<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Dos Reis RS</submitter><funding>Conselho Nacional de Desenvolvimento Científico e Tecnológico</funding><funding>NINDS NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIH HHS</funding><pagination>107</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11043047</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(1)</volume><pubmed_abstract>Neuroinflammation and synaptodendritic damage represent the pathological hallmarks of HIV-1 associated cognitive disorders (HAND). The post-synaptic protein neurogranin (Nrgn) is significantly reduced in the frontal cortex of postmortem brains from people with HIV (PWH) and it is associated with inflammatory factors released by infected microglia/macrophages. However, the mechanism involved in synaptic loss have yet to be elucidated. In this study, we characterized a newly identified long non-coding RNA (lncRNA) transcript (RP11-677M14.2), which is antisense to the NRGN locus and is highly expressed in the frontal cortex of HIV-1 individuals. Further analysis indicates an inverse correlation between the expression of RP11-677M14.2 RNA and Nrgn mRNA. Additionally, the Nrgn-lncRNA axis is dy</pubmed_abstract><journal>Journal of neuroinflammation</journal><pubmed_title>Neuroinflammation driven by human immunodeficiency virus-1 (HIV-1) directs the expression of long noncoding RNA RP11-677M14.2 resulting in dysregulation of neurogranin in vivo and in vitro.</pubmed_title><pmcid>PMC11043047</pmcid><funding_grant_id>R24 NS104160</funding_grant_id><funding_grant_id>R56 NS122567</funding_grant_id><funding_grant_id>R56NS122567</funding_grant_id><funding_grant_id>221281/2014-2</funding_grant_id><pubmed_authors>Dos Reis RS</pubmed_authors><pubmed_authors>Wagner MCE</pubmed_authors><pubmed_authors>Ayyavoo V</pubmed_authors><pubmed_authors>McKenna S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Neuroinflammation driven by human immunodeficiency virus-1 (HIV-1) directs the expression of long noncoding RNA RP11-677M14.2 resulting in dysregulation of neurogranin in vivo and in vitro.</name><description>Neuroinflammation and synaptodendritic damage represent the pathological hallmarks of HIV-1 associated cognitive disorders (HAND). The post-synaptic protein neurogranin (Nrgn) is significantly reduced in the frontal cortex of postmortem brains from people with HIV (PWH) and it is associated with inflammatory factors released by infected microglia/macrophages. However, the mechanism involved in synaptic loss have yet to be elucidated. In this study, we characterized a newly identified long non-coding RNA (lncRNA) transcript (RP11-677M14.2), which is antisense to the NRGN locus and is highly expressed in the frontal cortex of HIV-1 individuals. Further analysis indicates an inverse correlation between the expression of RP11-677M14.2 RNA and Nrgn mRNA. Additionally, the Nrgn-lncRNA axis is dy</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Apr</publication><modification>2025-04-22T20:44:19.994Z</modification><creation>2025-04-06T03:15:19.838Z</creation></dates><accession>S-EPMC11043047</accession><cross_references><pubmed>38659061</pubmed><doi>10.1186/s12974-024-03102-x</doi></cross_references></HashMap>