Fasting plasma and CSF amino acid levels in amyotrophic lateral sclerosis: a subtype analysis.
Identifieur interne : 001710 ( PubMed/Corpus ); précédent : 001709; suivant : 001711Fasting plasma and CSF amino acid levels in amyotrophic lateral sclerosis: a subtype analysis.
Auteurs : W. Camu ; M. Billiard ; M. Baldy-MoulinierSource :
- Acta neurologica Scandinavica [ 0001-6314 ] ; 1993.
English descriptors
- KwdEn :
- Amino Acids (blood), Amino Acids (cerebrospinal fluid), Amino Acids (metabolism), Amyotrophic Lateral Sclerosis (blood), Amyotrophic Lateral Sclerosis (cerebrospinal fluid), Amyotrophic Lateral Sclerosis (metabolism), Fasting (blood), Female, Glutamates (blood), Glutamates (cerebrospinal fluid), Glutamates (metabolism), Glutamine (blood), Glutamine (cerebrospinal fluid), Glutamine (metabolism), Hereditary Sensory and Autonomic Neuropathies (blood), Hereditary Sensory and Autonomic Neuropathies (cerebrospinal fluid), Hereditary Sensory and Autonomic Neuropathies (metabolism), Humans, Male, Parkinson Disease (blood), Parkinson Disease (cerebrospinal fluid), Parkinson Disease (diagnosis), Plasma (chemistry).
- MESH :
- chemical , blood : Amino Acids, Glutamates, Glutamine.
- chemical , cerebrospinal fluid : Amino Acids, Glutamates, Glutamine.
- chemical , metabolism : Amino Acids, Glutamates, Glutamine.
- blood : Amyotrophic Lateral Sclerosis, Fasting, Hereditary Sensory and Autonomic Neuropathies, Parkinson Disease.
- cerebrospinal fluid : Amyotrophic Lateral Sclerosis, Hereditary Sensory and Autonomic Neuropathies, Parkinson Disease.
- chemistry : Plasma.
- diagnosis : Parkinson Disease.
- metabolism : Amyotrophic Lateral Sclerosis, Hereditary Sensory and Autonomic Neuropathies.
- Female, Humans, Male.
Abstract
Data from the literature about plasma and CSF amino acid (AA) levels in amyotrophic lateral sclerosis (ALS) remain controversial. To refine such analyses we used HPLC, and report a study of plasma and CSF AA concentrations in patients with ALS, the type of the disease (spinal and bulbar onset) being precisely determined. In ALS, there is a decrease in the plasma levels of the large neutral amino acids (LNAA) alanine, isoleucine, leucine, methionine and tyrosine which was particularly striking in the bulbar type (p < 0.05). Plasma glutamate levels do not differ between ALS and controls, but are significantly increased in ALS with spinal onset and decreased in the bulbar type (p < 0.05 vs controls, p < 0.001 bulbar vs spinal). In CSF, the analysis of the whole ALS group shows no difference from controls. However, there is an increase of CSF serine, glutamine and alanine in ALS with spinal onset (p < 0.05). Our results do not support an abnormal profile of excitatory AA concentrations in ALS. The heterogeneous changes we observed, mainly concerning LNAAs, may be explained by a blood-CSF barrier disturbance in the disease. As AA levels clearly differ between ALS types, with low concentrations in bulbar ALS, this dual profile probably explains some of the discrepancies between previous studies.
PubMed: 8372631
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pubmed:8372631Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Fasting plasma and CSF amino acid levels in amyotrophic lateral sclerosis: a subtype analysis.</title><author><name sortKey="Camu, W" sort="Camu, W" uniqKey="Camu W" first="W" last="Camu">W. Camu</name><affiliation><nlm:affiliation>Service de Neurologie B, Hôpital Gui-de-Chauliac, Hérault, France.</nlm:affiliation></affiliation></author><author><name sortKey="Billiard, M" sort="Billiard, M" uniqKey="Billiard M" first="M" last="Billiard">M. Billiard</name></author><author><name sortKey="Baldy Moulinier, M" sort="Baldy Moulinier, M" uniqKey="Baldy Moulinier M" first="M" last="Baldy-Moulinier">M. Baldy-Moulinier</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1993">1993</date><idno type="RBID">pubmed:8372631</idno><idno type="pmid">8372631</idno><idno type="wicri:Area/PubMed/Corpus">001710</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001710</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Fasting plasma and CSF amino acid levels in amyotrophic lateral sclerosis: a subtype analysis.</title><author><name sortKey="Camu, W" sort="Camu, W" uniqKey="Camu W" first="W" last="Camu">W. Camu</name><affiliation><nlm:affiliation>Service de Neurologie B, Hôpital Gui-de-Chauliac, Hérault, France.</nlm:affiliation></affiliation></author><author><name sortKey="Billiard, M" sort="Billiard, M" uniqKey="Billiard M" first="M" last="Billiard">M. Billiard</name></author><author><name sortKey="Baldy Moulinier, M" sort="Baldy Moulinier, M" uniqKey="Baldy Moulinier M" first="M" last="Baldy-Moulinier">M. Baldy-Moulinier</name></author></analytic><series><title level="j">Acta neurologica Scandinavica</title><idno type="ISSN">0001-6314</idno><imprint><date when="1993" type="published">1993</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acids (blood)</term><term>Amino Acids (cerebrospinal fluid)</term><term>Amino Acids (metabolism)</term><term>Amyotrophic Lateral Sclerosis (blood)</term><term>Amyotrophic Lateral Sclerosis (cerebrospinal fluid)</term><term>Amyotrophic Lateral Sclerosis (metabolism)</term><term>Fasting (blood)</term><term>Female</term><term>Glutamates (blood)</term><term>Glutamates (cerebrospinal fluid)</term><term>Glutamates (metabolism)</term><term>Glutamine (blood)</term><term>Glutamine (cerebrospinal fluid)</term><term>Glutamine (metabolism)</term><term>Hereditary Sensory and Autonomic Neuropathies (blood)</term><term>Hereditary Sensory and Autonomic Neuropathies (cerebrospinal fluid)</term><term>Hereditary Sensory and Autonomic Neuropathies (metabolism)</term><term>Humans</term><term>Male</term><term>Parkinson Disease (blood)</term><term>Parkinson Disease (cerebrospinal fluid)</term><term>Parkinson Disease (diagnosis)</term><term>Plasma (chemistry)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Amino Acids</term><term>Glutamates</term><term>Glutamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="cerebrospinal fluid" xml:lang="en"><term>Amino Acids</term><term>Glutamates</term><term>Glutamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amino Acids</term><term>Glutamates</term><term>Glutamine</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Amyotrophic Lateral Sclerosis</term><term>Fasting</term><term>Hereditary Sensory and Autonomic Neuropathies</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="cerebrospinal fluid" xml:lang="en"><term>Amyotrophic Lateral Sclerosis</term><term>Hereditary Sensory and Autonomic Neuropathies</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Plasma</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Amyotrophic Lateral Sclerosis</term><term>Hereditary Sensory and Autonomic Neuropathies</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Female</term><term>Humans</term><term>Male</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Data from the literature about plasma and CSF amino acid (AA) levels in amyotrophic lateral sclerosis (ALS) remain controversial. To refine such analyses we used HPLC, and report a study of plasma and CSF AA concentrations in patients with ALS, the type of the disease (spinal and bulbar onset) being precisely determined. In ALS, there is a decrease in the plasma levels of the large neutral amino acids (LNAA) alanine, isoleucine, leucine, methionine and tyrosine which was particularly striking in the bulbar type (p < 0.05). Plasma glutamate levels do not differ between ALS and controls, but are significantly increased in ALS with spinal onset and decreased in the bulbar type (p < 0.05 vs controls, p < 0.001 bulbar vs spinal). In CSF, the analysis of the whole ALS group shows no difference from controls. However, there is an increase of CSF serine, glutamine and alanine in ALS with spinal onset (p < 0.05). Our results do not support an abnormal profile of excitatory AA concentrations in ALS. The heterogeneous changes we observed, mainly concerning LNAAs, may be explained by a blood-CSF barrier disturbance in the disease. As AA levels clearly differ between ALS types, with low concentrations in bulbar ALS, this dual profile probably explains some of the discrepancies between previous studies.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">8372631</PMID><DateCreated><Year>1993</Year><Month>10</Month><Day>08</Day></DateCreated><DateCompleted><Year>1993</Year><Month>10</Month><Day>08</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0001-6314</ISSN><JournalIssue CitedMedium="Print"><Volume>88</Volume><Issue>1</Issue><PubDate><Year>1993</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Acta neurologica Scandinavica</Title><ISOAbbreviation>Acta Neurol. Scand.</ISOAbbreviation></Journal><ArticleTitle>Fasting plasma and CSF amino acid levels in amyotrophic lateral sclerosis: a subtype analysis.</ArticleTitle><Pagination><MedlinePgn>51-5</MedlinePgn></Pagination><Abstract><AbstractText>Data from the literature about plasma and CSF amino acid (AA) levels in amyotrophic lateral sclerosis (ALS) remain controversial. To refine such analyses we used HPLC, and report a study of plasma and CSF AA concentrations in patients with ALS, the type of the disease (spinal and bulbar onset) being precisely determined. In ALS, there is a decrease in the plasma levels of the large neutral amino acids (LNAA) alanine, isoleucine, leucine, methionine and tyrosine which was particularly striking in the bulbar type (p < 0.05). Plasma glutamate levels do not differ between ALS and controls, but are significantly increased in ALS with spinal onset and decreased in the bulbar type (p < 0.05 vs controls, p < 0.001 bulbar vs spinal). In CSF, the analysis of the whole ALS group shows no difference from controls. However, there is an increase of CSF serine, glutamine and alanine in ALS with spinal onset (p < 0.05). Our results do not support an abnormal profile of excitatory AA concentrations in ALS. The heterogeneous changes we observed, mainly concerning LNAAs, may be explained by a blood-CSF barrier disturbance in the disease. As AA levels clearly differ between ALS types, with low concentrations in bulbar ALS, this dual profile probably explains some of the discrepancies between previous studies.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Camu</LastName><ForeName>W</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Service de Neurologie B, Hôpital Gui-de-Chauliac, Hérault, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Billiard</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Baldy-Moulinier</LastName><ForeName>M</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Denmark</Country><MedlineTA>Acta Neurol Scand</MedlineTA><NlmUniqueID>0370336</NlmUniqueID><ISSNLinking>0001-6314</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000596">Amino Acids</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005971">Glutamates</NameOfSubstance></Chemical><Chemical><RegistryNumber>0RH81L854J</RegistryNumber><NameOfSubstance UI="D005973">Glutamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Acta Neurol Scand. 1994 May;89(5):404-5</RefSource><PMID Version="1">8085443</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000596" MajorTopicYN="N">Amino Acids</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000134" MajorTopicYN="N">cerebrospinal fluid</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000690" MajorTopicYN="N">Amyotrophic Lateral Sclerosis</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="Y">blood</QualifierName><QualifierName UI="Q000134" MajorTopicYN="N">cerebrospinal fluid</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005215" MajorTopicYN="N">Fasting</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="Y">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005971" MajorTopicYN="N">Glutamates</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000134" MajorTopicYN="N">cerebrospinal fluid</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005973" MajorTopicYN="N">Glutamine</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000134" MajorTopicYN="N">cerebrospinal fluid</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009477" MajorTopicYN="N">Hereditary Sensory and Autonomic Neuropathies</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000134" MajorTopicYN="N">cerebrospinal fluid</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName><QualifierName UI="Q000134" MajorTopicYN="N">cerebrospinal fluid</QualifierName><QualifierName UI="Q000175" MajorTopicYN="N">diagnosis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010949" MajorTopicYN="N">Plasma</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1993</Year><Month>7</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1993</Year><Month>7</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1993</Year><Month>7</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8372631</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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