The presented data indicate that various combinations of human APP/PSEN/tau mutated genes determine the variability of the onset time and severity of cognitive deficits, as well as the sequence and site of appearance losses in energy synthesis (acetyl-CoA, ATP), cholinergic phenotypes and Aβ accumulation in various Tg models of AD [62,82,87,88]. The gene discussed is MAPT; the disease is Cognitive impairment.