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Degradation of amyloid β peptide by neprilysin expressed from Borna disease virus vector
Authors:Takuji Daito  Megumi Asada‐Utsugi  Yumiko Komatsu  Ayae Kinoshita  Takakuni Maki  Akira Kuzuya  Ryosuke Takahashi  Akiko Makino  Keizo Tomonaga
Institution:1. Research Center for Zoonosis Control, Biologics Development, Hokkaido University, North 20, West 10 Kita‐ku, Sapporo 001‐0020, Japan;2. School of Health Sciences, Graduate School of Medicine, Kyoto University, Yoshida‐Konoe‐cho, Sakyo‐ku, Kyoto 606‐8501, Japan;3. Laboratory of RNA Viruses, Institute for Frontier Life and Medical Sciences, Kyoto University, 53 Kawahara‐cho, Shogoin, Sakyo‐ku, Kyoto 606‐8507, Japan;4. Keihanshin Consortium for Fostering the Next Generation of Global Leaders in Research (K‐CONNEX), Kyoto University, Kyoto, Japan;5. Department of Neurology, Graduate School of Medicine, Kyoto University, Yoshida‐Konoe‐cho, Sakyo‐ku, Kyoto 606‐8501, Japan;6. Department of Mammalian Regulatory Network, Graduate School of Biostudies, Kyoto University, 53 Kawahara‐cho, Shogoin, Sakyo‐ku, Kyoto 606‐8507, Japan;7. Department of Molecular Virology, Graduate School of Medicine, Kyoto University, Kyoto, Japan
Abstract:
Accumulation of amyloid β (Aβ40 and Aβ42) in the brain is a characteristic of Alzheimer disease (AD). Because neprilysin (NEP) is a major Aβ‐degrading enzyme, NEP delivery in the brain is a promising gene therapy for AD. Borna disease virus (BoDV) vector enables long‐term transduction of foreign genes in the central nerve system. Here, the proteolytic ability of NEP transduced by the BoDV vector was evaluated and it was found that the amounts of Aβ40 and Aβ42 decreased significantly, suggesting that NEP expressed from the BoDV vector is functional in that it degrades Aβ.
Keywords:Alzheimer disease  amyloid β    Borna disease virus vector  neprilysin
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