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Some forms of familial Alzheimer's disease are caused by mutations in the amyloid β protein precursor (βAPP), and there is excellent evidence that these mutations foster amyloid deposition by increasing secretion of total amyloid β protein (Aβ) or the highly amyloidogenic Aβ1-42 form. These observations provide a powerful rationale for developing an animal model of AD by generating transgenic mice...
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