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In vitro studies have reported that pre- or simultaneous administration of myricetin (0.3, 1, 3 and/or 10 M, 48 h) can suppress A 1-42 -induced nuclear fragmentation and caspase-3 activation in primary cultured cortical neurons, and reduce A 1-40 /A 1-42 levels in neuronal culture media via the promotion of -secretase (ADAM10) expression and the inhibition of -secretase (BACE-1) activity (Shimmyo et al., 2008), suggesting that promoting neuronal survival and inhibiting A accumulation may mediate the anti-ADs effects of myricetin