This review attempts to provide integrated information at the levels of oxidative signaling mechanisms by which ethanol withdrawal (EW) provokes brain injuries and 17β-estradiol (E2) protects against it. Unmanaged sudden withdrawal from the excessive consumption of alcohol (ethanol) adversely alters neuronal integrity in vulnerable brain regions such as the cerebellum, hippocampus, or cortex.

Using thyrotropin-releasing hormone (TRH) as a model, paper explores whether synergistic combination of lipoamino acid(s) and a linker cleaved by prolyl oligopeptidase (POP) can be used as a promoiety for prodrug design for the preferential brain delivery of the peptide.