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Higher education moderates the effect of T2 lesion load and third ventricle width on cognition in multiple sclerosis
Previous work suggested greater intellectual enrichment might moderate the negative impact of brain atrophy on cognition. This awaits confirmation in independent cohorts including investigation of the role of T2-lesion load (T2-LL), which is another important determinant of cognition in MS. We here...
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Published in: | PloS one 2014-01, Vol.9 (1), p.e87567-e87567 |
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creator | Pinter, Daniela Sumowski, James DeLuca, John Fazekas, Franz Pichler, Alexander Khalil, Michael Langkammer, Christian Fuchs, Siegrid Enzinger, Christian |
description | Previous work suggested greater intellectual enrichment might moderate the negative impact of brain atrophy on cognition. This awaits confirmation in independent cohorts including investigation of the role of T2-lesion load (T2-LL), which is another important determinant of cognition in MS. We here thus aimed to test this cognitive reserve hypothesis by investigating whether educational attainment (EA) moderates the negative effects of both brain atrophy and T2-LL on cognitive function in a large sample of MS patients.
137 patients participated in the study. Cognition was assessed by the "Brief Repeatable Battery of Neuropsychological Tests." T2-LL, normalized brain volume (global volume loss) and third ventricle width (regional volume loss) served as MRI markers.
Both T2-LL and atrophy predicted worse cognition, with a stronger effect of T2-LL. Higher EA (as assessed by years of education) also predicted better cognition. Interactions showed that the negative effects of T2-LL and regional brain atrophy were moderated by EA.
In a cohort with different stages of MS, higher EA attenuated the negative effects of white matter lesion burden and third ventricle width (suggestive of thalamic atrophy) on cognitive performance. Actively enhancing cognitive reserve might thus be a means to reduce or prevent cognitive problems in MS in parallel to disease modifying drugs. |
doi_str_mv | 10.1371/journal.pone.0087567 |
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137 patients participated in the study. Cognition was assessed by the "Brief Repeatable Battery of Neuropsychological Tests." T2-LL, normalized brain volume (global volume loss) and third ventricle width (regional volume loss) served as MRI markers.
Both T2-LL and atrophy predicted worse cognition, with a stronger effect of T2-LL. Higher EA (as assessed by years of education) also predicted better cognition. Interactions showed that the negative effects of T2-LL and regional brain atrophy were moderated by EA.
In a cohort with different stages of MS, higher EA attenuated the negative effects of white matter lesion burden and third ventricle width (suggestive of thalamic atrophy) on cognitive performance. Actively enhancing cognitive reserve might thus be a means to reduce or prevent cognitive problems in MS in parallel to disease modifying drugs.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0087567</identifier><identifier>PMID: 24475309</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Archives & records ; Atrophy ; Atrophy - pathology ; Batteries ; Biology ; Brain ; Brain research ; Cognition ; Cognition & reasoning ; Cognition Disorders - etiology ; Cognition Disorders - physiopathology ; Cognitive ability ; Drugs ; Education ; Educational attainment ; Educational Status ; Female ; Gender differences ; Higher education ; Humans ; Hypotheses ; Image Processing, Computer-Assisted ; Magnetic Resonance Imaging ; Male ; Medical research ; Medicine ; Middle Aged ; Multiple sclerosis ; Multiple Sclerosis - complications ; Multiple Sclerosis - physiopathology ; Neurology ; Neuropsychological Tests ; Neurosciences ; NMR ; Nuclear magnetic resonance ; Patients ; Regression Analysis ; Social and Behavioral Sciences ; Standard deviation ; Studies ; Substantia alba ; Thalamus ; Third Ventricle - pathology ; Variables ; Ventricle ; Ventricles (cerebral)</subject><ispartof>PloS one, 2014-01, Vol.9 (1), p.e87567-e87567</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Pinter et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Pinter et al 2014 Pinter et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-661ccbfd770af655a81e2cae3a129f6732990ebbcfe742b975f9649211c114403</citedby><cites>FETCH-LOGICAL-c692t-661ccbfd770af655a81e2cae3a129f6732990ebbcfe742b975f9649211c114403</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1492015089/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1492015089?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25751,27922,27923,37010,37011,44588,53789,53791,74896</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24475309$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Weber, Martin Sebastian</contributor><creatorcontrib>Pinter, Daniela</creatorcontrib><creatorcontrib>Sumowski, James</creatorcontrib><creatorcontrib>DeLuca, John</creatorcontrib><creatorcontrib>Fazekas, Franz</creatorcontrib><creatorcontrib>Pichler, Alexander</creatorcontrib><creatorcontrib>Khalil, Michael</creatorcontrib><creatorcontrib>Langkammer, Christian</creatorcontrib><creatorcontrib>Fuchs, Siegrid</creatorcontrib><creatorcontrib>Enzinger, Christian</creatorcontrib><title>Higher education moderates the effect of T2 lesion load and third ventricle width on cognition in multiple sclerosis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Previous work suggested greater intellectual enrichment might moderate the negative impact of brain atrophy on cognition. This awaits confirmation in independent cohorts including investigation of the role of T2-lesion load (T2-LL), which is another important determinant of cognition in MS. We here thus aimed to test this cognitive reserve hypothesis by investigating whether educational attainment (EA) moderates the negative effects of both brain atrophy and T2-LL on cognitive function in a large sample of MS patients.
137 patients participated in the study. Cognition was assessed by the "Brief Repeatable Battery of Neuropsychological Tests." T2-LL, normalized brain volume (global volume loss) and third ventricle width (regional volume loss) served as MRI markers.
Both T2-LL and atrophy predicted worse cognition, with a stronger effect of T2-LL. Higher EA (as assessed by years of education) also predicted better cognition. Interactions showed that the negative effects of T2-LL and regional brain atrophy were moderated by EA.
In a cohort with different stages of MS, higher EA attenuated the negative effects of white matter lesion burden and third ventricle width (suggestive of thalamic atrophy) on cognitive performance. Actively enhancing cognitive reserve might thus be a means to reduce or prevent cognitive problems in MS in parallel to disease modifying drugs.</description><subject>Adult</subject><subject>Archives & records</subject><subject>Atrophy</subject><subject>Atrophy - pathology</subject><subject>Batteries</subject><subject>Biology</subject><subject>Brain</subject><subject>Brain research</subject><subject>Cognition</subject><subject>Cognition & reasoning</subject><subject>Cognition Disorders - etiology</subject><subject>Cognition Disorders - physiopathology</subject><subject>Cognitive ability</subject><subject>Drugs</subject><subject>Education</subject><subject>Educational attainment</subject><subject>Educational Status</subject><subject>Female</subject><subject>Gender differences</subject><subject>Higher education</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Image Processing, Computer-Assisted</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Middle Aged</subject><subject>Multiple sclerosis</subject><subject>Multiple Sclerosis - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pinter, Daniela</au><au>Sumowski, James</au><au>DeLuca, John</au><au>Fazekas, Franz</au><au>Pichler, Alexander</au><au>Khalil, Michael</au><au>Langkammer, Christian</au><au>Fuchs, Siegrid</au><au>Enzinger, Christian</au><au>Weber, Martin Sebastian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Higher education moderates the effect of T2 lesion load and third ventricle width on cognition in multiple sclerosis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-01-27</date><risdate>2014</risdate><volume>9</volume><issue>1</issue><spage>e87567</spage><epage>e87567</epage><pages>e87567-e87567</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Previous work suggested greater intellectual enrichment might moderate the negative impact of brain atrophy on cognition. This awaits confirmation in independent cohorts including investigation of the role of T2-lesion load (T2-LL), which is another important determinant of cognition in MS. We here thus aimed to test this cognitive reserve hypothesis by investigating whether educational attainment (EA) moderates the negative effects of both brain atrophy and T2-LL on cognitive function in a large sample of MS patients.
137 patients participated in the study. Cognition was assessed by the "Brief Repeatable Battery of Neuropsychological Tests." T2-LL, normalized brain volume (global volume loss) and third ventricle width (regional volume loss) served as MRI markers.
Both T2-LL and atrophy predicted worse cognition, with a stronger effect of T2-LL. Higher EA (as assessed by years of education) also predicted better cognition. Interactions showed that the negative effects of T2-LL and regional brain atrophy were moderated by EA.
In a cohort with different stages of MS, higher EA attenuated the negative effects of white matter lesion burden and third ventricle width (suggestive of thalamic atrophy) on cognitive performance. Actively enhancing cognitive reserve might thus be a means to reduce or prevent cognitive problems in MS in parallel to disease modifying drugs.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24475309</pmid><doi>10.1371/journal.pone.0087567</doi><tpages>e87567</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Archives & records Atrophy Atrophy - pathology Batteries Biology Brain Brain research Cognition Cognition & reasoning Cognition Disorders - etiology Cognition Disorders - physiopathology Cognitive ability Drugs Education Educational attainment Educational Status Female Gender differences Higher education Humans Hypotheses Image Processing, Computer-Assisted Magnetic Resonance Imaging Male Medical research Medicine Middle Aged Multiple sclerosis Multiple Sclerosis - complications Multiple Sclerosis - physiopathology Neurology Neuropsychological Tests Neurosciences NMR Nuclear magnetic resonance Patients Regression Analysis Social and Behavioral Sciences Standard deviation Studies Substantia alba Thalamus Third Ventricle - pathology Variables Ventricle Ventricles (cerebral) |
title | Higher education moderates the effect of T2 lesion load and third ventricle width on cognition in multiple sclerosis |
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