Nrf2 Suppresses Oxidative Stress and Inflammation in App Knock-In Alzheimer’s Disease Model Mice

Author:

Uruno Akira12,Matsumaru Daisuke3,Ryoke Rie4,Saito Ritsumi12,Kadoguchi Shiori2,Saigusa Daisuke12,Saito Takashi56,Saido Takaomi C.5,Kawashima Ryuta4,Yamamoto Masayuki12

Affiliation:

1. Department of Integrative Genomics, Tohoku Medical Megabank Organization, Tohoku University, Sendai, Miyagi, Japan

2. Department of Medical Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan

3. Center for Gene Research, Tohoku University, Sendai, Miyagi, Japan

4. Department of Advanced Brain Science, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Miyagi, Japan

5. Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Wako, Saitama, Japan

6. Department of Neurocognitive Science, Nagoya City University Graduate School of Medical Science, Nagoya, Aichi, Japan

Abstract

Nrf2 (NF-E2-related-factor 2) is a stress-responsive transcription factor that protects cells against oxidative stresses. To clarify whether Nrf2 prevents Alzheimer’s disease (AD), AD model App NL-G-F/NL-G-F knock-in ( App NLGF ) mice were studied in combination with genetic Nrf2 induction model Keap1 FA/FA mice. While App NLGF mice displayed shorter latency to escape than wild-type mice in the passive-avoidance task, the impairment was improved in App NLGF :: Keap1 FA/FA mice.

Funder

Takeda Science Foundation

Naito Foundation

Japan Agency for Medical Research and Development

Ministry of Education, Culture, Sports, Science and Technology

MEXT | Japan Society for the Promotion of Science

Publisher

American Society for Microbiology

Subject

Cell Biology,Molecular Biology

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