{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Branciamore S"],"funding":["National Library of Medicine","NIA NIH HHS","NIMH NIH HHS","National Cancer Institute","NCI NIH HHS","NINDS NIH HHS","NLM NIH HHS","National Institute on Aging"],"pagination":["14954"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11213882"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["While there are currently over 40 replicated genes with mapped risk alleles for Late Onset Alzheimer's disease (LOAD), the Apolipoprotein E locus E4 haplotype is still the biggest driver of risk, with odds ratios for neuropathologically confirmed E44 carriers exceeding 30 (95% confidence interval 16.59-58.75). We sought to address whether the APOE E4 haplotype modifies expression globally through networks of expression to increase LOAD risk. We have used the Human Brainome data to build expression networks comparing APOE E4 carriers to non-carriers using scalable mixed-datatypes Bayesian network (BN) modeling. We have found that VGF had the greatest explanatory weight. High expression of VGF is a protective signal, even on the background of APOE E4 alleles. LOAD risk signals, considering a"],"journal":["Scientific reports"],"pubmed_title":["Changes in expression of VGF, SPECC1L, HLA-DRA and RANBP3L act with APOE E4 to alter risk for late onset Alzheimer's disease."],"pmcid":["PMC11213882"],"funding_grant_id":["P30 AG013846","P50 AG005128","R01 LM013138","P30 AG053760","P50 AG005134","P50 AG005146","P50 AG005136","U01 AG016976","P30 CA033572","AG069008","P30 AG010161","P50 AG005681","P30CA033572","P50 AG005144","P30 AG072980","R01 AG069008","R01LM013138","P50 MH060451","P30 AG019610","P50 NS039764","P50 AG016570"],"pubmed_authors":["Rodin AS","Branciamore S","Gogoshin G","Myers AJ"],"additional_accession":[]},"is_claimable":false,"name":"Changes in expression of VGF, SPECC1L, HLA-DRA and RANBP3L act with APOE E4 to alter risk for late onset Alzheimer's disease.","description":"While there are currently over 40 replicated genes with mapped risk alleles for Late Onset Alzheimer's disease (LOAD), the Apolipoprotein E locus E4 haplotype is still the biggest driver of risk, with odds ratios for neuropathologically confirmed E44 carriers exceeding 30 (95% confidence interval 16.59-58.75). We sought to address whether the APOE E4 haplotype modifies expression globally through networks of expression to increase LOAD risk. We have used the Human Brainome data to build expression networks comparing APOE E4 carriers to non-carriers using scalable mixed-datatypes Bayesian network (BN) modeling. We have found that VGF had the greatest explanatory weight. High expression of VGF is a protective signal, even on the background of APOE E4 alleles. LOAD risk signals, considering a","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2026-05-29T17:37:05.364Z","creation":"2026-04-08T05:36:55.447Z"},"accession":"S-EPMC11213882","cross_references":{"pubmed":["38942763"],"doi":["10.1038/s41598-024-65010-7"]}}