Thus, comprehensive immunohistochemical assessment of the markers NSE and NeuN enables evaluation of the metabolic activity of penumbral neurons, while analysis of caspase-3 expression—the terminal effector of apoptosis—together with activation of the PI3K/Akt/mTOR and PI3K/Akt/FOXO3a signaling pathways allows not only clarification of the morphological boundaries of neuronal degeneration but also identification of the molecular mechanisms underlying the age-dependent imbalance between neuronal survival and death in stroke. This evidence concerns the gene AKT1 and stroke disorder.