Human cortical neuronal cell lints HCN-1A and HCN-2 are killed followi
ng exposure of the differentiated cells to amyloid beta-peptide(1-40),
a component of senile plaques and other amyloid deposits in brains fr
om Alzheimer's patients. We present a model of A beta toxicity uncompl
icated by the presence of other cell types that can be used to address
the mechanism of A beta neurotoxicity. This model will be useful in t
he evaluation of neuroprotective compounds which may attenuate cortica
l neuronal loss in Alzheimer's disease.