SET translocation is associated with increase in caspase cleaved amyloid precursor protein in CA1 of Alzheimer and Down syndrome patients.

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Serval ID
serval:BIB_A321D5D11223
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
SET translocation is associated with increase in caspase cleaved amyloid precursor protein in CA1 of Alzheimer and Down syndrome patients.
Journal
Neurobiology of Aging
Author(s)
Facchinetti P., Dorard E., Contremoulins V., Gaillard M.C., Déglon N., Sazdovitch V., Guihenneuc-Jouyaux C., Brouillet E., Duyckaerts C., Allinquant B.
ISSN
1558-1497 (Electronic)
ISSN-L
0197-4580
Publication state
Published
Issued date
2014
Volume
35
Number
5
Pages
958-968
Language
english
Notes
Publication types: Journal ArticlePublication Status: ppublish
Abstract
Caspase cleaved amyloid precursor protein (APPcc) and SET are increased and mislocalized in the neuronal cytoplasm in Alzheimer Disease (AD) brains. Translocated SET to the cytoplasm can induce tau hyperphosphorylation. To elucidate the putative relationships between mislocalized APPcc and SET, we studied their level and distribution in the hippocampus of 5 controls, 3 Down syndrome and 10 Alzheimer patients. In Down syndrome and Alzheimer patients, APPcc and SET levels were increased in CA1 and the frequency of both localizations in the neuronal cytoplasm was high in CA1, and low in CA4. As the increase of APPcc is already present at early stages of AD, we overexpressed APPcc in CA1 and the dentate gyrus neurons of adult mice with a lentiviral construct. APPcc overexpression in CA1 and not in the dentate gyrus induced endogenous SET translocation and tau hyperphosphorylation. These data suggest that increase in APPcc in CA1 neurons could be an early event leading to the translocation of SET and the progression of AD through tau hyperphosphorylation.
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Web of science
Create date
16/02/2014 19:27
Last modification date
19/06/2020 6:21
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