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在患有GBA1变体和亚体内深脑刺激的患者中,纵向认知功能的临床和生物学决定因素

Moritz A Loeffler^1,2, Philipp Klocke^1,2, Isabel Wurster^1,2

¹Centre for Neurology, Department of Neurodegenerative Diseases, University of Tübingen, Tübingen, Germany.

Annals of neurology

|January 16, 2026

概括

脑下深层刺激 (STN-DBS) 不能加速患有GBA1变异的帕金森病 (PD) 患者的认知衰退. 痴呆风险与GBA1状态,基线认知和年龄有关,而不是STN-DBS.

科学领域:

神经科学是一个神经科学.
遗传学遗传学是一个
神经学神经学

背景情况:

帕金森病 (PD) 是一种神经退行性疾病.
GBA1基因变异是PD的已知风险因素.
脑下深层刺激 (STN-DBS) 是PD的治疗方法,但其对GBA1变体携带者的认知效应仍有争议.

研究的目的:

调查STN-DBS是否加速了携带GBA1变异的PD患者的认知衰退.
在接受STN-DBS的PD患者中确定痴呆症的预测因素.

主要方法:

分析了患有或没有GBA1变体,有或没有STN-DBS的PD患者的匹配队列.
用蒙特利尔认知评估 (MoCA) 来评估认知功能,持续3年.
还分析了脑脊液生物标志物和转化为痴呆症.

主要成果:

在具有和没有STN-DBS的GBA1载体之间没有观察到认知衰退的显著差异.
痴呆症风险与GBA1状态,较低的基线MoCA得分和较高的基线年龄有关.
一个特定的视觉空间/执行域得分预测了GBA1载体的痴呆症.

结论:

在患有PD的GBA1变异携带者中,STN-DBS似乎不会加速认知衰退.
GBA1状态,基线认知和年龄是PD患者痴呆风险的重要预测因素.
调查结果可以为潜在的STN-DBS候选人提供咨询信息.

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