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The β-amyloid peptide (Aβ) and tau are key molecules in Alzheimer’s disease causing neuronal dysfunction and cell death. Evidence exists that tau mediates the pathology downstream of Aβ. N-methyl-D-aspartate receptors (NMDARs) are supposed to play an essential role in the pathophysiology of Aβ and tau. However, the exact mechanisms deciphering how Aβ could induce tau-dependent neuronal dysfunctions are still unclear. Here we show that virus-mediated expression of human tau causes neuronal degeneration in organotypic hippocampal slice cultures from APP transgenic mice but not in non-transgenic cultures. Treatment with therapeutically concentrations of NMDAR open channel blocker memantine completely abolished tau-dependent cell death in APP transgenic cultures. Removing extracellular calcium with calcium chelator BAPTA also prevented tau toxicity. Our data indicate that human tau-dependent neuronal cell death in APP transgenic slice cultures is mediated by calcium influx through NMDARs.

Human tau-dependent toxicity in APP transgenic cultures requires calcium influx through N-methyl-D-aspartate receptors