![]() Neuron 66: 631–645īarbero‐Camps E, Fernández A, Baulies A, Martinez L, Fernández‐Checa JC, Colell A (2014) Endoplasmic reticulum stress mediates amyloid β neurotoxicity via mitochondrial cholesterol trafficking. Published under the terms of the CC BY 4.0 license.Īshe KH, Zahs KR (2010) Probing the biology of Alzheimer's disease in mice. We advise AD researchers to consider the comparative strengths and limitations of each model against the scientific and therapeutic goal of a prospective preclinical study.ĪPP transgenic Alzheimer's disease App knock‐in amyloid precursor protein amyloid β peptide. These mice show Aβ accumulation without phenotypes related to overexpression but are not yet a clinical recapitulation of human AD In this review, we evaluate different APP mouse models of AD, and review recent studies using the second-generation mice. These mice exhibit AD pathology, but the overexpression paradigm may cause additional phenotypes unrelated to AD Second-generation mouse models contain humanized sequences and clinical mutations in the endogenous mouse App gene. The Alzheimer's disease (AD) research community has historically used first-generation transgenic (Tg) mouse models that overexpress proteins linked to familial AD (FAD), mutant amyloid precursor protein (APP), or APP and presenilin (PS).
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