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It was reported that GLP-1 (9-36) decreased the level of nuclear factor kappa-B (NF-B) in astrocytes after oxygen-glucose deprivation/reoxygenation (OGD/R) damage and inhibited neuronal apoptosis around the infarct area against CIR, the mechanism of which might be relying on the activation of the IGF-1 receptor rather than the GLP-1 receptor (91)

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10.1186/s12951-025-03415-w 64 LuS

Dyslipidemia affected approximately 40%

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Neuronal energy is primarily supplied by bloodderived glucose and its metabolite lactate, whereas astrocytes provide a major buffering node through glycogen mobilization during hypoglycemia and are widely regarded as the predominant site of fatty acid oxidation in the adult brain (Morant-Ferrando et al., 2023)