Authors
Ze Li, QiuLi Ming, LinPeng Fu, JingShuang Yang, YiLin Lv, BingQian Chen, ZhaoFeng Lu
Published in
Frontiers in nutrition. Volume 13. Pages 1886340. Epub Jul 08, 2026.
Abstract
Alzheimer's disease is increasingly viewed as a disorder in which age-related disturbances in microglial metabolism and the handling of nutritional substrates contribute to progressive loss of protective function. This review examines how lipids and ketone bodies shape microglial metabolic fitness in the aging brain and in Alzheimer's disease, and how these effects intersect with triggering receptor expressed on myeloid cells 2 (TREM2) signaling and translational biomarkers. Available evidence indicates that early compensatory glycolysis may give way to chronic bioenergetic failure, while cholesterol and lipoprotein trafficking, lipid droplet accumulation, ketone-body signaling, and TREM2-associated lysosomal pathways influence plaque engagement, phagocytosis, and inflammatory responses. The review also considers how apolipoprotein E genotype, brain region, sex, disease stage, and model system condition translation from experimental models to human disease. Fluid, imaging, and tissue readouts are therefore discussed as stage- and context-dependent proxies rather than fixed signatures. Overall, nutritional strategies and microglia-targeted interventions are most likely to be informative when aligned with disease stage and biological context.
PMID:
42488212
Bibliographic data and abstract were imported from PubMed on 15 Sep 2026.
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