volume 29, issue 4, P827-840 2012
DOI: 10.3233/jad-2012-111604
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Mark S. Kindy, Jin Yu, Hong Zhu, Salim S. El-Amouri, Vivian Hook, Gregory R. Hook

Abstract: Therapeutic agents that improve the memory loss of Alzheimer’s disease (AD) may eventually be developed if drug targets are identified that improve memory deficits in appropriate AD animal models. One such target is β-secretase which, in most AD patients, cleaves the wild-type (WT) β-secretase site sequence of the amyloid-β protein precursor (AβPP) to produce neurotoxic amyloid-β (Aβ). Thus, an animal model representing most AD patients for evaluating β-secretase effects on memory deficits is one that express…

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