TgF344-AD Rat Model: Cognitive Impairment and Hippocampal Neuropathology at age 10 months

Alzheimer’s Disease is an untreatable progressive neurodegenerative disease, affecting a growing number of people as expected lifespans increase. Animal models allow for examination of the disease in vivo, thereby facilitating learning about disease etiology and testing of potential treatments. One animal model, the TgF344-AD rat model (Cohen et al., 2013), is particularly promising as these rats display more features of Alzheimer’s Disease than most other animal models currently used. The TgF344-AD model seems healthy at 6 months of age but displays cognitively impairment at 15 months and neuropathological signs at 16 months. The aim of the current study was to examine spatial learning and memory and the presence of β-amyloid in the hippocampus at age 10 months, to provide a more detailed understanding of the disease development. 8 transgenic, homozygous rats (4 male, 4 female) and 8 healthy matched wildtype controls were used in the study. Spatial learning and memory were assessed using the Barnes Maze (1979), and hippocampal sections were examined using immunohistochemical staining. No gender differences were found. No significant differences were found between the genotypes with regards to learning assessed on day 1 and 2, nor with regards to memory assessed on day 3. On day 10 the transgenic rats showed significantly impaired spatial memory. Moreover, the transgenic model had a significantly higher β-amyloid plaque load in the hippocampus than the controls. However, no significant association between the amount of β-amyloid and memory impairment was found in the study. Additionally, post-hoc tests suggested a possibility of anxiety in the transgenic rats, relative to the wildtype rats. The results add support to the utility of the TgF344-AD model as and Alzheimer’s Disease model, suggesting that the rats are at a middle stage of the disease course at age 10 months.