{"doi":"10.1016/j.jalz.2016.06.875","title":"P1‐127: Assessing Trem2 Risk Variants in Alzheimer's Disease with RNA‐SEQ","abstract":null,"journal":"Alzheimer's &amp; Dementia","year":2016,"id":624092,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":0,"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":598781,"name":"Hong Wang","orcid":"0000-0002-0213-3523","position":1,"is_corresponding":false},{"id":1510638,"name":"John Ryder","orcid":null,"position":2,"is_corresponding":false},{"id":117939,"name":"David A. Collier","orcid":null,"position":3,"is_corresponding":false},{"id":1510639,"name":"Michael J. O'Neill","orcid":null,"position":4,"is_corresponding":false},{"id":1613190,"name":"Richard JB. Dobson","orcid":null,"position":5,"is_corresponding":false},{"id":1510641,"name":"Stephen J. Newhouse","orcid":null,"position":6,"is_corresponding":false},{"id":1510637,"name":"Guillermo Carbajosa","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"P1‐127: Assessing Trem2 Risk Variants in Alzheimer's Disease with RNA‐SEQ","abstract":"Rare heterozygous variants in the Triggering Receptor Expressed on Myeloid cells 2 (TREM2) gene are associated with increased susceptibility to late-onset Alzheimer's disease, with an odds ratio of about 3, a similar risk to the common ApoE4 allele, the strongest known single genetic risk factor for Alzheimer's disease (AD). It has been proposed that TREM2 is able to detect damage-associated lipid patterns associated with neurodegeneration, sustaining the microglial response to Aβ accumulation. Previous reports analyzing microarray gene expression data in postmortem brain have described a TREM2-associated mRNA co-expression network enriched for innate immunity and microgial expressed genes to be perturbed in AD brain. Despite these reports TREM2 has yet to be extensively studied. Furthermore, all the previous studies established co-expression networks did not directly study expression levels for individuals that were TREM2 variant positive (TREM2+), that is they did not observe the effects of the AD-associated variants themselves. Our project involves RNA sequencing (RNAseq) on brain tissue using human brain samples with rare TREM2 risk variants, and also on a parallel mouse model using TREM2 KO mice brain samples analyzed at 4 and 8 months of age. To further link the studies to an AD relevant model we also generated RNAseq data for various time points for the tg4510 tau transgenic model. The work will be followed up by further in vitro an in vivo studies to further understand the function of TREM2. We will report on the progress of the project which will include bioinformatic analyses on the TREM2 KO RNAseq mice data. These initial efforts will focus on characterizing the gene and network level changes. Overall the key goal of our project is to gain an understanding of the TREM2 biology, the functional impact of TREM variants in AD and elucidate how TREM2 impacts inflammation in the central nervous system. We intend to achieve this goal using transcriptome RNAseq data on both human brain samples harboring the rare TREM2 risk variant and mouse model systems and further use these model systems to validate our findings. By accomplishing it we hope to make an important contribution to our understanding of AD pathogenesis.","is_dataset_classified":null,"base_score":0.0,"endowment":0.0,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"19910364","pmcid":null,"openalex_id":"https://openalex.org/W2532570235","authors":[],"funders":[],"total_grants":0,"fwci":0.0,"citation_percentile":0.11817238,"influential_citations":0,"citation_trend":[],"oa_status":"closed","license":"http://onlinelibrary.wiley.com/termsAndConditions#vor","oa_locations":[{"url":"https://api.elsevier.com/content/article/PII:S1552526016311773?httpAccept=text/xml","host_type":"publisher"},{"url":"https://api.elsevier.com/content/article/PII:S1552526016311773?httpAccept=text/plain","host_type":"publisher"},{"url":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1016%2Fj.jalz.2016.06.875","host_type":"publisher"},{"url":"https://onlinelibrary.wiley.com/doi/pdf/10.1016/j.jalz.2016.06.875","host_type":"publisher"},{"url":"https://onlinelibrary.wiley.com/doi/full-xml/10.1016/j.jalz.2016.06.875","host_type":"publisher"},{"url":"https://alz-journals.onlinelibrary.wiley.com/doi/pdf/10.1016/j.jalz.2016.06.875","host_type":"publisher"},{"url":"https://doi.org/10.1016/j.jalz.2016.06.875","host_type":"journal"}],"fields_of_study":["Neuroinflammation and Neurodegeneration Mechanisms","Neurological Disease Mechanisms and Treatments","Inflammation biomarkers and pathways"],"mesh_terms":[],"keywords":["TREM2","Neurodegeneration","Biology","Disease","Gene","Microarray analysis techniques","Allele","Microarray","Genetics","Gene expression","Computational biology","Neuroscience","Receptor","Medicine","Internal medicine"],"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":"2026-08-04T02:36:58.410452Z","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":[]}