2018 Fiscal Year Final Research Report
Behavioral and electrophysiological analyses of new Alzheimer's disease model mouse that express amyloid beta oligomer intraneuronally
| Project/Area Number |
16K12944
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Rehabilitation science/Welfare engineering
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| Research Institution | National Institute of Advanced Industrial Science and Technology |
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Principal Investigator |
OCHIISHI TOMOYO 国立研究開発法人産業技術総合研究所, 生命工学領域, 主任研究員 (30356729)
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| Co-Investigator(Kenkyū-buntansha) |
角 正美 植草学園大学, 保健医療学部, 講師 (30646261)
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| Research Collaborator |
Ebihara Tatsuhiko
Kiyosue Kazuyuki
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Keywords | アルツハイマー病 / アミロイドβタンパク質 / シナプス / オリゴマー / トランスジェニックマウス / 運動 |
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| Outline of Final Research Achievements |
Soluble amyloid β protein (Aβ) oligomers in neurons are neurotoxic and play crucial roles in synaptic transmission and cognitive function in Alzheimer’s disease (AD) patients. In this study, using GFP-fused human Aβ, which only forms low molecular weight oligomers, we developed a new mouse model that expresses Aβ oligomers throughout their life. They exhibit memory and long-term potentiation impairments already in young age. However, these mice showed improvement in cognitive function due to the spontaneous load of running wheel for about 2 months. Thus, the Aβ-GFP Tg mouse is a unique tool specialized to investigate the toxicity of Aβ oligomers inside neurons and the effect of exercise against the impairment of cognitive function induced by Aβ oligomer.
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| Free Research Field |
神経細胞生物学
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| Academic Significance and Societal Importance of the Research Achievements |
高齢化社会とあいまって、認知症の半数以上を占めるADの原因解明、治療法の確立は社会的要請となっている。MCIの患者における習慣的な運動の効果のメカニズムの解明は、認知症の予防や運動が効果を示す病理学的な時期の予想、また、非薬物的介入のみでなく運動による効果を高める物質等、薬物的治療法の開発など全く新しい治療法の開発に大きく貢献することが期待できる。
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