Figure 1.3.

Molecular mechanism of AEG-1 function in HAD- and glioma-induced neurodegeneration. The EAAT2 in normal astrocytes is responsible for clearing extracellular glutamate to minimize excitotoxicity, and astrocytes convert glutamate to glutamine via the glutamine synthetase. Increased AEG-1 in HIV-infected astrocytes and glioma reduces EAAT2 expression and boosts synaptic glutamate concentrations. Increased synaptic glutamate overactivates glutamate receptors (GluRs), especially NMDA receptors (NMDARs) in postsynaptic neurons, resulting in induction of high levels of Ca²⁺ influx and apoptotic cell death.