Affiliations: [a] Department of Food and Nutrition, Kyoto Women’s University, Kyoto, Japan
| [b] Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan
| [c] Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako, Saitama, Japan
| [d] Department of Neurocognitive Science, Institute of Brain Science, Nagoya City University Graduate School of Medical Science, Nagoya, Aichi, Japan
Correspondence:
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Corresponding authors: Masataka Narukawa, PhD, Department of Food and Nutrition, Kyoto Women’s University, 35 Imakumano, Higashiyama-ku, Kyoto 605-8501, Japan. Tel.: +81 75 531 7131; E-mail: narukawa@kyoto-wu.ac.jp; Takumi Misaka, PhD, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan. Tel.: +81 3 5841 8117; Fax: +81 3 5841 8100; E-mail: amisaka@mail.ecc.u-tokyo.ac.jp.
Abstract: Using an amyloid precursor protein (App) gene knock-in (KI) mouse of Alzheimer’s disease (AD), we investigated the expression of olfactory-related genes in olfactory impairment caused by AD. We observed the change in olfactory behavior in the App-KI mice. There was no significant difference, however, in the mRNA expression levels of olfactory-related genes between the olfactory epithelia of wild-type (WT) and App-KI mice. Amyloid-β deposition was confirmed throughout the olfactory pathway in App-KI mice, but not in WT mice. These show that the change in olfactory behavior in the App-KI mice might cause by the impairment of the olfactory pathway.
