What question did this study set out to answer?

The aim is to explore the role of GM3 accumulation in microglia and its impact on Aβ phagocytosis and neuroinflammation in Alzheimer's disease.

February 9, 2026NeurotherapeuticsOpen Access

Microglial GM3 accumulation impairs Aβ phagocytic activity and promotes neuroinflammation in Alzheimer's disease

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Demonstrates that GM3 accumulation in microglia impairs Aβ clearance in Alzheimer's disease, suggesting therapeutic potential for HexA.

The aim is to explore the role of GM3 accumulation in microglia and its impact on Aβ phagocytosis and neuroinflammation in Alzheimer's disease.
Analysis of GM3 accumulation in 5xFAD mouse models.
Examination of Hexa and Hexb gene expression in different brain cell types.
Functional studies assessing the effects of Hexa and Hexb overexpression and knockdown in microglial cells.
Elevated GM3 levels were linked to increased expression of HexA and HexB in microglia.
Overexpression of HexA and HexB impaired Aβ phagocytosis and increased proinflammatory cytokines.
Microglia-specific knockdown of HexA and HexB improved cognitive function and reduced Aβ pathology and neuroinflammation.

Park et al. (2026) studied this question.

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