In this study, we used the transgenic TgF344-AD rat model, which overexpresses mutant human amyloid precursor protein and presenilin, recapitulates hallmark AD pathologies, including age-dependent increases in amyloid-beta plaques, neurofibrillary tangles, microglia activation, neuronal loss, and cognitive deficits, making it a robust platform for detailed investigation of AD pathogenesis. This evidence concerns the gene APP and Alzheimer disease.