Document Detail

BACE1 levels by APOE genotype in non-demented and Alzheimer's post-mortem brains.
MedLine Citation:
PMID:  23036023     Owner:  NLM     Status:  MEDLINE    
The APOE genotype is a known susceptibility factor for Alzheimer's disease (AD). It is apparent that the presence of the APOE ε40 allele increases the risk for developing AD, lowers the age of onset in AD, and may influence the pathological burden seen in AD. In this study, we asked whether BACE1 levels differ by APOE genotype in the AD and non-demented (ND) brain. We isolated mid-frontal cortex (MFC) and mid-temporal cortex (MTC) from post-mortem ND and AD subjects that were APOE ε3/3, ε3/4, ε4/4 carriers. All AD subjects met NINDS-ADRDA and NIA-Reagan criteria for a diagnosis of AD. The MFC and MTC were homogenized and the lysates underwent ELISA and Western blotting for BACE1. The ELISA revealed that total BACE1 levels were lower in the MFC of AD compared to ND subjects. Furthermore, in APOE ε4 carriers BACE1 levels were lower than ε3/3 carriers in the ND frontal cortex. No difference in BACE1 levels was observed in AD MFC and in ND and AD MTC tissues. The ELISA results were confirmed by Western blotting. Our data suggest that brain BACEl levels may be influenced by the apolipoprotein E genotype before the onset of AD, providing an alternative explanation for the lower amyloid beta 42 levels in CSF in ND and AD subjects.
Boris Decourt; Amanda Gonzales; Thomas G Beach; Michael Malek-Ahmadi; Aaron Walker; Lucia Sue; Douglas G Walker; Marwan N Sabbagh
Related Documents :
16079403 - Temporal patterns of fos expression in the dentate gyrus after spontaneous seizures in ...
9637603 - Ictal scalp eeg in unilateral mesial temporal lobe epilepsy.
15622013 - A rodent model for investigating the neurobiology of contralateral neglect.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Current Alzheimer research     Volume:  10     ISSN:  1875-5828     ISO Abbreviation:  Curr Alzheimer Res     Publication Date:  2013 Mar 
Date Detail:
Created Date:  2013-04-18     Completed Date:  2013-11-11     Revised Date:  2014-08-06    
Medline Journal Info:
Nlm Unique ID:  101208441     Medline TA:  Curr Alzheimer Res     Country:  United Arab Emirates    
Other Details:
Languages:  eng     Pagination:  309-15     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Aged, 80 and over
Alzheimer Disease / enzymology*,  genetics*
Amyloid Precursor Protein Secretases / analysis,  metabolism*
Apolipoproteins E / genetics*
Aspartic Acid Endopeptidases / analysis,  metabolism*
Blotting, Western
Brain / enzymology*
Enzyme-Linked Immunosorbent Assay
Genetic Predisposition to Disease / genetics
Polymerase Chain Reaction
Grant Support
5P30AG019610-12/AG/NIA NIH HHS; P30 AG019610/AG/NIA NIH HHS; P30 AG19610/AG/NIA NIH HHS; P30AG019610-09/AG/NIA NIH HHS; R01 AG034155/AG/NIA NIH HHS; R01AG034155/AG/NIA NIH HHS
Reg. No./Substance:
0/Apolipoproteins E; EC 3.4.-/Amyloid Precursor Protein Secretases; EC 3.4.23.-/Aspartic Acid Endopeptidases; EC protein, human

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

Previous Document:  Valproic acid attenuates neuronal loss in the brain of APP/PS1 double transgenic Alzheimer's disease...
Next Document:  Hypoglycemia induces tau hyperphosphorylation.