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Fig. 3 | Molecular Neurodegeneration

Fig. 3

From: TREM2 in the pathogenesis of AD: a lipid metabolism regulator and potential metabolic therapeutic target

Fig. 3

Macrophages with a high expression of TREM2 influence the metabolic comorbidities of AD. After sensing peripheral microenvironmental stimuli, macrophages transit into different phenotypes, such as LAMs, TREM2 hi macrophages, and hepatic transitional macrophages. LAMs play a protective role in obesity through the formation of crown-like structures in adipose tissue. TREM2 hi macrophages increase lipid metabolism in atherosclerotic plaques, although they may reduce the stability of plaques. The hepatic transitional macrophages express high levels of TREM2 and can then transform into Kupffer cells to promote the repair of liver tissue damage and influence the pathogenesis of NAFLD. In addition, Trem2-deficient macrophages in the liver increase the synthesis of ceramides and release exosomes that could impair hepatocytic energy supply in NAFLD

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Molecular Neurodegeneration

ISSN: 1750-1326