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Abstract
Alzheimer's disease is associated with dysregulated at the neurovascular-glia-neuron interface.
- Systemic metabolic stressors such as insulin resistance and obesity may reprogram brain immune cells and sustain inflammation.
- In microglia, changes in energy pathways could influence the clearance of amyloid and tau proteins, affecting synaptic health.
- Impaired delivery of nutrients in the brain, linked to endothelial GLUT1 loss, may accelerate amyloid buildup and neuronal damage.
- Lipid metabolism is connected to inflammation, with APOE4-related changes in microglial lipid droplets potentially linking genetics to inflammatory responses.
- NLRP3 may play a role in integrating metabolic signals into ongoing neuroinflammation.
- Emerging metabolic treatments, such as GLP-1 receptor agonists and SGLT2 inhibitors, could modify glial metabolism and inflammation.
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