The Alzheimer's disease prevention and treatment by nutritional increase in endogenous neuro-protective mediator, kynurenic acid in brain
| Project/Area Number |
25750068
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Eating habits
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| Research Institution | National Center for Geriatrics and Gerontology |
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Principal Investigator |
OKUNO Alato 国立研究開発法人国立長寿医療研究センター, ラジオアイソトープ管理室, 研究員 (50623980)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | トリプトファン / キヌレン酸 / キノリン酸 / 栄養 / アルツハイマー病 / アミロイドβ |
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| Outline of Final Research Achievements |
Tryptophan (Trp) metabolism within the mammalian brain mainly occurs through the kynurenine pathway, where both the endogenous neuro-protective mediator, kynurenic acid (KYNA) and the endogenous excitatory neurotoxin, quinolinic acid (QA) are generated. Increase in KYNA/QA ratio in the brain is thought to be neuro-protective against some neurodegenerative diseases. To examine the possible effect of Trp intake on the change of the KYNA/QA ration in the brain, 0, 0.5, 1.0, 2.0, 5.0% Trp supplementation to 20% casein diet were fed to 20 weeks old C57BL6/J male mice for 28 weeks. As a result, the 1-5% Trp supplementation caused a decrease in the KYNA/QA ratio in brain. Furthermore, a systemic inflammation (a 5-fold increase in plasma level of IFN-γ). These results suggest that a simple Trp supplementation to AD patients worsens rather than suppresses neural degeneration by decrease in the KYNA/QA ratio and by increase in systemic inflammation.
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Report
(4 results)
Research Products
(17 results)
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[Journal Article] Lipidomic analysis of brain tissues and plasma in a mouse model expressing mutated human amyloid precursor protein/tau for Alzheimer's disease.2013
Author(s)
Tajima Y, Ishikawa M, Maekawa K, Murayama M, Senoo Y, Nishimaki-Mogami T, Nakanishi H, Ikeda K, Arita M, Taguchi R, Okuno A, Mikawa R, Niida S, Takikawa O, Saito Y.
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Journal Title
Lipids Health Dis
Volume: 12
Issue: 1
Pages: 68-68
DOI
Related Report
Peer Reviewed
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[Presentation] Lipidomic analysis of brain tissues and plasma in a mouse model expressing mutated human amyloid precursor protein/tau for Alzheimer’s disease.2013
Author(s)
Tajima Y, Maekawa Keiko, Ishikawa M, Murayama M, Senoo Y, Nishimaki-Mogami T, Nakanishi H, Kazutaka I, Arita M, Taguchi R, Okuno A, Mikawa R, Niida S, Takikawa O, Saito Y.
Organizer
The 9th Annual Conference of the Metabolomics Society
Place of Presentation
Glasgow, Scotland
Related Report
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