<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Salminen LE</submitter><funding>NIH/National Institute of Neurological Disorders and Stroke</funding><funding>NCATS NIH HHS</funding><funding>NIH/National Institute of Mental Health</funding><funding>NIA NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>Australian National Health and Medical Research Council</funding><funding>National Institutes of Health (NIH)/National Institute on Aging</funding><pagination>111-119</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5515475</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>329</volume><pubmed_abstract>Oxidative stress is a key mechanism of the aging process that can cause damage to brain white matter and cognitive functions. Polymorphisms in the superoxide dismutase 2 (SOD2) and catalase (CAT) genes have been associated with abnormalities in antioxidant enzyme activity in the aging brain, suggesting a risk for enhanced oxidative damage to white matter and cognition among older individuals with these genetic variants. The present study compared differences in white matter microstructure and cognition among 96 older adults with and without genetic risk factors of SOD2 (rs4880) and CAT (rs1001179). Results revealed higher radial diffusivity in the anterior thalamic radiation among SOD2 CC genotypes compared to CT/TT genotypes. Further, the CC genotype moderated the relationship between the</pubmed_abstract><journal>Behavioural brain research</journal><pubmed_title>Vulnerability of white matter tracts and cognition to the SOD2 polymorphism: A preliminary study of antioxidant defense genes in brain aging.</pubmed_title><pmcid>PMC5515475</pmcid><funding_grant_id>R01 NS039538</funding_grant_id><funding_grant_id>5F31AG050450</funding_grant_id><funding_grant_id>R01 NS052470</funding_grant_id><funding_grant_id>R01NS052470</funding_grant_id><funding_grant_id>R21MH090494</funding_grant_id><funding_grant_id>UL1 TR002345</funding_grant_id><funding_grant_id>F31 AG050450</funding_grant_id><funding_grant_id>R21 MH105822</funding_grant_id><funding_grant_id>1037196</funding_grant_id><funding_grant_id>R01NS039538</funding_grant_id><funding_grant_id>R21 MH090494</funding_grant_id><funding_grant_id>UL1 TR000448</funding_grant_id><pubmed_authors>Griffin MG</pubmed_authors><pubmed_authors>Salminen LE</pubmed_authors><pubmed_authors>Bolzenius JD</pubmed_authors><pubmed_authors>Schofield PR</pubmed_authors><pubmed_authors>Paul RH</pubmed_authors><pubmed_authors>Tate DF</pubmed_authors><pubmed_authors>Bruce SE</pubmed_authors><pubmed_authors>Conturo TE</pubmed_authors><pubmed_authors>Pierce KD</pubmed_authors><pubmed_authors>Cabeen RP</pubmed_authors><pubmed_authors>Laidlaw DH</pubmed_authors></additional><is_claimable>false</is_claimable><name>Vulnerability of white matter tracts and cognition to the SOD2 polymorphism: A preliminary study of antioxidant defense genes in brain aging.</name><description>Oxidative stress is a key mechanism of the aging process that can cause damage to brain white matter and cognitive functions. Polymorphisms in the superoxide dismutase 2 (SOD2) and catalase (CAT) genes have been associated with abnormalities in antioxidant enzyme activity in the aging brain, suggesting a risk for enhanced oxidative damage to white matter and cognition among older individuals with these genetic variants. The present study compared differences in white matter microstructure and cognition among 96 older adults with and without genetic risk factors of SOD2 (rs4880) and CAT (rs1001179). Results revealed higher radial diffusivity in the anterior thalamic radiation among SOD2 CC genotypes compared to CT/TT genotypes. Further, the CC genotype moderated the relationship between the</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Jun</publication><modification>2025-04-26T18:39:52.526Z</modification><creation>2019-03-26T23:44:04Z</creation></dates><accession>S-EPMC5515475</accession><cross_references><pubmed>28457881</pubmed><doi>10.1016/j.bbr.2017.04.041</doi></cross_references></HashMap>