Some reports suggest that Alzheimer's disease (AD) patients are more susceptible to viral infections (Honjo et al., 2009).  Most of these studies have been epidemiological in nature or have been based on histological assessment of human brain tissues.  What is lacking is an animal model to explore the consequences of infections with pre-existing pathologies. In this study, we are developing such a novel mouse model.  We aim to determine if a pre-existing, genetically driven tauopathy, which is found in AD, affects anti-viral immunity in aged mice or the converse - whether infection and inflammation exacerbate tauopathy. Mice expressing CD46, a human measles virus receptor, were crossed with mice over-expressing p25, a peptide that leads to tau pathologies.  The p25 transgene was tagged with green fluorescent protein (GFP).  Genotypes of the parent generations in mice off of a tetracycline diet for 7 and 30 days were determined by isolating DNA from 1.5 cm tail snips, followed by PCR then gel electrophoresis.  95% ethanol fixation followed by fluorescence microscopy validated p25 expression in the brains of the same mice.  Future directions aim to characterize immune profiles by gene expression and tau pathological changes by immunohistochemistry in the brains of CD46 x p25 mice at various ages and to establish the key link .between viral infection and tauopathy.

Genotyping CD46 and p25 transgenic mice to establish a novel mouse model of neuron-specific viral infection and tauopathy

243rd National Meeting (2012)

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