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Cerebral amyloid angiopathy and cortical microinfarcts as putative substrates of vascular dementia.

Haglund, Mattias LU ; Passant, Ulla LU ; Sjöbeck, Martin LU ; Ghebremedhin, Estifanos and Englund, Elisabet LU (2006) In International Journal of Geriatric Psychiatry 21(7). p.681-687
Abstract
Background and purpose Vascular dementia (VaD) has occasionally been associated with cerebral amyloid angiopathy (CAA), but the prevalence and significance of this counterintuitive relationship are poorly known. Therefore, we investigated the presence and characteristics of CAA in brains of VaD cases. Methods We examined temporal and parietal regions of the cerebral cortex of 26 consecutive VaD cases from the Lund Longitudinal Dementia Study. We carried out immunohistochemistry and routine stainings, determined Apolipoprotein E (ApoE) genotypes, and obtained clinical characteristics on the studied group for retrospective analysis. Results CAA was marked in eight out of 26 cases, and correlated strongly with the presence of cortical... (More)
Background and purpose Vascular dementia (VaD) has occasionally been associated with cerebral amyloid angiopathy (CAA), but the prevalence and significance of this counterintuitive relationship are poorly known. Therefore, we investigated the presence and characteristics of CAA in brains of VaD cases. Methods We examined temporal and parietal regions of the cerebral cortex of 26 consecutive VaD cases from the Lund Longitudinal Dementia Study. We carried out immunohistochemistry and routine stainings, determined Apolipoprotein E (ApoE) genotypes, and obtained clinical characteristics on the studied group for retrospective analysis. Results CAA was marked in eight out of 26 cases, and correlated strongly with the presence of cortical microinfarcts, both in the temporal lobe and in the parietal lobe. Based on comparisons with eight age-matched VaD cases without CAA, the clinical records suggested that VaD cases with CAA as a group exhibited less pronounced neurological symptoms. A clear contribution of the ApoE genotype could not be identified. Conclusions Based on a combination of the clinical and pathological data, we suggest that microinfarcts in the cerebral cortex associated with severe CAA may be the primary pathological substrate in a significant proportion of VaD cases. Future studies should be undertaken to confirm or dismiss the hypothesis that these cases exhibit a different symptom profile than VaD cases without CAA. Copyright (c) 2006 John Wiley & Sons, Ltd. (Less)
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author
organization
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type
Contribution to journal
publication status
published
subject
keywords
cerebrovascular disorder, histopathology, neuropathology, Alzheimer's disease
in
International Journal of Geriatric Psychiatry
volume
21
issue
7
pages
681 - 687
publisher
John Wiley and Sons Ltd
external identifiers
  • wos:000239288000009
  • scopus:33746463940
ISSN
1099-1166
DOI
10.1002/gps.1550
language
English
LU publication?
yes
id
973787e9-35ab-45f2-aeb3-b7c51d0b8f47 (old id 158078)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16802283&dopt=Abstract
date added to LUP
2007-07-13 14:57:28
date last changed
2019-04-02 01:38:12
@article{973787e9-35ab-45f2-aeb3-b7c51d0b8f47,
  abstract     = {Background and purpose Vascular dementia (VaD) has occasionally been associated with cerebral amyloid angiopathy (CAA), but the prevalence and significance of this counterintuitive relationship are poorly known. Therefore, we investigated the presence and characteristics of CAA in brains of VaD cases. Methods We examined temporal and parietal regions of the cerebral cortex of 26 consecutive VaD cases from the Lund Longitudinal Dementia Study. We carried out immunohistochemistry and routine stainings, determined Apolipoprotein E (ApoE) genotypes, and obtained clinical characteristics on the studied group for retrospective analysis. Results CAA was marked in eight out of 26 cases, and correlated strongly with the presence of cortical microinfarcts, both in the temporal lobe and in the parietal lobe. Based on comparisons with eight age-matched VaD cases without CAA, the clinical records suggested that VaD cases with CAA as a group exhibited less pronounced neurological symptoms. A clear contribution of the ApoE genotype could not be identified. Conclusions Based on a combination of the clinical and pathological data, we suggest that microinfarcts in the cerebral cortex associated with severe CAA may be the primary pathological substrate in a significant proportion of VaD cases. Future studies should be undertaken to confirm or dismiss the hypothesis that these cases exhibit a different symptom profile than VaD cases without CAA. Copyright (c) 2006 John Wiley & Sons, Ltd.},
  author       = {Haglund, Mattias and Passant, Ulla and Sjöbeck, Martin and Ghebremedhin, Estifanos and Englund, Elisabet},
  issn         = {1099-1166},
  keyword      = {cerebrovascular disorder,histopathology,neuropathology,Alzheimer's disease},
  language     = {eng},
  number       = {7},
  pages        = {681--687},
  publisher    = {John Wiley and Sons Ltd},
  series       = {International Journal of Geriatric Psychiatry},
  title        = {Cerebral amyloid angiopathy and cortical microinfarcts as putative substrates of vascular dementia.},
  url          = {http://dx.doi.org/10.1002/gps.1550},
  volume       = {21},
  year         = {2006},
}