Mechanisms of redox perturbation in the mouse model of Alzheimer's disease

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K19036
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Pathological medical chemistry
• Research Institution: Institute of Physical and Chemical Research
• Principal Investigator: Hashimoto Shoko 国立研究開発法人理化学研究所, 脳科学総合研究センター, 基礎科学特別研究員 (50632890)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: アルツハイマー病 / 酸化ストレス / グルタチオン / 神経炎症

Outline of Final Research Achievements

Oxidative stress is demonstrated to play an important role in the etiology of Alzheimer’s disease (AD). In order to defense against oxidative stress, organisms possess glutathione as an important antioxidant. However, glutathione level is decreased with ageing and progression of diseases including AD. We found that glutathione level is also lowered in App-knockin (App-KI) mice. In this study, we elucidated the mechanism by which glutathione level was decreased in App-KI, and the effect of glutathione reduction on AD progression. Consequently, we concluded that neuroinflammation induced by amyloid pathology decreased glutathione level, and resulted in further activation of neuroinflammation and neuronal cell death. The vicious cycle of neuroinflammation and oxidative stress may play an important role in AD progression.

Free Research Field

生化学