Research for the pathological relationship between Alzheimer Disease and depression
| Project/Area Number |
15K15438
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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 |
Psychiatric science
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| Research Institution | Tokyo Metropolitan Institute of Medical Science |
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Principal Investigator |
TATEBAYASHI Yoshitaka 公益財団法人東京都医学総合研究所, 精神行動医学研究分野, プロジェクトリーダー (80342814)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | オリゴデンドロサイト前駆細胞 / アルツハイマー病 / 大うつ病 / plexin-B3 / 老人斑 / アミロイドβ / オリゴデンデロサイト前駆細胞 / 気分障害 / うつ病 / オリゴデンドロサイト / plexin B3 / γセクレターゼ / Aβ / Notch |
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| Outline of Final Research Achievements |
The roles of oligodendrocyte (OL) lineage cells, the largest glial population in the adult CNS, in the pathogenesis of Alzheimer’s disease (AD) remain elusive. Here, we show a newly developed culture method for adult OL progenitor cells (aOPCs) and identify novel plexin-B3-expressing aOPCs as β amyloid peptides (Aβ)-secreting cells. A small population of plexin-B3+ aOPCs was found in NG2+ aOPC cultures (> 95%) growing in FGF2. FGF2 withdrawal decreased NG2+, but increased plexin-B3+ aOPCs with increased Aβ1-40, -42 secretions and Aβ1-42/total Aβ ratios. In vivo, plexin-B3+ aOPCs are distributed throughout the adult brain, although less densely so than NG2+ aOPCs. Spreading depolarization, a type of brain injury, induced unique delayed cortical plexin-B3+ aOPC gliosis. In AD brains, virtually all senile plaques were immunostained with plexin-B3 antibodies. These findings suggest that plexin-B3+ aOPCs play important roles in AD pathogenesis as a natural Aβ source.
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Report
(4 results)
Research Products
(13 results)
