The bad seed in Alzheimer's disease.
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 Abeta40 or Abeta42 and prove that Abeta42 is critical for the formation of amyloid deposits in vivo.
Fryer
John D
JD
Department of Neurology and Molecular Biology and Pharmacology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, USA.
Holtzman
David M
DM
D000544:Alzheimer Disease / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D000818:Animals; D016657:Cerebral Amyloid Angiopathy; D004195:Disease Models, Animal; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D010446:Peptide Fragments; D058225:Plaque, Amyloid / Q000378:metabolism / Q000473:pathology*
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments