APOE associations with severe CAA-associated vasculopathic changes: collaborative meta-analysis
| Journal Title: | Journal of neurology neurosurgery and psychiatry, 2014-03, Vol.85 (3), p.300-305 |
| Main Author: | Rannikmäe, Kristiina |
| Other Authors: | Kalaria, Rajesh N , Greenberg, Steven M , Chui, Helena C , Schmitt, Frederick A , Samarasekera, Neshika , Al-Shahi Salman, Rustam , Sudlow, Cathie L M |
| Format: |
 Electronic Article
|
| Language: |
English |
| Subjects: | |
| Publisher: | England: BMJ Publishing Group Ltd |
| ID: | ISSN: 0022-3050 |
| Link: | https://www.ncbi.nlm.nih.gov/pubmed/24163429 |
| Zum Text: |
SendSend as email
Add to Book BagAdd to Book Bag
Staff View
| recordid: | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4018226 |
| title: | APOE associations with severe CAA-associated vasculopathic changes: collaborative meta-analysis |
| format: | Article |
| creator: |
|
| subjects: |
|
| ispartof: | Journal of neurology, neurosurgery and psychiatry, 2014-03, Vol.85 (3), p.300-305 |
| description: | Objectives Cerebral amyloid angiopathy (CAA) is associated with lobar intracerebral haemorrhage (ICH). While only the ε4 allele of the apolipoprotein E (APOE) gene is associated with the presence of CAA, both APOE-ε4 and ε2 are associated with lobar ICH. The generally accepted explanation is that APOE-ε4 promotes vascular amyloid deposition, while APOE-ε2 promotes progression to severe CAA with associated vasculopathic changes that cause vessel rupture and ICH. We assessed the evidence for these allele-specific effects. Methods We systematically identified published studies with data on APOE genotype and histopathological assessment of postmortem brains for CAA severity. We obtained unpublished data from these for meta-analyses of the effects of ε4-containing (ε4+) and ε2-containing (ε2+) genotypes on progression to severe CAA. Results Of six eligible studies (543 eligible participants), data were available from 5 (497 participants, 353 with CAA). Meta-analyses showed a possible association of ε4+ genotypes with severe CAA (ε4+ vs ε4−: severe vs mild/moderate CAA, OR 2.5, 95% CI 1.4 to 4.5, p=0.002; severe vs moderate CAA, OR 1.7, 95% CI 0.9 to 3.1, p=0.11). For ε2+ versus ε2− genotypes, there was no significant association, but the very small number of participants with ε2+ genotypes (22) precluded reliable estimates. Conclusions We found a possible association of severe CAA with APOE-ε4 but not APOE-ε2. However, our findings do not exclude a biologically meaningful association between APOE-ε2 and severe CAA. Further work is needed to elucidate fully the allele-specific associations of APOE with CAA and their mechanisms. |
| language: | eng |
| source: | |
| identifier: | ISSN: 0022-3050 |
| fulltext: | no_fulltext |
| issn: |
|
| url: | Link |
| @attributes |
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| PrimoNMBib |
|