BAX and Alzheimer disease: PARP-1 activation at early stages of amyloid deposit. Crossing of PARP-1 [−/−] mouse with AD transgenic mouse prevented synaptic damage, cognitive dysfunction and microglial activation. p53, PARP-1, NF-κB, Bax overexpression, decreased Bcl-2 levels in Aβ [1–42] treated group while upregulation in Bcl-2 and downregulated PARP-1, NF-κB, p53, and Bax levels with NA treatment. Aβ42 induced hippocampal neurotoxicity by oxidative stress-mediated PARP1 activation, TRPM2 activation, Ca2+ influx and mitochondrial dysfunction.