Fig. 2Figure 2
Schematic representation of astrocytic activation and neuroinflammatory pathways in Alzheimer’s disease (AD). Exposure to amyloid-β (Aβ) or injury triggers reactive astrocytosis with increased GFAP, vimentin, and nestin expression, leading to neurotoxic or neuroprotective phenotypes. Activated astrocytes release nitric oxide (NO) via iNOS and monoamine oxidase-B (MAO-B), producing excessive γ-aminobutyric acid (GABA) and gliotransmitters (GABA, glutamate, ATP), disrupting neuronal signaling and impairing memory. Microglial activation, ROS generation, and NF-κB signaling further exacerbate neurodegeneration and Aβ plaque accumulation. ATP adenosine triphosphate, GABA γ-aminobutyric acid, GFAP glial fibrillary acidic protein, iNOS inducible nitric oxide synthase, MAO-B monoamine oxidase-B, NF-κB nuclear factor kappa-light-chain-enhancer of activated B cells, NO nitric oxide, ROS reactive oxygen species