(6) EGCG treatment attenuated early aged hypertension-activated neural mitochondrial-mediated Caspase-dependent apoptotic pathway, in which the evidence was based on decreases in expression levels of t-Bid, Bax/Bcl-2, Bak/Bcl-xL, Apaf-1, cytosolic Cytochrome C, Caspase-9, and Caspase-3 in the cerebral cortex; (7) EGCG treatment enhanced Bcl-2 family-related pro-survival protein levels (Bcl-2, Bcl-xL, p-Bad, 14-3-3) and Sirt1/PI3K/AKT related pro-survival protein levels (Sirt1, p-PI3K/PI3K, p-AKT/AKT) in the early aged hypertensive cerebral cortex. Here, BID is linked to hypertensive disorder.