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Post-mortem analysis of human brains from AD patients showed that that A 40 discriminated between AD patients and high pathology controls more readily than A 42 (Gao et al., 40 oligomers have been shown to induce neurotoxicity and disrupt brain lipid bilayers while other amyloid species do not (Bode et al., 40 is induced by an increase in intracellular Ca 2+ , and this has led to the hypothesis that the accumulation of intracellular A may occur as an early event in the pathogenesis of AD (Itkin et al., 2+ ] i and may enhance Ca 2+ -mediated excitotoxicity, which may induce progressive memory loss and cognitive deficits and enhance neuronal cell apoptosis

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