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EFAD transgenic mice as a human APOE relevant preclinical model of Alzheimer's disease

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journal contribution
posted on 29.06.2018 by LM Tai, D Balu, E Avila-Munoz, L Abdullah, R Thomas, N Collins, AC Valencia-Olvera, MJ LaDu
Identified in 1993, APOE4 is the greatest genetic risk factor for sporadic Alzheimer's disease (AD), increasing risk up to 15-fold compared with APOE3, with APOE2 decreasing AD risk. However, the functional effects of APOE4 on AD pathology remain unclear and, in some cases, controversial. In vivo progress to understand how the human (h)-APOE genotypes affect AD pathology has been limited by the lack of a tractable familial AD-transgenic (FAD-Tg) mouse model expressing h-APOE rather than mouse (m)-APOE. The disparity between m-and h-apoE is relevant for virtually every AD-relevant pathway, including amyloid-beta (A beta) deposition and clearance, neuroinflammation, tau pathology, neural plasticity and cerebrovascular deficits. EFAD mice were designed as a temporally useful preclinical FAD-Tg-mouse model expressing the h-APOE genotypes for identifying mechanisms underlying APOE-modulated symptoms of AD pathology. From their first description in 2012, EFAD mice have enabled critical basic and therapeutic research. Here we review insights gleaned from the EFAD mice and summarize future directions.-Tai, L. M., D. Balu, E. Avila-Munoz, L. Abdullah, R. Thomas, N. Collins, A. C. Valencia-Olvera, and M. J. LaDu. EFAD transgenic mice as a human APOE relevant preclinical model of Alzheimer's disease.

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Publisher Statement

"This is a copy of an article published in the JOURNAL OF LIPID RESEARCH © 2017 AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC"

Publisher

AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC

Language

en_US

issn

0022-2275

Issue date

01/09/2017

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