| Project/Area Number |
18K15495
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 52030:Psychiatry-related
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| Research Institution | Nippon Medical School |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2024-03-31
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| Project Status |
Completed (Fiscal Year 2023)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2021: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2020: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2019: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 老年期うつ病 / タウ蛋白 / ドパミントランスポータ / PET / ドパミントランスポーター / タウイメージング |
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| Outline of Final Research Achievements |
Some depression in elderly people may be a symptom caused by degenerative diseases. In this study, 18 patients with depression aged 65 years or older were evaluated for tau protein accumulation using [18F]PM-PBB3 PET, and five of them were also evaluated for dopamine function using [18F]FE-PE2I PET. Tau protein accumulation was positively correlated with the age at onset of depression, suggesting that local neuronal loss due to tau protein accumulation may be involved in the pathology of depression that occurs in old age. Furthermore, a negative correlation was found between tau protein accumulation and dopamine transporter function, suggesting that reduced dopamine function caused by local neuronal loss resulting from tau protein accumulation may be involved in the emergence and progression of depressive symptoms.
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| Academic Significance and Societal Importance of the Research Achievements |
これまで、老年期うつ病とアミロイドβとの関連はPETにおいて数多く検討されているが、老年期うつ病と脳内タウ蛋白との関連を検討したPET研究は数少なく、タウ蛋白とドパミン機能との関連を検討した研究はさらに少ない。老年期うつ病治療においては、通常の薬物療法に反応が乏しいことがしばしば見受けられるが、本研究で示したように老年期うつ病の病態と脳内タウ蛋白やドパミン機能との関連を明らかにすることにより、治療開始時期や治療の選択、薬物の適正使用などの点で新たな治療戦略につながると考える。
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