{"doi":"10.1136/jnnp-2013-306485","title":"APOE associations with severe CAA-associated vasculopathic changes: collaborative meta-analysis","abstract":null,"journal":"Journal of Neurology, Neurosurgery & Psychiatry","year":2014,"id":602260,"datarank":0.7289718606542509,"base_score":4.859812404361672,"endowment":4.859812404361672,"self_citation_contribution":0.7289718606542509,"citation_network_contribution":0.0,"self_endowment_contribution":0.7289718606542509,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":128,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1544489,"name":"R. N. Kalaria","orcid":null,"position":1,"is_corresponding":false},{"id":1544490,"name":"S. M. Greenberg","orcid":null,"position":2,"is_corresponding":false},{"id":1544491,"name":"H. C. Chui","orcid":null,"position":3,"is_corresponding":false},{"id":1544494,"name":"F. A. Schmitt","orcid":null,"position":4,"is_corresponding":false},{"id":1544496,"name":"N. Samarasekera","orcid":null,"position":5,"is_corresponding":false},{"id":1544498,"name":"R. Al-Shahi Salman","orcid":null,"position":6,"is_corresponding":false},{"id":1544501,"name":"C. L. M. Sudlow","orcid":null,"position":7,"is_corresponding":false},{"id":1544488,"name":"K. Rannikmae","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"APOE associations with severe CAA-associated vasculopathic changes: collaborative meta-analysis","abstract":"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.","is_dataset_classified":null,"base_score":4.859812404361672,"endowment":4.859812404361672,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"24163429","pmcid":"PMC4018226","openalex_id":"https://openalex.org/W2117130548","authors":[],"funders":[{"funder_name":"Medical Research Council","grant_id":"G0400074","title":null},{"funder_name":"NIA NIH HHS","grant_id":"P30AG028383","title":null},{"funder_name":"NIA NIH HHS","grant_id":"R01 AG019241","title":null},{"funder_name":"Medical Research Council","grant_id":"MR/K026992/1","title":null},{"funder_name":"NIA NIH HHS","grant_id":"R01 AG038651","title":null},{"funder_name":"NICHD NIH HHS","grant_id":"R01 HD064993","title":null},{"funder_name":"Medical Research Council","grant_id":"G0700718B","title":null},{"funder_name":"Medical Research Council","grant_id":"G1100540","title":null},{"funder_name":"NIA NIH HHS","grant_id":"P50 AG005142","title":null},{"funder_name":"NIA NIH HHS","grant_id":"R01 AG026484","title":null},{"funder_name":"Medical Research Council","grant_id":"G0900652","title":null},{"funder_name":"Medical Research Council","grant_id":"G1002605","title":null},{"funder_name":"NIA NIH HHS","grant_id":"2R01AG26484","title":null},{"funder_name":"Medical Research Council","grant_id":"G0502157","title":null},{"funder_name":"Medical Research Council","grant_id":"G0900428","title":null}],"total_grants":15,"fwci":4.8635,"citation_percentile":0.95597507,"influential_citations":0,"citation_trend":[{"year":2014,"count":7},{"year":2015,"count":12},{"year":2016,"count":6},{"year":2017,"count":4},{"year":2018,"count":9},{"year":2019,"count":10},{"year":2020,"count":7},{"year":2021,"count":12},{"year":2022,"count":17},{"year":2023,"count":8},{"year":2024,"count":15},{"year":2025,"count":11},{"year":2026,"count":10}],"oa_status":"green","license":null,"oa_locations":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/4018226","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/4018226","host_type":"repository"},{"url":"https://syndication.highwire.org/content/doi/10.1136/jnnp-2013-306485","host_type":"publisher"},{"url":"https://doi.org/10.1136/jnnp-2013-306485","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/24163429","host_type":"repository"},{"url":"http://jnnp.bmj.com/cgi/content/short/85/3/300","host_type":"repository"}],"fields_of_study":["Intracerebral and Subarachnoid Hemorrhage Research","Alzheimer's disease research and treatments","Dementia and Cognitive Impairment Research","Aged","Aged, 80 and over","Apolipoprotein E2","Apolipoprotein E4","Apolipoproteins E","Cerebral Amyloid Angiopathy","Disease Progression","Female","Genetic Association Studies","Genotype","Humans","Intracranial Hemorrhages","Male","Severity of Illness Index"],"mesh_terms":["Aged","Aged, 80 and over","Apolipoproteins E","Female","Genotype","Humans","Male","Severity of Illness Index","Cerebral Amyloid Angiopathy","Disease Progression","Intracranial Hemorrhages","Apolipoprotein E4","Apolipoprotein E2","Genetic Association Studies"],"keywords":["Cerebral amyloid angiopathy","Apolipoprotein E","Genotype","Medicine","Allele","Internal medicine","Intracerebral hemorrhage","Pathology","Biology","Gene","Disease","Genetics","Dementia","Apolipoproteins","Amyloid","Meta-analysis","Cerebrovascular disease","Systematic Reviews"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Good health and well-being"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-07-29T18:51:18.894435Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}