Microglial MS4A4A Protects against Epileptic Seizures in Alzheimer's Disease

Abstract Alzheimer's disease (AD) is a predominant neurodegenerative disorder worldwide, with epileptic seizures being a common comorbidity that can exacerbate cognitive deterioration in affected individuals, thus highlighting the importance of early therapeutic intervention. It is determined t...

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Main Authors: Meng Jiang, Qingqing Li, Jianhui Chen, Ruochong Li, Jun Yao, Yong Hu, Haizheng Zhang, Lixin Cai, Maoguo Luo, Yu Sun, Wenwen Zeng
Format: Article
Language:English
Published: Wiley 2025-06-01
Series:Advanced Science
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Online Access:https://doi.org/10.1002/advs.202417733
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author Meng Jiang
Qingqing Li
Jianhui Chen
Ruochong Li
Jun Yao
Yong Hu
Haizheng Zhang
Lixin Cai
Maoguo Luo
Yu Sun
Wenwen Zeng
author_facet Meng Jiang
Qingqing Li
Jianhui Chen
Ruochong Li
Jun Yao
Yong Hu
Haizheng Zhang
Lixin Cai
Maoguo Luo
Yu Sun
Wenwen Zeng
author_sort Meng Jiang
collection DOAJ
description Abstract Alzheimer's disease (AD) is a predominant neurodegenerative disorder worldwide, with epileptic seizures being a common comorbidity that can exacerbate cognitive deterioration in affected individuals, thus highlighting the importance of early therapeutic intervention. It is determined that deletion of Ms4a4a, an AD‐associated gene, exacerbates seizures in amyloid β (Aβ)‐driven AD mouse model. MS4A4A is significantly upregulated in brain lesions in patients with epilepsy. Single‐cell sequencing reveals that MS4A4A is highly expressed in microglia within these lesions, linked to enhanced phagocytic activity. Mechanistic investigation delineates that deletion of Ms4a4a impairs microglial phagocytosis, accompanied by diminished calcium influx and disruptions in mitochondrial metabolic fitness. The cytosolic fragment of Ms4a4a is anchored to the cytoskeletal components, supporting its critical role in mediating phagocytosis. Induction of Ms4a4a through central delivery of LNP‐Il4 alleviates seizure conditions. Collectively, these findings identify Ms4a4a as a potential therapeutic target for managing seizures in AD treatment.
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institution Kabale University
issn 2198-3844
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publisher Wiley
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series Advanced Science
spelling doaj-art-aec7a2b7848340a887edbf53903d6ff72025-08-20T03:44:51ZengWileyAdvanced Science2198-38442025-06-011222n/an/a10.1002/advs.202417733Microglial MS4A4A Protects against Epileptic Seizures in Alzheimer's DiseaseMeng Jiang0Qingqing Li1Jianhui Chen2Ruochong Li3Jun Yao4Yong Hu5Haizheng Zhang6Lixin Cai7Maoguo Luo8Yu Sun9Wenwen Zeng10Institute for Immunology and School of Basic Medical Sciences and Beijing Key Laboratory of Immunological Research of Allergy (LIRA) Tsinghua University Beijing 100084 ChinaInstitute for Immunology and School of Basic Medical Sciences and Beijing Key Laboratory of Immunological Research of Allergy (LIRA) Tsinghua University Beijing 100084 ChinaInstitute for Immunology and School of Basic Medical Sciences and Beijing Key Laboratory of Immunological Research of Allergy (LIRA) Tsinghua University Beijing 100084 ChinaSchool of Life Sciences Tsinghua University Beijing 100084 ChinaENO Bio mRNA Innovation Institute Shenzhen Rhegen Biotechnology Co. Ltd Shenzhen 518000 ChinaENO Bio mRNA Innovation Institute Shenzhen Rhegen Biotechnology Co. Ltd Shenzhen 518000 ChinaSchool of Life Sciences Tsinghua University Beijing 100084 ChinaPediatric Epilepsy Center Peking University First Hospital Beijing 100034 ChinaSchool of Life Sciences Tsinghua University Beijing 100084 ChinaPediatric Epilepsy Center Peking University First Hospital Beijing 100034 ChinaInstitute for Immunology and School of Basic Medical Sciences and Beijing Key Laboratory of Immunological Research of Allergy (LIRA) Tsinghua University Beijing 100084 ChinaAbstract Alzheimer's disease (AD) is a predominant neurodegenerative disorder worldwide, with epileptic seizures being a common comorbidity that can exacerbate cognitive deterioration in affected individuals, thus highlighting the importance of early therapeutic intervention. It is determined that deletion of Ms4a4a, an AD‐associated gene, exacerbates seizures in amyloid β (Aβ)‐driven AD mouse model. MS4A4A is significantly upregulated in brain lesions in patients with epilepsy. Single‐cell sequencing reveals that MS4A4A is highly expressed in microglia within these lesions, linked to enhanced phagocytic activity. Mechanistic investigation delineates that deletion of Ms4a4a impairs microglial phagocytosis, accompanied by diminished calcium influx and disruptions in mitochondrial metabolic fitness. The cytosolic fragment of Ms4a4a is anchored to the cytoskeletal components, supporting its critical role in mediating phagocytosis. Induction of Ms4a4a through central delivery of LNP‐Il4 alleviates seizure conditions. Collectively, these findings identify Ms4a4a as a potential therapeutic target for managing seizures in AD treatment.https://doi.org/10.1002/advs.202417733Alzheimer's diseaseepilepsymicrogliaMS4A4Aphagocytosis
spellingShingle Meng Jiang
Qingqing Li
Jianhui Chen
Ruochong Li
Jun Yao
Yong Hu
Haizheng Zhang
Lixin Cai
Maoguo Luo
Yu Sun
Wenwen Zeng
Microglial MS4A4A Protects against Epileptic Seizures in Alzheimer's Disease
Advanced Science
Alzheimer's disease
epilepsy
microglia
MS4A4A
phagocytosis
title Microglial MS4A4A Protects against Epileptic Seizures in Alzheimer's Disease
title_full Microglial MS4A4A Protects against Epileptic Seizures in Alzheimer's Disease
title_fullStr Microglial MS4A4A Protects against Epileptic Seizures in Alzheimer's Disease
title_full_unstemmed Microglial MS4A4A Protects against Epileptic Seizures in Alzheimer's Disease
title_short Microglial MS4A4A Protects against Epileptic Seizures in Alzheimer's Disease
title_sort microglial ms4a4a protects against epileptic seizures in alzheimer s disease
topic Alzheimer's disease
epilepsy
microglia
MS4A4A
phagocytosis
url https://doi.org/10.1002/advs.202417733
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