Cerebral amyloid angiopathy in traumatic brain injury: association with apolipoprotein E genotype

In view of the association of the apolipoprotein E (APOE) epsilon 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.

Tissue sections from the frontal and temporal lobes were immunostained for amyloid-beta peptide (A beta) 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.

CAA was present in 7/40 (18%) epsilon 4 carriers compared with 1/48 (2%) non-epsilon 4 carriers (p = 0.021, 95% confidence interval (CI) for difference in proportions with CAA 3% to 29%) with 6/40 (4 with CAA) epsilon 4 carriers being homozygotes. Thus the risk of having CAA for epsilon 4 carriers was 8.4 times that for the non-epsilon 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).

Presence of CAA in head injured cases was significantly associated with possession of an APOE epsilon 4 allele but not with the severity of contusions.