Histochemical & Behavioral Analysis of the 3xTg‐AD Mouse Model of Alzheimer's Disease

Abstract

Alzheimer's disease (AD) is an incurable neurodegenerative disease that affects about 11% of Americans age 65 and over and has very few FDA‐approved treatments. As the primary areas affected within the brain are the hippocampus and the cortex, the main reported symptoms of this disease are memory loss and confusion. However, the disease can also affect olfactory function, a symptom that develops prior to changes in cognitive function. Due to the lack of effective treatments, developing an animal model that most closely resembles human AD is crucial. The goal of this study was to further validate a mouse model of AD, the 3xTg‐AD mouse which expresses both the amyloid plaques and neurofibrillary tangles in the brain, to determine if the mice express olfactory deficits seen in humans. To do this, we used a buried food test in which mice were food deprived for 24 hours and then placed in a rat cage with a piece of rodent chow buried beneath the bedding. We timed, up to 15 minutes, how long it took the mice to uncover the buried food as a way to measure olfactory detection. The 3xTg‐AD mice were compared to their background and parental strains (C57Bl/6, 129Sv/E, and a hybrid of the C57Bl/6 and 129Sv/E). Preliminary results indicate that over the span of 52 weeks, the 3xTg‐AD mice take significantly longer than the other strains to find the buried food. In order to correlate the behavioral observations with anatomical changes, the Congo Red staining technique was employed to identify whether or not amyloid plaques develop in the olfactory bulbs of the mice. Thus far we have observed plaque accumulation in the glomerular layer of the olfactory bulbs of the 3xTg‐AD mice. Overall, the results of this study increase the validity of the 3xTg‐AD mouse as a model of human AD and leads to new areas of study to determine where else in the brain olfactory function is affected by AD.Support or Funding InformationThis work was supported in part by Award No. 17‐2 from the Commonwealth of Virginia's Alzheimer's and Related Diseases Research Award Fund, administered by the Virginia Center on Aging, School of Allied Health Professions, Virginia Commonwealth University (to D.A. Mitrano & L.S. Webb)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.