Olfactory dysfunction occurs in transgenic mice overexpressing human tau protein.

Disorders of olfaction are among the first clinical signs of neurodegenerative diseases such as Alzheimer's disease (AD) and idiopathic Parkinson's disease (PD). In this study, we employed an odor habituation paradigm to evaluate the olfactory function of T alpha 1-3RT transgenic mice that overexpress tau, a key pathogenic protein in AD, and compared such function to that of wild-type controls who do not overexpress this protein. The T alpha 1-3RT mice, but not the controls, exhibited responses indicative of decreased olfactory function. These data lend support to the notion that tau may be involved in the pathogenesis of the olfactory dysfunction of some neurodegenerative diseases. Future studies need to similarly assess other pathogenic markers, as well as their distribution within various sectors of the brain, to determine the specificity of this phenomenon.