Document Detail


Cell cycle-driven neuronal apoptosis specifically linked to amyloid peptide Abeta1-42 exposure is not exacerbated in a mouse model of presenilin-1 familial Alzheimer's disease.
MedLine Citation:
PMID:  18466334     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have shown previously that beta-catenin and cyclin D1 are up-regulated in cortical neurons from homozygous mice carrying the familial Alzheimer's disease (FAD) presenilin-1 M146V mutation in a knock-in model (PS1 KI(M146V) mice), leading to cell cycle-associated apoptosis. Here, we have aimed to determine (i) whether this phenotype is present in heterozygous PS1 KI(M146V) mice, which reflects more accurately the PS1 FAD condition in humans and (ii) whether Abeta(1-42), which is invariably present in the PS1 FAD brain and is thought to affect neuronal cell cycle kinetics, may contribute to the abnormal cell cycle/cell death phenotype seen in PS1 KI(M146V) mice. We demonstrate that cell cycle-linked apoptosis occurs in heterozygous PS1 KI(M146V) post-mitotic neurons. In addition, there is a significant Abeta-associated increase in cell cycle and cell death that is not further modified by the PS1 KI(M146V) mutation. Our results are consistent with a cell cycle-associated neurodegeneration model in the PS1 FAD brain in which the loss of PS1-dependent beta-catenin regulatory function is sufficient to commit susceptible neurons to an abortive cell cycle, and may act synergistically with the Abeta cytotoxic challenge present in the PS1 FAD brain to expand the neuronal population susceptible to cell cycle-driven apoptosis.
Authors:
Bilal Malik; Antonio Currais; Salvador Soriano
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-05-02
Journal Detail:
Title:  Journal of neurochemistry     Volume:  106     ISSN:  1471-4159     ISO Abbreviation:  J. Neurochem.     Publication Date:  2008 Jul 
Date Detail:
Created Date:  2008-08-08     Completed Date:  2008-09-16     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  England    
Other Details:
Languages:  eng     Pagination:  912-6     Citation Subset:  IM    
Affiliation:
Department of Neuroscience, MRC Centre for Neurodegeneration Research, Institute of Psychiatry, King's College London, De Crespigny Park, London, UK.
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MeSH Terms
Descriptor/Qualifier:
Alzheimer Disease / genetics
Amyloid beta-Protein / pharmacology*
Analysis of Variance
Animals
Apoptosis / physiology*
Bromodeoxyuridine / metabolism
Cell Cycle / physiology*
Cells, Cultured
Cerebral Cortex / pathology
Cyclin D1 / metabolism
Disease Models, Animal
Embryo, Mammalian
Hippocampus / metabolism
Humans
Mice
Mice, Transgenic
Mutation / genetics
Neurons / drug effects*,  physiology*
Peptide Fragments / pharmacology*
Presenilin-1 / genetics
Up-Regulation / physiology
beta Catenin / metabolism
Chemical
Reg. No./Substance:
0/Amyloid beta-Protein; 0/Peptide Fragments; 0/Presenilin-1; 0/amyloid beta-protein (1-42); 0/beta Catenin; 136601-57-5/Cyclin D1; 59-14-3/Bromodeoxyuridine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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