Olfactory deficits induce neurofilament hyperphosphorylation.

Abstract

Olfactory dysfunction, including structural abnormalities of the olfactory epithelium, the olfactory bulb and the central olfactory cortices is recognized as an early feature of Alzheimer disease (AD), the most prevalent neurodegenerative disease in aged population characterized by intracellular neurofibrillary tangles (NFTs). How olfactory deficits are linked with AD-like neuropathological changes is still unknown. Here, by using two anosmia animal models, bilateral olfactory bulbectomy (OBX) rats and Cnga2(-/Y) mice, which lack intact olfactory CNG channels, we found the immunoreactivity of phosphorylated neurofilament (NF) are highly increased in the neurites at both the hippocampus and the cortex. As hyperphosphorylated NF is one of the main components of NFTs, our study strongly suggested the underlying correlation of olfactory deficits with AD-like pathological impairments.