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Abstract
Neuroinflammation is increasingly recognized as a central and modifiable factor in Alzheimer's disease pathogenesis.
- Microglia and astrocytes play dual roles in neuroinflammation, with potential protective and harmful effects.
- Microglial activation and astrocytic polarization into neurotoxic A1 and neuroprotective A2 subtypes influence amyloid-β clearance and tau pathology.
- Disruption of the blood-brain barrier and activation of inflammasome pathways like NLRP3 are associated with chronic inflammation and neurodegeneration.
- Advances in single-cell transcriptomics and lipidomics have identified glial heterogeneity and new molecular targets for treatment.
- Genetic risk factors, such as apolipoprotein E variants, may further modulate inflammatory responses in Alzheimer's disease.
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