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Characterizing the APOE4/Trem2R47H Mouse Model for Late Onset Alzheimer’s Disease
Poster Title: Characterizing the APOE4/Trem2R47H Mouse Model for Late Onset Alzheimer’s Disease
Submitted on 14 Aug 2018
Author(s): Harriet Williams on behalf of the MODEL-AD Consortium
Affiliations: The Jackson Laboratory, Indiana University Stark Neuroscience Institute, Sage Bionetworks, University of California Irvine
This poster was presented at AAIC 2018
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Poster Information
Abstract: Alzheimer’s disease (AD) is a debilitating neurodegenerative disorder. More than 46
million people are affected worldwide, with no effective treatment currently available.
Research into fully understanding the disease has been fueled by animal models with
familial AD (fAD) mutations, which accounts for 2-5% of the AD population. While these
models have proved fruitful in understanding some of the baseline endophenotypes of
AD, they have not been adequate to develop therapeutics or fully elucidate the
processes leading to AD. One component of this lack of an effective therapeutic is due
to the inability to fully reproduce an AD phenotype in these animals.
Here, the MODEL-AD consortium presents a new mouse model for Late Onset
Alzheimer’s disease (LOAD). We have developed a model carrying the two highest
genetic risk factors for LOAD, the most common and strongest risk factor, APOE4, and
the R47H allele of Trem2. To characterize this model, we have looked at three time
points to understand the aging phenotype of these APOE4/Trem2*R47H mice.
At these three time points, mice were exposed to a battery of behavioral assays,
consisting of continuous activity monitoring, frailty assessment, open field, grip
strength, spontaneous alternation, rotarod, delayed spatial novelty, and episodic
memory. Once completed, brains are removed and assessed. We are primarily looking
for hallmark signs of AD, such as beta amyloid plaques and neurofibrillary tangles, as
well as levels of neuroinflammation, vascular compromise, and neuronal
The development of this new model will enable us to gain a deeper understanding into
the two of the genetic factors contributing to LOAD. Our goal is that the new models
will lead to better therapeutic testing as well as determining if any preventative actions
can be taken to impede the onset of AD. For more information see .
Summary: The characterization of the APOE4/Trem2R47H mouse model.Report abuse »
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