重视对阿尔茨海默病痫性发作易感性升高的识别与机制研究

doi:10.3969/j.issn.1672-6731.2026.03.001

中国现代神经疾病杂志 ›› 2026, Vol. 26 ›› Issue (3): 203-210. doi: 10.3969/j.issn.1672-6731.2026.03.001

2 重视对阿尔茨海默病痫性发作易感性升高的识别与机制研究

王群¹^,²^,*(), 王颖婷¹, 陈露¹

1. 100070 首都医科大学附属北京天坛医院神经病学中心国家神经系统疾病临床医学研究中心
2. 450046 郑州大学第一附属医院神经内科

收稿日期:2026-03-12 出版日期:2026-03-25 发布日期:2026-04-14
通讯作者: 王群
基金资助:
国家重点研发计划“常见多发病防治研究”重点专项(2022YFC2503800); 国家自然科学基金资助项目(82371449); 国家自然科学基金联合基金项目(U24A20695); 国家自然科学基金青年科学基金项目(82501735)

Emphasizing the identification and mechanistic study of increased seizure susceptibility in Alzheimer's disease

Qun WANG¹^,²^,*(), Ying-ting WANG¹, Lu CHEN¹

1. Center of Neurology, Beijing Tiantan Hospital, Capital Medical University; China National Clinical Research Center for Neurological Diseases, Beijing 100070, China
2. Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450046, He'nan, China

Received:2026-03-12 Online:2026-03-25 Published:2026-04-14
Contact: Qun WANG
Supported by:
National Key Research and Development Program of China "Common Disease Prevention and Control Research" Key Project(2022YFC2503800); the National Natural Science Foundation of China(82371449); the National Natural Science Foundation of China for Cooperative Fund Project(U24A20695); the National Natural Science Foundation of China for Young Scientists(82501735)

摘要/Abstract

摘要：

阿尔茨海默病不仅是传统的神经系统变性疾病，更是一种伴神经网络高兴奋性的疾病。其痫性发作易感性升高，常隐匿表现为亚临床癫痫样活动和高频振荡，且与认知功能下降形成恶性循环。核心病理学机制为β-淀粉样蛋白和tau蛋白病理级联反应触发的神经元兴奋/抑制失衡，进而演变为宏观神经网络高兴奋性，且受神经炎症、血脑屏障破坏和脑网络重组的共同驱动。受限于电生理表现的隐匿性与脑深部起源，临床主要依靠长程视频脑电图、高密度脑电图和脑磁图进行精准识别。但在临床认知、检测设备普及和技术标准化方面仍存挑战，未来亟待借助人工智能构建标准化智能监测体系，探索以调控神经网络高兴奋性为靶点的治疗新策略及多模态标志物的联合应用，旨在为阿尔茨海默病共病癫痫的早期精准诊疗提供全新维度。

关键词: 阿尔茨海默病, 癫痫, 脑电描记术, 脑磁图描记术, 综述

Abstract:

Alzheimer's disease (AD) is increasingly recognized not merely as a classic neurodegenerative disorder, but as a condition fundamentally characterized by network hyperexcitability. Recent studies demonstrate that AD patients exhibit significantly increased seizure susceptibility, which frequently manifests insidiously as subclinical epileptiform activity (SEA) and high-frequency oscillation (HFO), driving a vicious cycle that accelerates cognitive decline. The core pathological mechanism stems from the disruption of neuronal excitation/inhibition (E/I) homeostasis induced by amyloid β-protein (Aβ) and tau pathological cascades. This E/I imbalance ultimately leads to large-scale network hyperexcitability, a process further co-driven by neuroinflammation, blood-brain barrier (BBB) disruption, and extensive brain network remodeling. Given the insidious nature and deep-brain origins of these aberrant electrophysiological activities, precise clinical identification currently relies heavily on long-term video electroencephalography (LT-VEEG), high-density electroencephalography (HD-EEG) and magnetoencephalography (MEG). Despite considerable progress, significant challenges remain regarding clinical awareness, the widespread accessibility of detection equipment, and technical standardization. Future research must urgently leverage artificial intelligence (AI) to establish standardized, intelligent monitoring systems. Exploring novel therapeutic strategies targeting network hyperexcitability, combined with multimodal biomarkers, will ultimately provide a new dimension for the early, precise diagnosis and targeted intervention of AD.

Key words: Alzheimer disease, Epilepsy, Electroencephalography, Magnetoencephalography, Review

中图分类号:

R741

王群, 王颖婷, 陈露. 重视对阿尔茨海默病痫性发作易感性升高的识别与机制研究[J]. 中国现代神经疾病杂志, 2026, 26(3): 203-210.

Qun WANG, Ying-ting WANG, Lu CHEN. Emphasizing the identification and mechanistic study of increased seizure susceptibility in Alzheimer's disease[J]. Chinese Journal of Contemporary Neurology and Neurosurgery, 2026, 26(3): 203-210.

https://journal11.magtechjournal.com/cjcnn/CN/Y2026/V26/I3/203

图/表 1

图 1 阿尔茨海默病痫性发作易感性升高的多维度机制 1a 微观层面：Aβ和tau蛋白病理介导的细胞与突触兴奋/抑制失衡 1b 局部环路层面：特征性异常电生理活动如亚临床癫痫样活动和高频振荡 1c 宏观层面：脑磁图映射的全脑神经网络功能连接损害和过度活跃病灶 Aβ，β‑淀粉样蛋白

Figure 1 Multidimensional mechanisms of increased seizure susceptibility in AD Microscopic level: cellular and synaptic E/I imbalance driven by Aβ and tau pathology (Panel 1a). Local circuit level: characteristic abnormal electrophysiological activities (e.g., SEA and HFO; Panel 1b). Macroscopic level: impaired network functional connectivity and hyperactive foci mapped by MEG (Panel 1c).

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