Objective Alzheimers disease (AD) is the most common neurodegenerative disorder characterized by the progressive deterioration of cognition and memory in association with the presence of senile plaques (SP),neurofibrillary tangles(NFT),and massive loss of neurons,primarily in the cerebral cortex and hippocampus.The NFT contain paired helical filaments (PHF),which are mostly composed of a hyperphosphorylated tau.Recent studies have suggested that the abnormal hyperphosphorylation of tau could be the result of up-regulation of protein kinases or down-regulation of protein phosphatases.Okadaic acid (OA) is a extractive of marine life,which can selected inhibit protein phosphatases such as PP2A,cause tau hyperphosphorylation and result in neurotoxicity.A novel peptide termed humanin (HN) was recently reported to rescue neurons in vitro from the toxicity induced by familial AD (FAD)-linked mutant genes and the Alzheimers amyloid-β (Aβ) peptides (full length Aβ peptide and Aβ25-35 fragment).