パーキンソン病の神経基盤となる脳ネットワークを特定(Brain Network Responsible for Parkinson’s Disease Identified)

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2026-02-04 ワシントン大学セントルイス校

米国ワシントン大学セントルイス校の研究チームは、パーキンソン病の運動症状に直接関与する脳ネットワークを特定した。研究では、脳深部刺激療法(DBS)を受ける患者の脳活動データと神経回路解析を組み合わせ、症状改善と強く相関する特定の神経ネットワークを同定した。このネットワークは大脳基底核と皮質領域を結び、異常活動が振戦や運動緩慢などの症状を引き起こす中枢的役割を果たすことが示された。成果により、DBSの刺激部位や設定を患者ごとに最適化できる可能性が高まり、より効果的で副作用の少ない個別化治療への道が開かれた。本研究は、パーキンソン病を「局所障害」ではなく「脳回路疾患」として理解する新たな視点を提示している。

パーキンソン病の神経基盤となる脳ネットワークを特定(Brain Network Responsible for Parkinson’s Disease Identified)
The brain network that links thinking with movement, called SCAN, was first described by WashU Medicine researchers in 2023 and has been identified in a new study as the neurological basis of Parkinson’s disease. An experimental therapy that targeted this network more than doubled symptom improvement in a small group of patients with Parkinson’s, which is characterized by hyperconnectivity (left side of illustration) between SCAN and the brain’s subcortex. (Image: Sara Moser/WashU Medicine)

<関連情報>

パーキンソン病は体性認知行動ネットワーク障害である Parkinson’s disease as a somato-cognitive action network disorder

Jianxun Ren,Wei Zhang,Louisa Dahmani,Evan M. Gordon,Shenshen Li,Ying Zhou,Yang Long,Jianting Huang,Yafei Zhu,Ning Guo,Changqing Jiang,Feng Zhang,Yan Bai,Wei Wei,Yaping Wu,Alan Bush,Matteo Vissani,Luhua Wei,Carina R. Oehrn,Melanie A. Morrison,Ying Zhu,Chencheng Zhang,Qingyu Hu,Yilin Yin,… Hesheng Liu
Nature  Published:04 February 2026
DOI:https://doi.org/10.1038/s41586-025-10059-1

Abstract

Parkinson’s disease (PD) is an incurable neurological disorder that often begins insidiously with sleep disturbances and somatic symptoms, progressing to whole-body motor and cognitive symptoms1,2,3,4,5. Dysfunction of the somato-cognitive action network (SCAN)—which is thought to control action execution6,7 by coordinating arousal, organ physiology and whole-body motor plans with behavioural motivation—is a potential contributor to the diverse clinical manifestations of PD. To investigate the role of the SCAN in PD pathophysiology and treatments (medications, deep-brain stimulation (DBS), transcranial magnetic stimulation (TMS) and MRI-guided focused ultrasound stimulation (MRgFUS)), we built a large (n = 863), multimodal, multi-intervention clinical imaging dataset. Resting-state functional connectivity revealed that the substantia nigra and all PD DBS targets (subthalamic nucleus, globus pallidus and ventral intermediate thalamus) are selectively connected to the SCAN rather than to effector-specific motor regions. Importantly, PD was characterized by specific hyperconnectivity between the SCAN and the subcortex. We therefore followed six PD cohorts undergoing DBS, TMS, MRgFUS and levodopa therapy using precision resting-state functional connectivity and electrocorticography recording. Efficacious treatments reduced SCAN-to-subcortex hyperconnectivity. Targeting the SCAN instead of effector regions doubled the efficacy of TMS treatments. Focused ultrasound treatment benefits increased when the target was closer to the thalamic SCAN sweet spot. Thus, SCAN hyperconnectivity is central to PD pathophysiology and its alleviation is a hallmark of successful neuromodulation. Targeting functionally defined subcortical SCAN nodes may improve existing therapies (DBS, MRgFUS), whereas cortical SCAN targets offer effective non-invasive or minimally invasive neuromodulation for PD.

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