Document Detail


Association between severe cerebral amyloid angiopathy and cerebrovascular lesions in Alzheimer disease is not a spurious one attributable to apolipoprotein E4.
MedLine Citation:
PMID:  10867785     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: We have previously reported an association between severe cerebral amyloid angiopathy (CAA) and cerebrovascular lesions in Alzheimer disease (AD), which is particularly strong for microinfarcts, hemorrhages, and multiple lesion types. Cerebral amyloid angiopathy has also been associated with the apolipoprotein E4 (APOE4) genotype, which is in turn associated with premature coronary artery disease and atherosclerosis. OBJECTIVE: To test whether severe CAA would be more strongly associated with cerebrovascular lesions than would APOE4 genotype. METHODS: We reviewed 306 cases of autopsy-confirmed AD (from the University of California, San Diego, brain autopsy series) to assess whether APOE genotype and other clinical risk factors were predictive of vascular lesions (VLs) in AD. Cerebral amyloid angiopathy severity was assessed using a semiquantitative scale in 4 brain regions (ie, hippocampus, midfrontal cortex, inferior parietal cortex, and superior temporal cortex) and an average score was computed for each case. RESULTS: We found that severe CAA was associated with an increased frequency of VLs (33% of the cases of severe CAA had VLs vs 19% of the cases of mild or absent CAA; P=.02). While the APOE4/4 genotype was associated with an increased severity of CAA, there was no significant relationship between APOE genotype and frequency of VLs. Logistic regression models showed that severe CAA, advanced age, atherosclerosis, and Hachinski Ischemia Scale score of 7 or more were all significantly associated with VLs, but the number of APOE4 alleles, history of hypertension, coronary artery disease, sex, and serum cholesterol levels had nonsignificant effects. Within strata of APOE genotype, the presence of severe CAA was associated with increased frequency of VLs (eg, within APOE4/4 homozygotes, VLs were present within 47% of the cases of severe CAA vs 9.5% of the cases of mild or absent CAA; P=.01). CONCLUSIONS: Severe CAA confers a greater risk of VLs in AD, even within strata of APOE genotype. Therefore, the association between severe CAA and VLs in AD is not a spurious one owing to APOE4. Overall, our cases of AD with APOE4 do not seem to be a more "vasculopathic" subtype of AD. The mechanisms by which CAA produces VLs of various types need to be further elucidated, as these are probably important in producing the common entity of "mixed" AD/vascular dementia. Arch Neurol. 2000.
Authors:
J M Olichney; L A Hansen; C R Hofstetter; J H Lee; R Katzman; L J Thal
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Publication Detail:
Type:  Clinical Trial; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Archives of neurology     Volume:  57     ISSN:  0003-9942     ISO Abbreviation:  Arch. Neurol.     Publication Date:  2000 Jun 
Date Detail:
Created Date:  2000-07-13     Completed Date:  2000-07-13     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0372436     Medline TA:  Arch Neurol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  869-74     Citation Subset:  AIM; IM    
Affiliation:
Neurology Service (127), Veterans Administration Medical Center, 3350 La Jolla Village Dr, San Diego, CA 92161, USA.
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MeSH Terms
Descriptor/Qualifier:
Aged
Alzheimer Disease / genetics,  metabolism,  pathology*
Apolipoprotein E4
Apolipoproteins E / genetics,  physiology*
Cerebral Amyloid Angiopathy / genetics,  metabolism,  pathology*
Cerebrovascular Disorders / genetics,  metabolism,  pathology*
Female
Genotype
Humans
Male
Neurofibrillary Tangles / pathology
Reverse Transcriptase Polymerase Chain Reaction
Risk Factors
Senile Plaques / pathology
Stroke / complications,  pathology
Grant Support
ID/Acronym/Agency:
AG 05131/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/Apolipoprotein E4; 0/Apolipoproteins E

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