2016 Fiscal Year Final Research Report
ABCA1 and ABCA7: what are their roles in the pathogenesis of Alzheimer's disease?
Project/Area Number |
25461375
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Metabolomics
|
Research Institution | Nagoya City University |
Principal Investigator |
|
Project Period (FY) |
2013-04-01 – 2017-03-31
|
Keywords | ABCA7 / ABCA1 / HDL / アルツハイマー病 / 動脈硬化 |
Outline of Final Research Achievements |
ABCA7 knock-out mice displayed an increased production of endogenous murine amyloid Aβ42 species. Crossing ABCA7-deficient animals to an APP transgenic model resulted in significant increases in the soluble Aβ as compared with mice expressing normal levels of ABCA7. In vitro studies indicated a more rapid endocytosis of APP in ABCA7 knock-out cells that is mechanistically consistent with the increased Aβ production. Phagocytotic activities in peritoneal macrophages were lower even in ABCA7 heterozygous deficiency.
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Free Research Field |
生化学
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