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<p>Fatigue is a common and debilitating non-motor symptom in patients with Parkinson’s disease (PD). By integrating the activation likelihood estimation (ALE) meta-analysis and activation network mapping (ANM) technique, the brain network underlying fatigue (referred to as “fatigue-related network”) in PD was identified, comprising widespread brain regions primarily involving the somatomotor and frontoparietal networks. This network was interpreted through transcriptomic patterns, chemoarchitectures, and behavioral relevance. Fatigue-related genes were predominantly enriched in synaptic and actin filament-related biological processes and showed primary expression in neurons and oligodendrocytes. The fatigue-related network closely corresponded to the spatial distribution of acetylcholine, glutamate, and norepinephrine systems and was primarily linked to motor function. This study defines a distinct brain network substrate underlying fatigue in PD, advancing our understanding of the neurobiological mechanisms and facilitating the development of effective therapies for affected patients.</p>

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Mapping the neural and molecular basis underlying fatigue in Parkinson’s disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月29日

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  • Futing Yang,
  • Junyi Shen,
  • Zhiqin Sun,
  • Lingli Tan,
  • Rucheng Yang,
  • Lina Zhu,
  • Yin Mo,
  • Heng Shao,
  • Jianhong Hou,
  • Zanzong Sun,
  • Yuan Gao,
  • Yanbing Hou,
  • Jiaojian Wang

摘要

Fatigue is a common and debilitating non-motor symptom in patients with Parkinson’s disease (PD). By integrating the activation likelihood estimation (ALE) meta-analysis and activation network mapping (ANM) technique, the brain network underlying fatigue (referred to as “fatigue-related network”) in PD was identified, comprising widespread brain regions primarily involving the somatomotor and frontoparietal networks. This network was interpreted through transcriptomic patterns, chemoarchitectures, and behavioral relevance. Fatigue-related genes were predominantly enriched in synaptic and actin filament-related biological processes and showed primary expression in neurons and oligodendrocytes. The fatigue-related network closely corresponded to the spatial distribution of acetylcholine, glutamate, and norepinephrine systems and was primarily linked to motor function. This study defines a distinct brain network substrate underlying fatigue in PD, advancing our understanding of the neurobiological mechanisms and facilitating the development of effective therapies for affected patients.