Alternative explanations for the phenotypes observed include (i) the absence of murine tau, (ii) multiple effects of the expression of human tau in a murine environment, such as interactions of htau with crucial murine AD-related pathways that are different from interactions of murine tau, or the lack of a proper interaction of htau with these pathways, i.e., a loss of function, (iii) an expression pattern of the different htau isoforms that deviates in time and quantity from the intrinsic profile of murine tau. The gene discussed is MAPT; the disease is Alzheimer disease.