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2016 Fiscal Year Final Research Report

ABCA1 and ABCA7: what are their roles in the pathogenesis of Alzheimer's disease?

Research Project

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Project/Area Number 25461375
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Metabolomics
Research InstitutionNagoya City University

Principal Investigator

ABE-DOHMAE Sumiko  名古屋市立大学, 大学院医学研究科, 准教授 (70227700)

Project Period (FY) 2013-04-01 – 2017-03-31
KeywordsABCA7 / 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.

Free Research Field

生化学

URL: 

Published: 2018-03-22  

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