Alterations in frontal white matter neurochemistry and microstructure in schizophrenia: implications for neuroinflammation
We investigated in vivo neurochemical markers reflective of neuronal health and glial activation to determine if these could yield clues regarding the reduced fractional anisotropy (FA) of white matter and accelerated decline of FA with age in schizophrenia. Participants with schizophrenia and healt...
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| Veröffentlicht in: | Translational psychiatry 2015-04, Vol.5 (4), p.e548-e548 |
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| creator | Chiappelli, J Hong, L E Wijtenburg, S A Du, X Gaston, F Kochunov, P Rowland, L M |
| description | We investigated
in vivo
neurochemical markers reflective of neuronal health and glial activation to determine if these could yield clues regarding the reduced fractional anisotropy (FA) of white matter and accelerated decline of FA with age in schizophrenia. Participants with schizophrenia and healthy controls completed diffusion tensor imaging to assess FA and proton magnetic resonance spectroscopy to assess neurochemical metabolites in the same frontal region. Frontal FA was significantly lower in the schizophrenia and declined more rapidly with age compared with the healthy control group. In both groups,
N
-acetylaspartate (NAA), a putative marker of neuronal integrity, and glutamate declined with age, and this decline was stronger in patients. Myo-inositol, a marker of glial cells, was negatively related to FA in both groups. The relationship between FA and age remained significant in schizophrenia even when controlling for all metabolites. The relationships of FA, NAA and myo-inositol to age appear to be independent of one another. The relationship between FA and myo-inositol was independently present in both patients and controls, even after controlling for age, indicating a potential general effect of neuroinflammation on white matter microstructure. Further studies are warranted to determine the underlying mechanism driving the accelerated FA decline with age in schizophrenia. |
| doi_str_mv | 10.1038/tp.2015.43 |
| format | Article |
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in vivo
neurochemical markers reflective of neuronal health and glial activation to determine if these could yield clues regarding the reduced fractional anisotropy (FA) of white matter and accelerated decline of FA with age in schizophrenia. Participants with schizophrenia and healthy controls completed diffusion tensor imaging to assess FA and proton magnetic resonance spectroscopy to assess neurochemical metabolites in the same frontal region. Frontal FA was significantly lower in the schizophrenia and declined more rapidly with age compared with the healthy control group. In both groups,
N
-acetylaspartate (NAA), a putative marker of neuronal integrity, and glutamate declined with age, and this decline was stronger in patients. Myo-inositol, a marker of glial cells, was negatively related to FA in both groups. The relationship between FA and age remained significant in schizophrenia even when controlling for all metabolites. The relationships of FA, NAA and myo-inositol to age appear to be independent of one another. The relationship between FA and myo-inositol was independently present in both patients and controls, even after controlling for age, indicating a potential general effect of neuroinflammation on white matter microstructure. Further studies are warranted to determine the underlying mechanism driving the accelerated FA decline with age in schizophrenia.</description><identifier>ISSN: 2158-3188</identifier><identifier>EISSN: 2158-3188</identifier><identifier>DOI: 10.1038/tp.2015.43</identifier><identifier>PMID: 25871973</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>59/57 ; 692/699/476/1799 ; Adult ; Age Factors ; Anisotropy ; Aspartic Acid - analogs & derivatives ; Aspartic Acid - metabolism ; Behavioral Sciences ; Biological Psychology ; Case-Control Studies ; Choline - metabolism ; Creatine - metabolism ; Diffusion Tensor Imaging ; Female ; Frontal Lobe - metabolism ; Frontal Lobe - pathology ; Glutamic Acid - metabolism ; Humans ; Inflammation ; Inositol - metabolism ; Magnetic Resonance Spectroscopy ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Neuroglia - metabolism ; Neurosciences ; Original ; original-article ; Pharmacotherapy ; Psychiatry ; Schizophrenia - metabolism ; Schizophrenia - pathology ; White Matter - metabolism ; White Matter - pathology ; Young Adult</subject><ispartof>Translational psychiatry, 2015-04, Vol.5 (4), p.e548-e548</ispartof><rights>The Author(s) 2015</rights><rights>Copyright Nature Publishing Group Apr 2015</rights><rights>Copyright © 2015 Macmillan Publishers Limited 2015 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-56ebede55e861d4057a0923e0c29053838218bc106df51584396071f824af9d63</citedby><cites>FETCH-LOGICAL-c508t-56ebede55e861d4057a0923e0c29053838218bc106df51584396071f824af9d63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4462606/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4462606/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,41120,42189,51576,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25871973$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chiappelli, J</creatorcontrib><creatorcontrib>Hong, L E</creatorcontrib><creatorcontrib>Wijtenburg, S A</creatorcontrib><creatorcontrib>Du, X</creatorcontrib><creatorcontrib>Gaston, F</creatorcontrib><creatorcontrib>Kochunov, P</creatorcontrib><creatorcontrib>Rowland, L M</creatorcontrib><title>Alterations in frontal white matter neurochemistry and microstructure in schizophrenia: implications for neuroinflammation</title><title>Translational psychiatry</title><addtitle>Transl Psychiatry</addtitle><addtitle>Transl Psychiatry</addtitle><description>We investigated
in vivo
neurochemical markers reflective of neuronal health and glial activation to determine if these could yield clues regarding the reduced fractional anisotropy (FA) of white matter and accelerated decline of FA with age in schizophrenia. Participants with schizophrenia and healthy controls completed diffusion tensor imaging to assess FA and proton magnetic resonance spectroscopy to assess neurochemical metabolites in the same frontal region. Frontal FA was significantly lower in the schizophrenia and declined more rapidly with age compared with the healthy control group. In both groups,
N
-acetylaspartate (NAA), a putative marker of neuronal integrity, and glutamate declined with age, and this decline was stronger in patients. Myo-inositol, a marker of glial cells, was negatively related to FA in both groups. The relationship between FA and age remained significant in schizophrenia even when controlling for all metabolites. The relationships of FA, NAA and myo-inositol to age appear to be independent of one another. The relationship between FA and myo-inositol was independently present in both patients and controls, even after controlling for age, indicating a potential general effect of neuroinflammation on white matter microstructure. Further studies are warranted to determine the underlying mechanism driving the accelerated FA decline with age in schizophrenia.</description><subject>59/57</subject><subject>692/699/476/1799</subject><subject>Adult</subject><subject>Age Factors</subject><subject>Anisotropy</subject><subject>Aspartic Acid - analogs & derivatives</subject><subject>Aspartic Acid - metabolism</subject><subject>Behavioral Sciences</subject><subject>Biological Psychology</subject><subject>Case-Control Studies</subject><subject>Choline - metabolism</subject><subject>Creatine - metabolism</subject><subject>Diffusion Tensor Imaging</subject><subject>Female</subject><subject>Frontal Lobe - metabolism</subject><subject>Frontal Lobe - pathology</subject><subject>Glutamic Acid - metabolism</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inositol - metabolism</subject><subject>Magnetic Resonance Spectroscopy</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Neuroglia - metabolism</subject><subject>Neurosciences</subject><subject>Original</subject><subject>original-article</subject><subject>Pharmacotherapy</subject><subject>Psychiatry</subject><subject>Schizophrenia - metabolism</subject><subject>Schizophrenia - pathology</subject><subject>White Matter - metabolism</subject><subject>White Matter - pathology</subject><subject>Young Adult</subject><issn>2158-3188</issn><issn>2158-3188</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNplkctu1DAUhi1E1VZtN30AFIkNAs3gexwWSFVFAakSG1hbHuekcZXYwXaK2qfH6UyrgXrjy_-d3-eC0DnBa4KZ-pinNcVErDl7hY4pEWrFiFKv985H6CylW1yW4IrU5BAdUaFq0tTsGD1cDBmiyS74VDlfdTH4bIbqT-8yVKPJRa08zDHYHkaXcryvjG-r0dkYym22eY6wRCbbu4cw9RG8M58qN06DszvjLuxMnO8GM46Pz6fooDNDgrPdfoJ-XX35efltdf3j6_fLi-uVFVjllZCwgRaEACVJy7GoDW4oA2xpgwVTTFGiNpZg2Xai1MxZI3FNOkW56ZpWshP0ees7zZsRWgs-RzPoKbrRxHsdjNP_Kt71-ibcac4llXgxeLcziOH3DCnr0ggLw2A8hDlpImtWN4xKUdC3_6G3YY6-lKdJ3RDCMOO8UO-31NLDFKF7ToZgvUxV50kvU9WcFfjNfvrP6NMMC_BhC6Qi-RuIe3--tPsLARiuiQ</recordid><startdate>20150414</startdate><enddate>20150414</enddate><creator>Chiappelli, J</creator><creator>Hong, L E</creator><creator>Wijtenburg, S A</creator><creator>Du, X</creator><creator>Gaston, F</creator><creator>Kochunov, P</creator><creator>Rowland, L M</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150414</creationdate><title>Alterations in frontal white matter neurochemistry and microstructure in schizophrenia: implications for neuroinflammation</title><author>Chiappelli, J ; Hong, L E ; Wijtenburg, S A ; Du, X ; Gaston, F ; Kochunov, P ; Rowland, L M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-56ebede55e861d4057a0923e0c29053838218bc106df51584396071f824af9d63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>59/57</topic><topic>692/699/476/1799</topic><topic>Adult</topic><topic>Age Factors</topic><topic>Anisotropy</topic><topic>Aspartic Acid - analogs & derivatives</topic><topic>Aspartic Acid - metabolism</topic><topic>Behavioral Sciences</topic><topic>Biological Psychology</topic><topic>Case-Control Studies</topic><topic>Choline - metabolism</topic><topic>Creatine - metabolism</topic><topic>Diffusion Tensor Imaging</topic><topic>Female</topic><topic>Frontal Lobe - metabolism</topic><topic>Frontal Lobe - pathology</topic><topic>Glutamic Acid - metabolism</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inositol - metabolism</topic><topic>Magnetic Resonance Spectroscopy</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Neuroglia - metabolism</topic><topic>Neurosciences</topic><topic>Original</topic><topic>original-article</topic><topic>Pharmacotherapy</topic><topic>Psychiatry</topic><topic>Schizophrenia - metabolism</topic><topic>Schizophrenia - pathology</topic><topic>White Matter - metabolism</topic><topic>White Matter - pathology</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chiappelli, J</creatorcontrib><creatorcontrib>Hong, L E</creatorcontrib><creatorcontrib>Wijtenburg, S A</creatorcontrib><creatorcontrib>Du, X</creatorcontrib><creatorcontrib>Gaston, F</creatorcontrib><creatorcontrib>Kochunov, P</creatorcontrib><creatorcontrib>Rowland, L M</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Translational psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chiappelli, J</au><au>Hong, L E</au><au>Wijtenburg, S A</au><au>Du, X</au><au>Gaston, F</au><au>Kochunov, P</au><au>Rowland, L M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alterations in frontal white matter neurochemistry and microstructure in schizophrenia: implications for neuroinflammation</atitle><jtitle>Translational psychiatry</jtitle><stitle>Transl Psychiatry</stitle><addtitle>Transl Psychiatry</addtitle><date>2015-04-14</date><risdate>2015</risdate><volume>5</volume><issue>4</issue><spage>e548</spage><epage>e548</epage><pages>e548-e548</pages><issn>2158-3188</issn><eissn>2158-3188</eissn><abstract>We investigated
in vivo
neurochemical markers reflective of neuronal health and glial activation to determine if these could yield clues regarding the reduced fractional anisotropy (FA) of white matter and accelerated decline of FA with age in schizophrenia. Participants with schizophrenia and healthy controls completed diffusion tensor imaging to assess FA and proton magnetic resonance spectroscopy to assess neurochemical metabolites in the same frontal region. Frontal FA was significantly lower in the schizophrenia and declined more rapidly with age compared with the healthy control group. In both groups,
N
-acetylaspartate (NAA), a putative marker of neuronal integrity, and glutamate declined with age, and this decline was stronger in patients. Myo-inositol, a marker of glial cells, was negatively related to FA in both groups. The relationship between FA and age remained significant in schizophrenia even when controlling for all metabolites. The relationships of FA, NAA and myo-inositol to age appear to be independent of one another. The relationship between FA and myo-inositol was independently present in both patients and controls, even after controlling for age, indicating a potential general effect of neuroinflammation on white matter microstructure. Further studies are warranted to determine the underlying mechanism driving the accelerated FA decline with age in schizophrenia.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>25871973</pmid><doi>10.1038/tp.2015.43</doi><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | 59/57 692/699/476/1799 Adult Age Factors Anisotropy Aspartic Acid - analogs & derivatives Aspartic Acid - metabolism Behavioral Sciences Biological Psychology Case-Control Studies Choline - metabolism Creatine - metabolism Diffusion Tensor Imaging Female Frontal Lobe - metabolism Frontal Lobe - pathology Glutamic Acid - metabolism Humans Inflammation Inositol - metabolism Magnetic Resonance Spectroscopy Male Medicine Medicine & Public Health Middle Aged Neuroglia - metabolism Neurosciences Original original-article Pharmacotherapy Psychiatry Schizophrenia - metabolism Schizophrenia - pathology White Matter - metabolism White Matter - pathology Young Adult |
| title | Alterations in frontal white matter neurochemistry and microstructure in schizophrenia: implications for neuroinflammation |
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