Examination of Mouse Facial Nerve Transection Model Focusing on Glial Cells

2021 Fiscal Year Final Research Report

• Project/Area Number: 20K18274
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 56050:Otorhinolaryngology-related
• Research Institution: Kanazawa University
• Principal Investigator: TAKASO YUJI 金沢大学, 医学系, 協力研究員 (00866444)
• Project Period (FY): 2020-04-01 – 2022-03-31
• Keywords: 顔面神経 / CD38 / NAD+ / 神経変性

Outline of Final Research Achievements

The effect of Nicotinamide adenine dinucleotide (NAD+) on nerve injury was investigated using a CD38 knockout mouse with a high NAD + concentration and a model in which the concentration was increased by administering a NAD+ precursor. No neuroprotective effect was observed in the facial nerve nucleus after nerve transection, but degeneration of peripheral nerves was delayed. From this, it was found that a high concentration of NAD+ has an effect of protecting nerves from nerve injury, and that the effect can be obtained by administering a NAD+ precursor.

Free Research Field

顔面神経

Academic Significance and Societal Importance of the Research Achievements

以前からNicotinamide adenine dinucleotide（NAD+）の神経変性に対する保護効果は指摘されていたが、今回は末梢神経においても同様の効果を認めることがわかり、また投薬での人為的なNAD+濃度の上昇でもその効果が得られることがわかった。これにより神経傷害後にNAD+濃度を高めるような治療が神経変性を抑制する可能性が示唆され、神経傷害後の新たな治療法の開発につながることが考えられる。