In vivo neurometabolic profiling in patients with spinocerebellar ataxia types 1, 2, 3, and 7.
Identifieur interne : 000222 ( PubMed/Curation ); précédent : 000221; suivant : 000223In vivo neurometabolic profiling in patients with spinocerebellar ataxia types 1, 2, 3, and 7.
Auteurs : Isaac M. Adanyeguh [France] ; Pierre-Gilles Henry ; Tra M. Nguyen ; Daisy Rinaldi ; Celine Jauffret ; Romain Valabregue ; Uzay E. Emir ; Dinesh K. Deelchand ; Alexis Brice ; Lynn E. Eberly ; Gülin Öz ; Alexandra Durr ; Fanny MochelSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2015.
Abstract
Spinocerebellar ataxias (SCAs) belong to polyglutamine repeat disorders and are characterized by a predominant atrophy of the cerebellum and the pons. Proton magnetic resonance spectroscopy ((1) H MRS) using an optimized semiadiabatic localization by adiabatic selective refocusing (semi-LASER) protocol was performed at 3 T to determine metabolite concentrations in the cerebellar vermis and pons of a cohort of patients with SCA1 (n=16), SCA2 (n=12), SCA3 (n=21), and SCA7 (n=12) and healthy controls (n=33). Compared with controls, patients displayed lower total N-acetylaspartate and, to a lesser extent, lower glutamate, reflecting neuronal loss/dysfunction, whereas the glial marker, myoinositol (myo-Ins), was elevated. Patients also showed higher total creatine as reported in Huntington's disease, another polyglutamine repeat disorder. A strong correlation was found between the Scale for the Assessment and Rating of Ataxia and the neurometabolites in both affected regions of patients. Principal component analyses confirmed that neuronal metabolites (total N-acetylaspartate and glutamate) were inversely correlated in the vermis and the pons to glial (myo-Ins) and energetic (total creatine) metabolites, as well as to disease severity (motor scales). Neurochemical plots with selected metabolites also allowed the separation of SCA2 and SCA3 from controls. The neurometabolic profiles detected in patients underlie cell-specific changes in neuronal and astrocytic compartments that cannot be assessed by other neuroimaging modalities. The inverse correlation between metabolites from these two compartments suggests a metabolic attempt to compensate for neuronal damage in SCAs. Because these biomarkers reflect dynamic aspects of cellular metabolism, they are good candidates for proof-of-concept therapeutic trials. © 2015 International Parkinson and Movement Disorder Society.
DOI: 10.1002/mds.26181
PubMed: 25773989
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Nguyen</name></author><author><name sortKey="Rinaldi, Daisy" sort="Rinaldi, Daisy" uniqKey="Rinaldi D" first="Daisy" last="Rinaldi">Daisy Rinaldi</name></author><author><name sortKey="Jauffret, Celine" sort="Jauffret, Celine" uniqKey="Jauffret C" first="Celine" last="Jauffret">Celine Jauffret</name></author><author><name sortKey="Valabregue, Romain" sort="Valabregue, Romain" uniqKey="Valabregue R" first="Romain" last="Valabregue">Romain Valabregue</name></author><author><name sortKey="Emir, Uzay E" sort="Emir, Uzay E" uniqKey="Emir U" first="Uzay E" last="Emir">Uzay E. Emir</name></author><author><name sortKey="Deelchand, Dinesh K" sort="Deelchand, Dinesh K" uniqKey="Deelchand D" first="Dinesh K" last="Deelchand">Dinesh K. Deelchand</name></author><author><name sortKey="Brice, Alexis" sort="Brice, Alexis" uniqKey="Brice A" first="Alexis" last="Brice">Alexis Brice</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="Oz, Gulin" sort="Oz, Gulin" uniqKey="Oz G" first="Gülin" last="Öz">Gülin Öz</name></author><author><name sortKey="Durr, Alexandra" sort="Durr, Alexandra" uniqKey="Durr A" first="Alexandra" last="Durr">Alexandra Durr</name></author><author><name sortKey="Mochel, Fanny" sort="Mochel, Fanny" uniqKey="Mochel F" first="Fanny" last="Mochel">Fanny Mochel</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="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Spinocerebellar ataxias (SCAs) belong to polyglutamine repeat disorders and are characterized by a predominant atrophy of the cerebellum and the pons. Proton magnetic resonance spectroscopy ((1) H MRS) using an optimized semiadiabatic localization by adiabatic selective refocusing (semi-LASER) protocol was performed at 3 T to determine metabolite concentrations in the cerebellar vermis and pons of a cohort of patients with SCA1 (n=16), SCA2 (n=12), SCA3 (n=21), and SCA7 (n=12) and healthy controls (n=33). Compared with controls, patients displayed lower total N-acetylaspartate and, to a lesser extent, lower glutamate, reflecting neuronal loss/dysfunction, whereas the glial marker, myoinositol (myo-Ins), was elevated. Patients also showed higher total creatine as reported in Huntington's disease, another polyglutamine repeat disorder. A strong correlation was found between the Scale for the Assessment and Rating of Ataxia and the neurometabolites in both affected regions of patients. Principal component analyses confirmed that neuronal metabolites (total N-acetylaspartate and glutamate) were inversely correlated in the vermis and the pons to glial (myo-Ins) and energetic (total creatine) metabolites, as well as to disease severity (motor scales). Neurochemical plots with selected metabolites also allowed the separation of SCA2 and SCA3 from controls. The neurometabolic profiles detected in patients underlie cell-specific changes in neuronal and astrocytic compartments that cannot be assessed by other neuroimaging modalities. The inverse correlation between metabolites from these two compartments suggests a metabolic attempt to compensate for neuronal damage in SCAs. Because these biomarkers reflect dynamic aspects of cellular metabolism, they are good candidates for proof-of-concept therapeutic trials. © 2015 International Parkinson and Movement Disorder Society.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="In-Process"><PMID Version="1">25773989</PMID><DateCreated><Year>2015</Year><Month>04</Month><Day>13</Day></DateCreated><DateRevised><Year>2015</Year><Month>05</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>5</Issue><PubDate><Year>2015</Year><Month>Apr</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>In vivo neurometabolic profiling in patients with spinocerebellar ataxia types 1, 2, 3, and 7.</ArticleTitle><Pagination><MedlinePgn>662-70</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.26181</ELocationID><Abstract><AbstractText>Spinocerebellar ataxias (SCAs) belong to polyglutamine repeat disorders and are characterized by a predominant atrophy of the cerebellum and the pons. Proton magnetic resonance spectroscopy ((1) H MRS) using an optimized semiadiabatic localization by adiabatic selective refocusing (semi-LASER) protocol was performed at 3 T to determine metabolite concentrations in the cerebellar vermis and pons of a cohort of patients with SCA1 (n=16), SCA2 (n=12), SCA3 (n=21), and SCA7 (n=12) and healthy controls (n=33). Compared with controls, patients displayed lower total N-acetylaspartate and, to a lesser extent, lower glutamate, reflecting neuronal loss/dysfunction, whereas the glial marker, myoinositol (myo-Ins), was elevated. Patients also showed higher total creatine as reported in Huntington's disease, another polyglutamine repeat disorder. A strong correlation was found between the Scale for the Assessment and Rating of Ataxia and the neurometabolites in both affected regions of patients. Principal component analyses confirmed that neuronal metabolites (total N-acetylaspartate and glutamate) were inversely correlated in the vermis and the pons to glial (myo-Ins) and energetic (total creatine) metabolites, as well as to disease severity (motor scales). Neurochemical plots with selected metabolites also allowed the separation of SCA2 and SCA3 from controls. The neurometabolic profiles detected in patients underlie cell-specific changes in neuronal and astrocytic compartments that cannot be assessed by other neuroimaging modalities. The inverse correlation between metabolites from these two compartments suggests a metabolic attempt to compensate for neuronal damage in SCAs. Because these biomarkers reflect dynamic aspects of cellular metabolism, they are good candidates for proof-of-concept therapeutic trials. © 2015 International Parkinson and Movement Disorder Society.</AbstractText><CopyrightInformation>© 2015 International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Adanyeguh</LastName><ForeName>Isaac M</ForeName><Initials>IM</Initials><AffiliationInfo><Affiliation>INSERM U 1127, Sorbonne Universités, UPMC Univ Paris Institut du Cerveau et de la Moelle épinière, ICM, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Henry</LastName><ForeName>Pierre-Gilles</ForeName><Initials>PG</Initials></Author><Author ValidYN="Y"><LastName>Nguyen</LastName><ForeName>Tra M</ForeName><Initials>TM</Initials></Author><Author ValidYN="Y"><LastName>Rinaldi</LastName><ForeName>Daisy</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Jauffret</LastName><ForeName>Celine</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Valabregue</LastName><ForeName>Romain</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Emir</LastName><ForeName>Uzay E</ForeName><Initials>UE</Initials></Author><Author ValidYN="Y"><LastName>Deelchand</LastName><ForeName>Dinesh K</ForeName><Initials>DK</Initials></Author><Author ValidYN="Y"><LastName>Brice</LastName><ForeName>Alexis</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Eberly</LastName><ForeName>Lynn E</ForeName><Initials>LE</Initials></Author><Author ValidYN="Y"><LastName>Öz</LastName><ForeName>Gülin</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Durr</LastName><ForeName>Alexandra</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Mochel</LastName><ForeName>Fanny</ForeName><Initials>F</Initials></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>ClinicalTrials.gov</DataBankName><AccessionNumberList><AccessionNumber>NCT01470729</AccessionNumber></AccessionNumberList></DataBank></DataBankList><GrantList CompleteYN="Y"><Grant><GrantID>P30 NS076408</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 NS076408</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P41 EB015894</GrantID><Acronym>EB</Acronym><Agency>NIBIB NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P41 EB015894</GrantID><Acronym>EB</Acronym><Agency>NIBIB NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DA023651</GrantID><Acronym>DA</Acronym><Agency>NIDA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NR010731</GrantID><Acronym>NR</Acronym><Agency>NINR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS070815</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS070815</GrantID><Acronym>NS</Acronym><Agency>NINDS 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><ArticleDate DateType="Electronic"><Year>2015</Year><Month>03</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Cerebellum. 2008;7(2):215-21</RefSource><PMID 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