<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kochunov P</submitter><funding>NIBIB NIH HHS</funding><funding>NIDA NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>NIAAA NIH HHS</funding><funding>PHS HHS</funding><pagination>41-9</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3144306</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>58(1)</volume><pubmed_abstract>We examined age trajectories of fractional anisotropy (FA) of cerebral white matter (WM) and thickness of cortical gray matter (GM) in 1031 healthy human subjects (aged 11-90 years). Whole-brain FA and GM thickness values followed quadratic trajectories with age but the relationship between them was linear, indicating that a putative biological mechanism may explain the non-linearity of their age trajectories. Inclusion of the FA values into the quadratic model of the whole-brain and regional GM thickness changes with age made the effect of the age(2) term no longer significant for the whole-brain GM thickness and greatly reduced its significance for regional GM thickness measurements. The phylogenetic order of cerebral myelination helped to further explain the intersubject variability in GM thickness. FA values for the early maturing WM were significantly better (p=10(-6)) at explaining variability in GM thickness in maturing (aged 11-20) subjects than FA values for the late maturing WM. The opposite trend was observed for aging subjects (aged 40-90) where FA values for the late maturing WM were better (p=10(-16)) at explaining the variability in GM thickness. We concluded that the non-linearity of the age trajectory for GM thickness, measured from T1-weighted MRI, was partially explained by the heterogeneity and the heterochronicity of the age-related changes in the microintegrity of cerebral WM. We consider these findings as the evidence that the measurements of age-related changes in GM thickness and FA are driven, in part, by a common biological mechanism, presumed to be related to changes in cerebral myelination.</pubmed_abstract><journal>NeuroImage</journal><pubmed_title>Fractional anisotropy of cerebral white matter and thickness of cortical gray matter across the lifespan.</pubmed_title><pmcid>PMC3144306</pmcid><funding_grant_id>R01 MH083824</funding_grant_id><funding_grant_id>R01 MH078111</funding_grant_id><funding_grant_id>MH0708143</funding_grant_id><funding_grant_id>K01EB006395</funding_grant_id><funding_grant_id>K01 EB006395-05</funding_grant_id><funding_grant_id>K01 EB006395</funding_grant_id><funding_grant_id>R01AA016274</funding_grant_id><funding_grant_id>P20 MH/DA52176</funding_grant_id><funding_grant_id>MH083824</funding_grant_id><funding_grant_id>HSC19940074H</funding_grant_id><funding_grant_id>K01 EB006395-04</funding_grant_id><funding_grant_id>K01 EB006395-03</funding_grant_id><funding_grant_id>R01 AA016274</funding_grant_id><funding_grant_id>MH078111</funding_grant_id><funding_grant_id>K01 EB006395-02</funding_grant_id><pubmed_authors>Fox P</pubmed_authors><pubmed_authors>Rogers B</pubmed_authors><pubmed_authors>Williamson DE</pubmed_authors><pubmed_authors>Kochunov V</pubmed_authors><pubmed_authors>Blangero J</pubmed_authors><pubmed_authors>Glahn DC</pubmed_authors><pubmed_authors>Thompson PM</pubmed_authors><pubmed_authors>Kochunov P</pubmed_authors><pubmed_authors>Lancaster J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Fractional anisotropy of cerebral white matter and thickness of cortical gray matter across the lifespan.</name><description>We examined age trajectories of fractional anisotropy (FA) of cerebral white matter (WM) and thickness of cortical gray matter (GM) in 1031 healthy human subjects (aged 11-90 years). Whole-brain FA and GM thickness values followed quadratic trajectories with age but the relationship between them was linear, indicating that a putative biological mechanism may explain the non-linearity of their age trajectories. Inclusion of the FA values into the quadratic model of the whole-brain and regional GM thickness changes with age made the effect of the age(2) term no longer significant for the whole-brain GM thickness and greatly reduced its significance for regional GM thickness measurements. The phylogenetic order of cerebral myelination helped to further explain the intersubject variability in GM thickness. FA values for the early maturing WM were significantly better (p=10(-6)) at explaining variability in GM thickness in maturing (aged 11-20) subjects than FA values for the late maturing WM. The opposite trend was observed for aging subjects (aged 40-90) where FA values for the late maturing WM were better (p=10(-16)) at explaining the variability in GM thickness. We concluded that the non-linearity of the age trajectory for GM thickness, measured from T1-weighted MRI, was partially explained by the heterogeneity and the heterochronicity of the age-related changes in the microintegrity of cerebral WM. We consider these findings as the evidence that the measurements of age-related changes in GM thickness and FA are driven, in part, by a common biological mechanism, presumed to be related to changes in cerebral myelination.</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Sep</publication><modification>2021-02-20T17:10:03Z</modification><creation>2019-03-27T03:07:25Z</creation></dates><accession>S-EPMC3144306</accession><cross_references><pubmed>21640837</pubmed><doi>10.1016/j.neuroimage.2011.05.050</doi></cross_references></HashMap>