M. Hesketh, P. Hinow
Alzheimer's disease (AD) is a devastating neurodegenerative disease whose etiology is poorly understood and for which current treatments provide only modest control of symptoms. To better investigate the causes and progression of the disease, the transgenic TgF344-AD rat model has emerged as a crucial tool. In this paper, we collect observations on the accumulation of amyloid-{beta}, changes in neuronal density, and a decline in cognitive performance in TgF344-AD and wild-type rats. We develop a compartmental ordinary differential equation model and determine its parameters by fitting the output to the experimental observations in the literature. Our model simulations are compatible with the hypothesis that the accumulation of amyloid-{beta} leads to a rapid decline in neuronal density followed by a significant loss in memory and learning ability. Our mathematical model can provide a bridge between AD research in rodent models and the human condition of AD.