Microglial glycolytic reprogramming in alzheimer’s disease: association with impaired phagocytic function and altered vascular proximity
Our study establishes that microglial glycolytic reprogramming via PKM2 promotes a proinflammatory HAM-like phenotype, phagocytic exhaustion, and peri-pathological accumulation with aggregates and cerebral vessels. Targeting glycolytic pathways represents a viable therapeutic strategy for alleviating microglial dysfunction and neuroinflammation in AD.
Authors
- Caiyun Zhu (ORCID: https://orcid.org/0000-0003-4405-0889)
- Qi Xu
- Nian Liu (ORCID: https://orcid.org/0000-0003-4518-4045)
- Ning Lü (ORCID: https://orcid.org/0000-0003-3992-0376)
- Zhongman Jin (ORCID: https://orcid.org/0009-0002-1927-6595)
- Hui Wei (ORCID: https://orcid.org/0000-0003-2078-8117)
Institutions
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Peking Union Medical College Hospital (CN)
Publication Details
- Journal
- Journal of Neuroinflammation
- Published
- 2025-10-02
- DOI
- https://doi.org/10.1186/s12974-025-03546-9
- Citations
- 5
- Primary Topic
- Neuroinflammation and Neurodegeneration Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 4.21
Funders
- Chinese Academy of Medical Sciences
- Peking Union Medical College Hospital
- National Key Research and Development Program of China