do brain cells die after stroke?
A large body of data suggest that it may be exciting (glutamate and excitotoxicity), radical (oxidative stress and free radicals), and suicidal (apoptotic-like pathways).4 6 Simply put, when brain fails to generate sufficient ATP, such as after oxygen and glucose deprivation, energy failure occurs and ionic gradients are lost. Glutamate is released, reuptake processes are impaired, and this excitatory amino acid binds to its postsynaptic receptors and promotes excessive calcium entry and calcium release. Calcium-dependent synthases and proteases contribute to cell and tissue demise by degrading key cytoskeletal and enzymatic proteins, and generating nitric oxide and peroxynitrite. Mitochondrial functions such as oxidative phosphorylation also fail and reactive oxygen radicals are released that further compromise cells by attacking proteins, lipids, and nucleic acids. Families of “executioner” molecules (eg, caspases, AIF) dismantle multiple cell processes in the cytoplasm and nucleus t
