In this issue of Neuron, McGowan et al. report on a new mouse model of amyloid deposition as occurs in Alzheimer's disease. Unlike previous models in which overexpression of the amyloid precursor protein results in amyloid plaque formation, McGowan et al. have produced mice that overexpress only Aβ40 or Aβ42 and prove that Aβ42 is critical for the formation of amyloid deposits in vivo.
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