| Project/Area Number |
17K09790
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Gunma University |
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Principal Investigator |
Tsuneo Yamazaki 群馬大学, 大学院保健学研究科, 教授 (80200658)
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| Co-Investigator(Kenkyū-buntansha) |
池田 佳生 群馬大学, 大学院医学系研究科, 教授 (00282400)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | アルツハイマー病 / 変性神経突起 / オートファジー / 顆粒空胞変性 / 神経原線維変化 / 脳神経疾患 / 認知症 |
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| Outline of Final Research Achievements |
According to the amyloid cascade theory of Alzheimer's disease, intracellular tau deposition is induced by extracellular amyloid β deposition. However, this mechanism is still yet unknown. In this study, I tried to search putative common pathological structures which connect both protein deposition by immunohistochemistry. My former studies clearly showed that autophagic vacuoles are related to amyloid β production,then paraffin sections of Alzheimer's brains were stained by anti-ATG9A antibody which recognizes primary stages of autophagic vacuoles. In results, ATG9A is expressed in degenerative neurites and the expressed pattern might be changed in different stages of amyloid β deposition.
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| Academic Significance and Societal Importance of the Research Achievements |
アルツハイマー病の発症メカニズムの解明は治療法の開発のために必要だが，未だ不明の部分も多い。特にアミロイドカスケードセオリーにおける，アミロイドβ蛋白とタウ蛋白沈着の関連解明は重要な課題と考えられる。本研究は両蛋白沈着の初期の共通構造物をオートファゴソームに求め，その結果神経変性突起の関与の可能性を指摘することができた。
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