Alzheimer’s disease (AD) is a neurodegenerative disease that causes a progressive decline in memory, thought, language, and behavior in patients. AD is hallmarked by the aggregation of B-amyloid proteins and neurofibrillary tangles. Age and obesity are some of the risk factors associated with AD, both of which alter glucose metabolism. On the other hand, the rate of adults with obesity reached 41.9% from 2017-2020 which raises questions about the impacts of a high fat diet and obesity on the development of AD. Our lab explores the effects of High Fat Diet (HFD) on transgenic (Tg) rats that were co-injected with two human genes known to cause early-onset AD when mutated: amyloid precursor protein (APP) and presenilin 1 (PS1). Preliminary results from our glucose monitoring data showed no significance between Tg and Wild-type (WT) rats. However, body composition data and western blot quantification displayed female Tg rats developing more neuropathologies than their WT counterparts. The results demonstrate how HFD may have an independent role in AD progression from the transgenes and that the presence of both can aggregate neuropathologies that induce AD.
