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Background Recent studies have indicated that an alteration in intracellular calcium homeostasis could contribute to the development of Alzheimer’s disease (AD) . Previous studies supported that sustained changes in intracellular free calcium concentration ([Ca]i ) homeostasis could provide the final common pathway for the neuropathological changes associated with AD. Calcium influx is play a key role in calcium overload. Calmodulin (CaM)/ Calmodulin-dependent protein kinase II /IV (/CaMK II /IV) is very important to regulate calcium homeostasis in the nervous system. (–)-Epigallocatechin-3-gallate (EGCG), which is classified the catechin family and is one of the major polyphenol constituents of green tea. Research has shown that EGCG could reduce [Ca]i, lessen mitochondrial damage, thereby prevent calcium overload and protect neurons. Transgenic mouse models have been created with mutations in genes related to AD. APP/PS1 double-transgenic mice, provide a valuable model for evaluating the pathogenesis of AD. Therefore, this study was designed to study the effect of EGCG and nimodipine on cognitive behavior, [Ca]i , CaM and CaMK II /IV in APP/PS1 double-transgenic mice.

EGCG and nimodipine improve the symptoms of AD by inhibiting [Ca2+]i in hippocampal neurons of APP/PS1 transgenic mice