Cerebral amyloid angiopathy in traumatic brain injury: association with apolipoprotein E genotype
Cerebral amyloid angiopathy in traumatic brain injury: association with apolipoprotein E genotype
Objective: In view of the association of the apolipoprotein E (APOE) {varepsilon}4 allele with poor outcome after traumatic brain injury we determined the frequency of cerebral amyloid angiopathy (CAA) and the extent of haemorrhagic pathology in relation to APOE genotype in an autopsy series of 88 head injured cases.
Methods: Tissue sections from the frontal and temporal lobes were immunostained for amyloid-ß peptide (Aß) and stained for Congo red to identify vascular amyloid pathology. A semiquantitative assessment of contusions, the total contusion index, was used to estimate the severity of the haemorrhagic pathology. APOE genotypes were determined by polymerase chain reaction of genomic DNA extracted from paraffin embedded tissue sections.
Results: CAA was present in 7/40 (18%) {varepsilon}4 carriers compared with 1/48 (2%) non-{varepsilon}4 carriers (p = 0.021, 95% confidence interval (CI) for difference in proportions with CAA 3% to 29%) with 6/40 (4 with CAA) {varepsilon}4 carriers being homozygotes. Thus the risk of having CAA for {varepsilon}4 carriers was 8.4 times that for the non-{varepsilon}4 carriers. However, there was no clear tendency for patients with CAA to have more severe or more numerous contusions (median contusion index 19 (CAA) v 14.5, p = 0.23, 95% CI for difference in medians –5 to 14).
Conclusions: Presence of CAA in head injured cases was significantly associated with possession of an APOE {varepsilon}4 allele but not with the severity of contusions.
apolipoprotein E, cerebral amyloid angiopathy, head injury
229-233
Leclercq, P.D.
cbd9f8a0-8dfe-4714-9092-ab720a6fc141
Murray, L.S.
9a2f2125-44de-4492-8ead-e9170b212b80
Smith, C.
2019b8d8-ee85-40ff-9bb1-76916a21de6b
Graham, D.I.
0b1c9c9e-94b2-44fa-b189-8e04501b3a67
Nicoll, J.A.R.
88c0685f-000e-4eb7-8f72-f36b4985e8ed
Gentleman, S.M.
5b93cc56-1fa8-4406-af6f-4177199da72a
2005
Leclercq, P.D.
cbd9f8a0-8dfe-4714-9092-ab720a6fc141
Murray, L.S.
9a2f2125-44de-4492-8ead-e9170b212b80
Smith, C.
2019b8d8-ee85-40ff-9bb1-76916a21de6b
Graham, D.I.
0b1c9c9e-94b2-44fa-b189-8e04501b3a67
Nicoll, J.A.R.
88c0685f-000e-4eb7-8f72-f36b4985e8ed
Gentleman, S.M.
5b93cc56-1fa8-4406-af6f-4177199da72a
Leclercq, P.D., Murray, L.S., Smith, C., Graham, D.I., Nicoll, J.A.R. and Gentleman, S.M.
(2005)
Cerebral amyloid angiopathy in traumatic brain injury: association with apolipoprotein E genotype.
Journal of Neurology, Neurosurgery, and Psychiatry, 76 (2), .
Abstract
Objective: In view of the association of the apolipoprotein E (APOE) {varepsilon}4 allele with poor outcome after traumatic brain injury we determined the frequency of cerebral amyloid angiopathy (CAA) and the extent of haemorrhagic pathology in relation to APOE genotype in an autopsy series of 88 head injured cases.
Methods: Tissue sections from the frontal and temporal lobes were immunostained for amyloid-ß peptide (Aß) and stained for Congo red to identify vascular amyloid pathology. A semiquantitative assessment of contusions, the total contusion index, was used to estimate the severity of the haemorrhagic pathology. APOE genotypes were determined by polymerase chain reaction of genomic DNA extracted from paraffin embedded tissue sections.
Results: CAA was present in 7/40 (18%) {varepsilon}4 carriers compared with 1/48 (2%) non-{varepsilon}4 carriers (p = 0.021, 95% confidence interval (CI) for difference in proportions with CAA 3% to 29%) with 6/40 (4 with CAA) {varepsilon}4 carriers being homozygotes. Thus the risk of having CAA for {varepsilon}4 carriers was 8.4 times that for the non-{varepsilon}4 carriers. However, there was no clear tendency for patients with CAA to have more severe or more numerous contusions (median contusion index 19 (CAA) v 14.5, p = 0.23, 95% CI for difference in medians –5 to 14).
Conclusions: Presence of CAA in head injured cases was significantly associated with possession of an APOE {varepsilon}4 allele but not with the severity of contusions.
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Published date: 2005
Keywords:
apolipoprotein E, cerebral amyloid angiopathy, head injury
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Local EPrints ID: 27636
URI: http://eprints.soton.ac.uk/id/eprint/27636
PURE UUID: 73444719-8685-4a22-a49c-5711eb4d44ea
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Date deposited: 25 Apr 2006
Last modified: 09 Jan 2022 03:09
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Author:
P.D. Leclercq
Author:
L.S. Murray
Author:
C. Smith
Author:
D.I. Graham
Author:
S.M. Gentleman
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