<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Altendahl M</submitter><funding>American Heart Association</funding><funding>National Institute of Neurological Disorders and Stroke</funding><funding>NIA NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>National Institute on Aging</funding><pagination>e0227835</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6980497</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(1)</volume><pubmed_abstract>Chronic systemic sterile inflammation is implicated in the pathogenesis of cerebrovascular disease and white matter injury. Non-invasive blood markers for risk stratification and dissection of inflammatory molecular substrates in vivo are lacking. We sought to identify whether an interconnected network of inflammatory biomarkers centered on IL-18 and all previously associated with white matter lesions could detect overt and antecedent white matter changes in two populations at risk for cerebral small vessel disease. In a cohort of 167 older adults (mean age: 76, SD 7.1, 83 females) that completed a cognitive battery, physical examination, and blood draw in parallel with MR imaging including DTI, we measured cerebral white matter hyperintensities (WMH) and free water (FW). Concurrently, ser</pubmed_abstract><journal>PloS one</journal><pubmed_title>An IL-18-centered inflammatory network as a biomarker for cerebral white matter injury.</pubmed_title><pmcid>PMC6980497</pmcid><funding_grant_id>UH3NS100608</funding_grant_id><funding_grant_id>UH3 NS100608</funding_grant_id><funding_grant_id>P30 AG062422</funding_grant_id><funding_grant_id>T32 AG023481</funding_grant_id><funding_grant_id>16GRNT31080021</funding_grant_id><funding_grant_id>RF1 AG032289</funding_grant_id><funding_grant_id>R01 AG032289</funding_grant_id><funding_grant_id>AG062422</funding_grant_id><funding_grant_id>T35 AG026736</funding_grant_id><funding_grant_id>#15CRP22900006</funding_grant_id><funding_grant_id>AG010129</funding_grant_id><funding_grant_id>R01 AG048234</funding_grant_id><funding_grant_id>P30 AG010129</funding_grant_id><funding_grant_id>UH2 NS100608</funding_grant_id><pubmed_authors>Elahi F</pubmed_authors><pubmed_authors>Kakarla V</pubmed_authors><pubmed_authors>Elashoff D</pubmed_authors><pubmed_authors>Singh B</pubmed_authors><pubmed_authors>Walters S</pubmed_authors><pubmed_authors>Leng M</pubmed_authors><pubmed_authors>Kramer JH</pubmed_authors><pubmed_authors>You M</pubmed_authors><pubmed_authors>Maillard P</pubmed_authors><pubmed_authors>Wolf A</pubmed_authors><pubmed_authors>Xiao G</pubmed_authors><pubmed_authors>Fox E</pubmed_authors><pubmed_authors>Cotter D</pubmed_authors><pubmed_authors>Hinman JD</pubmed_authors><pubmed_authors>Harvey D</pubmed_authors><pubmed_authors>Azizkhanian I</pubmed_authors><pubmed_authors>Altendahl M</pubmed_authors><pubmed_authors>Sheth SA</pubmed_authors><pubmed_authors>Decarli C</pubmed_authors></additional><is_claimable>false</is_claimable><name>An IL-18-centered inflammatory network as a biomarker for cerebral white matter injury.</name><description>Chronic systemic sterile inflammation is implicated in the pathogenesis of cerebrovascular disease and white matter injury. Non-invasive blood markers for risk stratification and dissection of inflammatory molecular substrates in vivo are lacking. We sought to identify whether an interconnected network of inflammatory biomarkers centered on IL-18 and all previously associated with white matter lesions could detect overt and antecedent white matter changes in two populations at risk for cerebral small vessel disease. In a cohort of 167 older adults (mean age: 76, SD 7.1, 83 females) that completed a cognitive battery, physical examination, and blood draw in parallel with MR imaging including DTI, we measured cerebral white matter hyperintensities (WMH) and free water (FW). Concurrently, ser</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020</publication><modification>2025-04-22T20:18:57.115Z</modification><creation>2020-05-22T09:22:44Z</creation></dates><accession>S-EPMC6980497</accession><cross_references><pubmed>31978079</pubmed><doi>10.1371/journal.pone.0227835</doi></cross_references></HashMap>