modulating TFEB expression as novel therapeutic approaches, highlighting the importance of developing such treatments to prevent disease progression.