Neurons and glial cells also synthesize and release tPA, which is highly expressed in the cortex, amygdala, hippocampus and cerebellum.13 Following brain insults such as epileptic seizure, trauma or stroke, increased synthesis of tPA can overactivate excitatory receptors such as the N-methyl-D-aspartate (NMDA) receptor, which increases calcium permeability, causing neuronal damage and death.14, 15 While excessive NMDA receptor activation can damage neurons, the same occurs with its reduced activity.14, 16. Here, PLAT is linked to stroke disorder.