Neurochemical alterations in spinocerebellar ataxia type 1 and their correlations with clinical status.
Identifieur interne : 001875 ( PubMed/Curation ); précédent : 001874; suivant : 001876Neurochemical alterations in spinocerebellar ataxia type 1 and their correlations with clinical status.
Auteurs : Gülin Oz [États-Unis] ; Diane Hutter ; Ivan Tkác ; H Brent Clark ; Myron D. Gross ; Hong Jiang ; Lynn E. Eberly ; Khalaf O. Bushara ; Christopher M. GomezSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2010.
English descriptors
- KwdEn :
- Analysis of Variance, Aspartic Acid (analogs & derivatives), Brain Chemistry, Case-Control Studies, Female, Functional Laterality, Glial Fibrillary Acidic Protein (cerebrospinal fluid), Humans, Inositol, Isoprostanes (cerebrospinal fluid), Magnetic Resonance Imaging (methods), Magnetic Resonance Spectroscopy (methods), Male, Middle Aged, Phosphocreatine, Protons (diagnostic use), Severity of Illness Index, Spinocerebellar Ataxias (metabolism), Spinocerebellar Ataxias (physiopathology), Statistics as Topic.
- MESH :
- chemical , analogs & derivatives : Aspartic Acid.
- chemical , cerebrospinal fluid : Glial Fibrillary Acidic Protein, Isoprostanes.
- chemical , diagnostic use : Protons.
- metabolism : Spinocerebellar Ataxias.
- methods : Magnetic Resonance Imaging, Magnetic Resonance Spectroscopy.
- physiopathology : Spinocerebellar Ataxias.
- Analysis of Variance, Brain Chemistry, Case-Control Studies, Female, Functional Laterality, Humans, Inositol, Male, Middle Aged, Phosphocreatine, Severity of Illness Index, Statistics as Topic.
Abstract
Robust biomarkers of neurodegeneration are critical for testing of neuroprotective therapies. The clinical applicability of such biomarkers requires sufficient sensitivity to detect disease in individuals. Here we tested the sensitivity of high field (4 tesla) proton magnetic resonance spectroscopy ((1)H MRS) to neurochemical alterations in the cerebellum and brainstem in spinocerebellar ataxia type 1 (SCA1). We measured neurochemical profiles that consisted of 10 to 15 metabolite concentrations in the vermis, cerebellar hemispheres and pons of patients with SCA1 (N = 9) and healthy controls (N = 15). Total NAA (N-acetylaspartate + N-acetylaspartylglutamate, tNAA) and glutamate were lower and glutamine, myo-inositol and total creatine (creatine + phosphocreatine, tCr) were higher in patients relative to controls, consistent with neuronal dysfunction/loss, gliotic activity, and alterations in glutamate-glutamine cycling and energy metabolism. Changes in tNAA, tCr, myo-inositol, and glutamate levels were discernible in individual spectra and the tNAA/myo-inositol ratio in the cerebellar hemispheres and pons differentiated the patients from controls with 100% specificity and sensitivity. In addition, tNAA, myo-inositol, and glutamate levels in the cerebellar hemispheres and the tNAA and myo-inositol levels in the pons correlated with ataxia scores (Scale for the Assessment and Rating of Ataxia, SARA). Two other biomarkers measured in the cerebrospinal fluid (CSF) of a subset of the volunteers (F(2)-isoprostanes asa marker of oxidative stress and glial fibrillary acidic protein (GFAP) as a marker of gliosis) were not different between patients and controls. These data demonstrate that (1)H MRS biomarkers can be utilized to noninvasively assess neuronal and glial status in individual ataxia patients.
DOI: 10.1002/mds.23067
PubMed: 20310029
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Gross</name></author><author><name sortKey="Jiang, Hong" sort="Jiang, Hong" uniqKey="Jiang H" first="Hong" last="Jiang">Hong Jiang</name></author><author><name sortKey="Eberly, Lynn E" sort="Eberly, Lynn E" uniqKey="Eberly L" first="Lynn E" last="Eberly">Lynn E. Eberly</name></author><author><name sortKey="Bushara, Khalaf O" sort="Bushara, Khalaf O" uniqKey="Bushara K" first="Khalaf O" last="Bushara">Khalaf O. Bushara</name></author><author><name sortKey="Gomez, Christopher M" sort="Gomez, Christopher M" uniqKey="Gomez C" first="Christopher M" last="Gomez">Christopher M. Gomez</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="doi">10.1002/mds.23067</idno><idno type="RBID">pubmed:20310029</idno><idno type="pmid">20310029</idno><idno type="wicri:Area/PubMed/Corpus">001875</idno><idno type="wicri:Area/PubMed/Curation">001875</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Neurochemical alterations in spinocerebellar ataxia type 1 and their correlations with clinical status.</title><author><name sortKey="Oz, Gulin" sort="Oz, Gulin" uniqKey="Oz G" first="Gülin" last="Oz">Gülin Oz</name><affiliation wicri:level="1"><nlm:affiliation>Center for MR Research, Department of Radiology, Medical School, University of Minnesota, Minneapolis, Minnesota 55455, USA. gulin@cmrr.umn.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Center for MR Research, Department of Radiology, Medical School, University of Minnesota, Minneapolis, Minnesota 55455</wicri:regionArea></affiliation></author><author><name sortKey="Hutter, Diane" sort="Hutter, Diane" uniqKey="Hutter D" first="Diane" last="Hutter">Diane Hutter</name></author><author><name sortKey="Tkac, Ivan" sort="Tkac, Ivan" uniqKey="Tkac I" first="Ivan" last="Tkác">Ivan Tkác</name></author><author><name sortKey="Clark, H Brent" sort="Clark, H Brent" uniqKey="Clark H" first="H Brent" last="Clark">H Brent Clark</name></author><author><name sortKey="Gross, Myron D" sort="Gross, Myron D" uniqKey="Gross M" first="Myron D" last="Gross">Myron D. Gross</name></author><author><name sortKey="Jiang, Hong" sort="Jiang, Hong" uniqKey="Jiang H" first="Hong" last="Jiang">Hong Jiang</name></author><author><name sortKey="Eberly, Lynn E" sort="Eberly, Lynn E" uniqKey="Eberly L" first="Lynn E" last="Eberly">Lynn E. Eberly</name></author><author><name sortKey="Bushara, Khalaf O" sort="Bushara, Khalaf O" uniqKey="Bushara K" first="Khalaf O" last="Bushara">Khalaf O. Bushara</name></author><author><name sortKey="Gomez, Christopher M" sort="Gomez, Christopher M" uniqKey="Gomez C" first="Christopher M" last="Gomez">Christopher M. Gomez</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Analysis of Variance</term><term>Aspartic Acid (analogs & derivatives)</term><term>Brain Chemistry</term><term>Case-Control Studies</term><term>Female</term><term>Functional Laterality</term><term>Glial Fibrillary Acidic Protein (cerebrospinal fluid)</term><term>Humans</term><term>Inositol</term><term>Isoprostanes (cerebrospinal fluid)</term><term>Magnetic Resonance Imaging (methods)</term><term>Magnetic Resonance Spectroscopy (methods)</term><term>Male</term><term>Middle Aged</term><term>Phosphocreatine</term><term>Protons (diagnostic use)</term><term>Severity of Illness Index</term><term>Spinocerebellar Ataxias (metabolism)</term><term>Spinocerebellar Ataxias (physiopathology)</term><term>Statistics as Topic</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Aspartic Acid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="cerebrospinal fluid" xml:lang="en"><term>Glial Fibrillary Acidic Protein</term><term>Isoprostanes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Protons</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Spinocerebellar Ataxias</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Magnetic Resonance Imaging</term><term>Magnetic Resonance Spectroscopy</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Spinocerebellar Ataxias</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Brain Chemistry</term><term>Case-Control Studies</term><term>Female</term><term>Functional Laterality</term><term>Humans</term><term>Inositol</term><term>Male</term><term>Middle Aged</term><term>Phosphocreatine</term><term>Severity of Illness Index</term><term>Statistics as Topic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Robust biomarkers of neurodegeneration are critical for testing of neuroprotective therapies. The clinical applicability of such biomarkers requires sufficient sensitivity to detect disease in individuals. Here we tested the sensitivity of high field (4 tesla) proton magnetic resonance spectroscopy ((1)H MRS) to neurochemical alterations in the cerebellum and brainstem in spinocerebellar ataxia type 1 (SCA1). We measured neurochemical profiles that consisted of 10 to 15 metabolite concentrations in the vermis, cerebellar hemispheres and pons of patients with SCA1 (N = 9) and healthy controls (N = 15). Total NAA (N-acetylaspartate + N-acetylaspartylglutamate, tNAA) and glutamate were lower and glutamine, myo-inositol and total creatine (creatine + phosphocreatine, tCr) were higher in patients relative to controls, consistent with neuronal dysfunction/loss, gliotic activity, and alterations in glutamate-glutamine cycling and energy metabolism. Changes in tNAA, tCr, myo-inositol, and glutamate levels were discernible in individual spectra and the tNAA/myo-inositol ratio in the cerebellar hemispheres and pons differentiated the patients from controls with 100% specificity and sensitivity. In addition, tNAA, myo-inositol, and glutamate levels in the cerebellar hemispheres and the tNAA and myo-inositol levels in the pons correlated with ataxia scores (Scale for the Assessment and Rating of Ataxia, SARA). Two other biomarkers measured in the cerebrospinal fluid (CSF) of a subset of the volunteers (F(2)-isoprostanes asa marker of oxidative stress and glial fibrillary acidic protein (GFAP) as a marker of gliosis) were not different between patients and controls. These data demonstrate that (1)H MRS biomarkers can be utilized to noninvasively assess neuronal and glial status in individual ataxia patients.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">20310029</PMID><DateCreated><Year>2010</Year><Month>07</Month><Day>26</Day></DateCreated><DateCompleted><Year>2010</Year><Month>11</Month><Day>04</Day></DateCompleted><DateRevised><Year>2014</Year><Month>12</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>9</Issue><PubDate><Year>2010</Year><Month>Jul</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Neurochemical alterations in spinocerebellar ataxia type 1 and their correlations with clinical status.</ArticleTitle><Pagination><MedlinePgn>1253-61</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.23067</ELocationID><Abstract><AbstractText>Robust biomarkers of neurodegeneration are critical for testing of neuroprotective therapies. The clinical applicability of such biomarkers requires sufficient sensitivity to detect disease in individuals. Here we tested the sensitivity of high field (4 tesla) proton magnetic resonance spectroscopy ((1)H MRS) to neurochemical alterations in the cerebellum and brainstem in spinocerebellar ataxia type 1 (SCA1). We measured neurochemical profiles that consisted of 10 to 15 metabolite concentrations in the vermis, cerebellar hemispheres and pons of patients with SCA1 (N = 9) and healthy controls (N = 15). Total NAA (N-acetylaspartate + N-acetylaspartylglutamate, tNAA) and glutamate were lower and glutamine, myo-inositol and total creatine (creatine + phosphocreatine, tCr) were higher in patients relative to controls, consistent with neuronal dysfunction/loss, gliotic activity, and alterations in glutamate-glutamine cycling and energy metabolism. Changes in tNAA, tCr, myo-inositol, and glutamate levels were discernible in individual spectra and the tNAA/myo-inositol ratio in the cerebellar hemispheres and pons differentiated the patients from controls with 100% specificity and sensitivity. In addition, tNAA, myo-inositol, and glutamate levels in the cerebellar hemispheres and the tNAA and myo-inositol levels in the pons correlated with ataxia scores (Scale for the Assessment and Rating of Ataxia, SARA). Two other biomarkers measured in the cerebrospinal fluid (CSF) of a subset of the volunteers (F(2)-isoprostanes asa marker of oxidative stress and glial fibrillary acidic protein (GFAP) as a marker of gliosis) were not different between patients and controls. These data demonstrate that (1)H MRS biomarkers can be utilized to noninvasively assess neuronal and glial status in individual ataxia patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Oz</LastName><ForeName>Gülin</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Center for MR Research, Department of Radiology, Medical School, University of Minnesota, Minneapolis, Minnesota 55455, USA. gulin@cmrr.umn.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hutter</LastName><ForeName>Diane</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Tkác</LastName><ForeName>Ivan</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Clark</LastName><ForeName>H Brent</ForeName><Initials>HB</Initials></Author><Author ValidYN="Y"><LastName>Gross</LastName><ForeName>Myron D</ForeName><Initials>MD</Initials></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Hong</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Eberly</LastName><ForeName>Lynn E</ForeName><Initials>LE</Initials></Author><Author ValidYN="Y"><LastName>Bushara</LastName><ForeName>Khalaf O</ForeName><Initials>KO</Initials></Author><Author ValidYN="Y"><LastName>Gomez</LastName><ForeName>Christopher M</ForeName><Initials>CM</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>1R01-AG026392</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>1R01-CA1205090</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>1R01-NR009212</GrantID><Acronym>NR</Acronym><Agency>NINR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>1R21-CA133263</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>1R21-NS060253</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>5-41230-G1/R01CA116795</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>M01 RR000400</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>M01 RR000400-416988</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>M01 RR00400</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS35192</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 HD039386</GrantID><Acronym>HD</Acronym><Agency>NICHD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01NS058901</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 NS057091</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 NS057091-04</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30-NS057091</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30NS057091</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P41 RR008079</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P41 RR008079</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P41 RR008079-175181</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P41RR008079</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 CA131013</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HD057064</GrantID><Acronym>HD</Acronym><Agency>NICHD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL093077</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS 22920-13</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS035192</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-HL53560-05</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 AG029582</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 NS056172</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 NS060253</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>RR00400</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UL1 TR000114</GrantID><Acronym>TR</Acronym><Agency>NCATS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005904">Glial Fibrillary Acidic Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D028421">Isoprostanes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011522">Protons</NameOfSubstance></Chemical><Chemical><RegistryNumber>020IUV4N33</RegistryNumber><NameOfSubstance UI="D010725">Phosphocreatine</NameOfSubstance></Chemical><Chemical><RegistryNumber>30KYC7MIAI</RegistryNumber><NameOfSubstance UI="D001224">Aspartic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>4L6452S749</RegistryNumber><NameOfSubstance UI="D007294">Inositol</NameOfSubstance></Chemical><Chemical><RegistryNumber>997-55-7</RegistryNumber><NameOfSubstance 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