MAPT and cardiac arrest: The effects were diminished by blocking the PI3K/Akt pathway with LY294002 (5 × 10−6m x 24 h).[72] H2S exposure (40 or 80 ppm × 1 h, given immediately after cardiac arrest and cardiopulmonary resuscitation in rats) impeded inflammation and oxidative stress by inhibiting NF‐κB activation and downstream proinflammatory mediators iNOS and ICAM‐1 to improve hippocampal neuron protection, neurological recovery, and animal survival.[73] Recently, it was reported that CSE/cystathionase, another crucial biosynthetic enzyme of H2S, failed to bind Tau P301L, a mutant Tau related to AD pathogenesis.