GULP1/CED-6 ameliorates amyloid-β toxicity in a Drosophila model of Alzheimer’s disease
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AbstractAmyloidogenic processing of APP by β- and γ-secretases leads to the generation of amyloid-β peptide (Aβ), and the accumulation of Aβ in senile plaques is a hallmark of Alzheimer’s disease (AD). Understanding the mechanisms of APP processing is therefore paramount. Increasing evidence suggests that APP intracellular domain (AICD) interacting proteins influence APP processing. In this study, we characterized the overexpression of AICD interactor GULP1 in a Drosophila AD model expressing human BACE and APP695. Transgenic GULP1 significantly lowered the levels of both Aβ1-40 and Aβ1-42 without decreasing the BACE and APP695 levels. Overexpression of GULP1 also reduced
APP/BACE-mediated retinal degeneration, rescued motor dysfunction and extended longevity of the flies. Our results indicate that GULP1 regulate APP processing and reduce neurotoxicity in a Drosophila AD model.
Acceptance Date30/07/2017
All Author(s) ListWai Yin Vivien Chiu, Alex Chun Koon, Jacky Chi Ki Ngo, Ho Yin Edwin Chan, Kwok-Fai Lau
Journal nameOncotarget
Volume Number8
Issue Number59
PublisherImpact Journals
Place of PublicationUSA
Pages99274 - 99283
LanguagesEnglish-United States
KeywordsCED-6, APP, Aβ, neurodegeneration, neurotoxicity

Last updated on 2020-28-06 at 01:37