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<p>Accumulating evidence implicates cholinergic dysfunction in freezing of gait (FOG) in Parkinson’s disease (PD). Given the basal forebrain (BF) provides the primary cholinergic input to the cortex, elucidating BF-cortical connectivity and its dynamic reconfiguration during motor challenges in PD-FOG is important. This study included 44 PD-FOG, 45 without FOG (PD-NFOG), and 27 healthy controls (HC). All underwent diffusion and resting-state functional MRI. A subgroup (27 PD-FOG, 20 PD-NFOG, 27 HC) also underwent gait-related task-based fMRI. Multimodal gradients of BF connectivity were compared across the three groups and between task and rest. BF free-water was elevated in both PD groups versus HC. Connectivity gradient analysis further revealed reduced structure-function coupling along the anteromedial-to-posterolateral BF axis, with weakest coupling in posterolateral subregions. Cortically, coupling progressively reduced from unimodal sensory to transmodal association cortex. While this topographic architecture was qualitatively preserved in both PD groups, during turning imagery, PD-FOG patients exhibited impaired adaptive decoupling in the somatomotor network, localized to an insular hub with attenuated task-evoked nodal responsivity. BF free-water elevation and hub dysfunction independently predicted clinical status along the continuum from healthy to PD-NFOG to PD-FOG. Our findings reveal a state-dependent reconfiguration failure in PD-FOG, suggesting a circuit-level, neurodynamic mechanism for FOG.</p>

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State-dependent reconfiguration failure of the basal forebrain-cortical gradient in Parkinson’s disease with freezing of gait

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月4日

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  • Hou Miaomiao,
  • Chen Liu,
  • Zhao Jiahao,
  • Lu Song,
  • Ying Wan,
  • Na Wu,
  • Xinxin Chen,
  • Yu Zhang,
  • Chen Qi,
  • Bingjie Ma,
  • Zhihua Liu,
  • Gaiying Li,
  • Jianqi Li,
  • Xi Wu,
  • Zhenguo Liu,
  • Jing Gan

摘要

Accumulating evidence implicates cholinergic dysfunction in freezing of gait (FOG) in Parkinson’s disease (PD). Given the basal forebrain (BF) provides the primary cholinergic input to the cortex, elucidating BF-cortical connectivity and its dynamic reconfiguration during motor challenges in PD-FOG is important. This study included 44 PD-FOG, 45 without FOG (PD-NFOG), and 27 healthy controls (HC). All underwent diffusion and resting-state functional MRI. A subgroup (27 PD-FOG, 20 PD-NFOG, 27 HC) also underwent gait-related task-based fMRI. Multimodal gradients of BF connectivity were compared across the three groups and between task and rest. BF free-water was elevated in both PD groups versus HC. Connectivity gradient analysis further revealed reduced structure-function coupling along the anteromedial-to-posterolateral BF axis, with weakest coupling in posterolateral subregions. Cortically, coupling progressively reduced from unimodal sensory to transmodal association cortex. While this topographic architecture was qualitatively preserved in both PD groups, during turning imagery, PD-FOG patients exhibited impaired adaptive decoupling in the somatomotor network, localized to an insular hub with attenuated task-evoked nodal responsivity. BF free-water elevation and hub dysfunction independently predicted clinical status along the continuum from healthy to PD-NFOG to PD-FOG. Our findings reveal a state-dependent reconfiguration failure in PD-FOG, suggesting a circuit-level, neurodynamic mechanism for FOG.