Alzheimer’s Disease has been known for more than 100 years, affecting more and more people as the human population grows ever older. To this day, the disease remains untreatable and unpreventable, and the full etiology has stayed unknown. Immense amounts of research about Alzheimer’s Disease are conducted every year to learn more about the disease that robs people of their memories, their personalities, and their elderly family members. Considerable progress has been made, and brain mapping has come a long way, opening doors for gaining knowledge about human Alzheimer’s Disease in vivo. When it comes to development of treatments, however, animal models of the disease are in the front of the field, yet treatment paradigms have failed repeatedly when applied to humans, in spite of working perfectly well in animal models. One possible reason for such dissonance is that the animal models employed may not be complex enough to fully mirror the disease. Granted, such models are invaluable when it comes to learning about the individual features of the disease, but they cannot stand as adequate models for developing broad treatments for Alzheimer’s Disease. One very promising, fairly recent animal model, the TgF344-AD rat model, developed by Cohen and colleagues in 2013, may provide a better integrative model, as these rats display more features of Alzheimer’s Disease than most other animal models. The model has been investigated with regards to both neuropathology, cognitive impairment, and neuropsychiatric symptoms, and shows great promise as a tool in the process of learning more about the disease that plagues more and more humans. Nonetheless, there is still knowledge to gain about this model. The aim of this thesis is to present current knowledge about Alzheimer’s Disease, as well as the TgF344-AD model, and to examine the presence of beta-amyloid in the hippocampus of the rats via immunohistochemistry. Furthermore, the study compares the beta-amyloid levels with impairments in memory, measured on the hippocampus-dependent spatial memory test, Barnes Maze. 8 10-month-old TgF344-AD rats and 8 Fisher 344 wildtype littermates matched for age and gender are employed in the study. A significant difference in beta-amyloid is found between the genotypes, with virtually none being present in the wildtype littermates, whereas on average 9.84% of the hippocampi of transgenic rats is covered in plaques. This is compared with the presence of beta-amyloid in a rat from a previous study, and the method of immunohistochemistry is discussed. As for memory impairments, no correlation is found with the amount of beta-amyloid present in the hippocampus, which is similar to results found in studies performed on human Alzheimer’s Disease patients. Confounding factors, including neuropsychiatric symptoms, are discussed. In sum, the results of this thesis continue to support the promising potential of the TgF344-AD rat model, as its disease course seems to be comparable with that of human Alzheimer’s Disease patients on several aspects.