Pathological changes of astrocytes in AD. Under physiological conditions, astrocytes are involved in the glutamate cycle between neurons. In early AD, Aβ formation impairs EAAT2 expression, while NMDAR activity increases compensatory, enhancing synaptic plasticity. In late-stage AD, Aβ fully inhibits EAAT2 on astrocytes, disrupting the glutamate cycle. Excessive reactive oxygen species are released from postsynaptic neurons, leading to neuronal necrosis.