Senescence-accelerated OXYS rats appears to be a suitable non-transgenic model of sporadic AD (which accounts for 95% of AD patients) as characterized by the progressive age-related aggregation of Aβ and hyperphosphorylation of τ protein as well as mitochondrial dysfunction, loss of synapses, neuronal death, and concomitant cognitive decline (72). The gene discussed is TBXT; the disease is Alzheimer disease.