Plasma catechols and monoamine oxidase metabolites in untreated Parkinson's and Alzheimer's diseases
Identifieur interne : 001710 ( Main/Corpus ); précédent : 001709; suivant : 001711Plasma catechols and monoamine oxidase metabolites in untreated Parkinson's and Alzheimer's diseases
Auteurs : J. Eric Ahlskog ; Ryan J. Uitti ; Gertrude M. Tyce ; John F. O'Brien ; Ronald C. Petersen ; Emre KokmenSource :
- Journal of the Neurological Sciences [ 0022-510X ] ; 1995.
Abstract
Prior studies have documented functional and pathological compromise of the peripheral sympathetic nervous system in patients with Parkinson's disease, suggesting the possibility of reduced catecholamine release into the circulation. We measured free plasma catechols in early and untreated patients with Parkinson's disease, but found no evidence of reduced concentrations, compared to control subjects or a group of patients with probable Alzheimer's disease. Rather, there was a significant elevation of plasma norepinephrine within the Parkinson's disease group. Furthermore, 6 of 15 untreated Parkinson's disease patients (40%) displayed markedly elevated plasma concentrations of the catecholamine MAO metabolites, DOPAC or DOPEG. Despite this finding, platelet MAO-B activity measured in these and all other Parkinson's disease patients fell well within the range of the control subjects, and was also statistically similar to the group with Alzheimer's type dementia. Plasma dopa levels were similar in all groups, whereas the majority of patients in the three groups had plasma free dopamine and epinephrine concentrations below the limits of detection. These trends toward increased, rather than decreased, circulating catechol concentrations suggest that peripheral sympathetic nervous system catecholamine production and release is not severely compromised in patients with early Parkinson's disease. In addition, we were unable to confirm certain previous reports of elevated MAO-B activity in patients with Parkinson's or Alzheimer's diseases.
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DOI: 10.1016/0022-510X(95)00318-V
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Tyce</name><affiliation><mods:affiliation>Department of Physiology and Biophysics, Mayo Clinic Rochester, Rochester, MN 55905, USA</mods:affiliation></affiliation></author><author><name sortKey="O Brien, John F" sort="O Brien, John F" uniqKey="O Brien J" first="John F." last="O'Brien">John F. O'Brien</name><affiliation><mods:affiliation>Department Laboratory Medicine and Pathology, Mayo Clinic Rochester, Rochester, MN 55905, USA</mods:affiliation></affiliation></author><author><name sortKey="Petersen, Ronald C" sort="Petersen, Ronald C" uniqKey="Petersen R" first="Ronald C." last="Petersen">Ronald C. 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Eric" last="Ahlskog">J. Eric Ahlskog</name><affiliation><mods:affiliation>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</mods:affiliation></affiliation></author><author><name sortKey="Uitti, Ryan J" sort="Uitti, Ryan J" uniqKey="Uitti R" first="Ryan J." last="Uitti">Ryan J. Uitti</name><affiliation><mods:affiliation>Department of Neurology, Mayo Clinic Jacksonville; Jacksonville, FL, USA</mods:affiliation></affiliation></author><author><name sortKey="Tyce, Gertrude M" sort="Tyce, Gertrude M" uniqKey="Tyce G" first="Gertrude M." last="Tyce">Gertrude M. Tyce</name><affiliation><mods:affiliation>Department of Physiology and Biophysics, Mayo Clinic Rochester, Rochester, MN 55905, USA</mods:affiliation></affiliation></author><author><name sortKey="O Brien, John F" sort="O Brien, John F" uniqKey="O Brien J" first="John F." last="O'Brien">John F. 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Petersen</name><affiliation><mods:affiliation>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</mods:affiliation></affiliation></author><author><name sortKey="Kokmen, Emre" sort="Kokmen, Emre" uniqKey="Kokmen E" first="Emre" last="Kokmen">Emre Kokmen</name><affiliation><mods:affiliation>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="ISSN">0022-510X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995">1995</date><biblScope unit="volume">136</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="162">162</biblScope><biblScope unit="page" to="168">168</biblScope></imprint><idno type="ISSN">0022-510X</idno></series><idno type="istex">F164C656FA89DA0907A2F1EBDEA8FAB39E920533</idno><idno type="DOI">10.1016/0022-510X(95)00318-V</idno><idno type="PII">0022-510X(95)00318-V</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-510X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Prior studies have documented functional and pathological compromise of the peripheral sympathetic nervous system in patients with Parkinson's disease, suggesting the possibility of reduced catecholamine release into the circulation. We measured free plasma catechols in early and untreated patients with Parkinson's disease, but found no evidence of reduced concentrations, compared to control subjects or a group of patients with probable Alzheimer's disease. Rather, there was a significant elevation of plasma norepinephrine within the Parkinson's disease group. Furthermore, 6 of 15 untreated Parkinson's disease patients (40%) displayed markedly elevated plasma concentrations of the catecholamine MAO metabolites, DOPAC or DOPEG. Despite this finding, platelet MAO-B activity measured in these and all other Parkinson's disease patients fell well within the range of the control subjects, and was also statistically similar to the group with Alzheimer's type dementia. Plasma dopa levels were similar in all groups, whereas the majority of patients in the three groups had plasma free dopamine and epinephrine concentrations below the limits of detection. These trends toward increased, rather than decreased, circulating catechol concentrations suggest that peripheral sympathetic nervous system catecholamine production and release is not severely compromised in patients with early Parkinson's disease. In addition, we were unable to confirm certain previous reports of elevated MAO-B activity in patients with Parkinson's or Alzheimer's diseases.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>J.Eric Ahlskog</name><affiliations><json:string>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</json:string></affiliations></json:item><json:item><name>Ryan J. Uitti</name><affiliations><json:string>Department of Neurology, Mayo Clinic Jacksonville; Jacksonville, FL, USA</json:string></affiliations></json:item><json:item><name>Gertrude M. Tyce</name><affiliations><json:string>Department of Physiology and Biophysics, Mayo Clinic Rochester, Rochester, MN 55905, USA</json:string></affiliations></json:item><json:item><name>John F. O'Brien</name><affiliations><json:string>Department Laboratory Medicine and Pathology, Mayo Clinic Rochester, Rochester, MN 55905, USA</json:string></affiliations></json:item><json:item><name>Ronald C. Petersen</name><affiliations><json:string>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</json:string></affiliations></json:item><json:item><name>Emre Kokmen</name><affiliations><json:string>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Clinical section</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Catecholamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Monoamine oxidase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Alzheimer's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>DOPAC</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>DOPEG</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Prior studies have documented functional and pathological compromise of the peripheral sympathetic nervous system in patients with Parkinson's disease, suggesting the possibility of reduced catecholamine release into the circulation. We measured free plasma catechols in early and untreated patients with Parkinson's disease, but found no evidence of reduced concentrations, compared to control subjects or a group of patients with probable Alzheimer's disease. Rather, there was a significant elevation of plasma norepinephrine within the Parkinson's disease group. Furthermore, 6 of 15 untreated Parkinson's disease patients (40%) displayed markedly elevated plasma concentrations of the catecholamine MAO metabolites, DOPAC or DOPEG. Despite this finding, platelet MAO-B activity measured in these and all other Parkinson's disease patients fell well within the range of the control subjects, and was also statistically similar to the group with Alzheimer's type dementia. Plasma dopa levels were similar in all groups, whereas the majority of patients in the three groups had plasma free dopamine and epinephrine concentrations below the limits of detection. These trends toward increased, rather than decreased, circulating catechol concentrations suggest that peripheral sympathetic nervous system catecholamine production and release is not severely compromised in patients with early Parkinson's disease. In addition, we were unable to confirm certain previous reports of elevated MAO-B activity in patients with Parkinson's or Alzheimer's diseases.</abstract><qualityIndicators><score>7.196</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612.28 x 792.28 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>7</keywordCount><abstractCharCount>1557</abstractCharCount><pdfWordCount>4628</pdfWordCount><pdfCharCount>30961</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>214</abstractWordCount></qualityIndicators><title>Plasma catechols and monoamine oxidase metabolites in untreated Parkinson's and Alzheimer's diseases</title><pii><json:string>0022-510X(95)00318-V</json:string></pii><genre><json:string>research-article</json:string></genre><serie><volume>Vol. XVII</volume><pages><last>698</last><first>692</first></pages><genre></genre><language><json:string>unknown</json:string></language><title>Part B</title></serie><host><volume>136</volume><pii><json:string>S0022-510X(00)X0005-6</json:string></pii><pages><last>168</last><first>162</first></pages><issn><json:string>0022-510X</json:string></issn><issue>1–2</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><title>Journal of the Neurological Sciences</title><publicationDate>1996</publicationDate></host><categories><wos><json:string>CLINICAL NEUROLOGY</json:string><json:string>NEUROIMAGING</json:string><json:string>NEUROSCIENCES</json:string></wos></categories><publicationDate>1995</publicationDate><copyrightDate>1996</copyrightDate><doi><json:string>10.1016/0022-510X(95)00318-V</json:string></doi><id>F164C656FA89DA0907A2F1EBDEA8FAB39E920533</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/F164C656FA89DA0907A2F1EBDEA8FAB39E920533/fulltext/pdf</uri></json:item><json:item><original>true</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/F164C656FA89DA0907A2F1EBDEA8FAB39E920533/fulltext/txt</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/F164C656FA89DA0907A2F1EBDEA8FAB39E920533/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/F164C656FA89DA0907A2F1EBDEA8FAB39E920533/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Plasma catechols and monoamine oxidase metabolites in untreated Parkinson's and Alzheimer's diseases</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>ELSEVIER</publisher><availability><p>ELSEVIER</p></availability><date>1996</date></publicationStmt><notesStmt><note type="content">Section title: Research article</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Plasma catechols and monoamine oxidase metabolites in untreated Parkinson's and Alzheimer's diseases</title><author><persName><forename type="first">J.Eric</forename><surname>Ahlskog</surname></persName><note type="correspondence"><p>Corresponding author. Tel.: +1 (507) 284-9231; Fax: +1 (507) 284-2203.</p></note><affiliation>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</affiliation></author><author><persName><forename type="first">Ryan J.</forename><surname>Uitti</surname></persName><affiliation>Department of Neurology, Mayo Clinic Jacksonville; Jacksonville, FL, USA</affiliation></author><author><persName><forename type="first">Gertrude M.</forename><surname>Tyce</surname></persName><affiliation>Department of Physiology and Biophysics, Mayo Clinic Rochester, Rochester, MN 55905, USA</affiliation></author><author><persName><forename type="first">John F.</forename><surname>O'Brien</surname></persName><affiliation>Department Laboratory Medicine and Pathology, Mayo Clinic Rochester, Rochester, MN 55905, USA</affiliation></author><author><persName><forename type="first">Ronald C.</forename><surname>Petersen</surname></persName><affiliation>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</affiliation></author><author><persName><forename type="first">Emre</forename><surname>Kokmen</surname></persName><affiliation>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</affiliation></author></analytic><monogr><title level="j">Journal of the Neurological Sciences</title><title level="j" type="abbrev">JNS</title><idno type="pISSN">0022-510X</idno><idno type="PII">S0022-510X(00)X0005-6</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995"></date><biblScope unit="volume">136</biblScope><biblScope unit="issue">1–2</biblScope><biblScope unit="page" from="162">162</biblScope><biblScope unit="page" to="168">168</biblScope></imprint></monogr><idno type="istex">F164C656FA89DA0907A2F1EBDEA8FAB39E920533</idno><idno type="DOI">10.1016/0022-510X(95)00318-V</idno><idno type="PII">0022-510X(95)00318-V</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1996</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Prior studies have documented functional and pathological compromise of the peripheral sympathetic nervous system in patients with Parkinson's disease, suggesting the possibility of reduced catecholamine release into the circulation. We measured free plasma catechols in early and untreated patients with Parkinson's disease, but found no evidence of reduced concentrations, compared to control subjects or a group of patients with probable Alzheimer's disease. Rather, there was a significant elevation of plasma norepinephrine within the Parkinson's disease group. Furthermore, 6 of 15 untreated Parkinson's disease patients (40%) displayed markedly elevated plasma concentrations of the catecholamine MAO metabolites, DOPAC or DOPEG. Despite this finding, platelet MAO-B activity measured in these and all other Parkinson's disease patients fell well within the range of the control subjects, and was also statistically similar to the group with Alzheimer's type dementia. Plasma dopa levels were similar in all groups, whereas the majority of patients in the three groups had plasma free dopamine and epinephrine concentrations below the limits of detection. These trends toward increased, rather than decreased, circulating catechol concentrations suggest that peripheral sympathetic nervous system catecholamine production and release is not severely compromised in patients with early Parkinson's disease. In addition, we were unable to confirm certain previous reports of elevated MAO-B activity in patients with Parkinson's or Alzheimer's diseases.</p></abstract><textClass><keywords scheme="keyword"><list><head>Article category</head><item><term>Clinical section</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Catecholamine</term></item><item><term>Monoamine oxidase</term></item><item><term>Parkinson's disease</term></item><item><term>Alzheimer's disease</term></item><item><term>DOPAC</term></item><item><term>DOPEG</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1995-09-27">Registration</change><change when="1995-09-19">Modified</change><change when="1995">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>JNS</jid><aid>9500318V</aid><ce:pii>0022-510X(95)00318-V</ce:pii><ce:doi>10.1016/0022-510X(95)00318-V</ce:doi><ce:copyright type="unknown" year="1996"></ce:copyright><ce:doctopics><ce:doctopic><ce:text>Clinical section</ce:text></ce:doctopic></ce:doctopics></item-info><head><ce:dochead><ce:textfn>Research article</ce:textfn></ce:dochead><ce:title>Plasma catechols and monoamine oxidase metabolites in untreated Parkinson's and Alzheimer's diseases</ce:title><ce:author-group><ce:author><ce:given-name>J.Eric</ce:given-name><ce:surname>Ahlskog</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Ryan J.</ce:given-name><ce:surname>Uitti</ce:surname><ce:cross-ref refid="AFF4"><ce:sup>d</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Gertrude M.</ce:given-name><ce:surname>Tyce</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>John F.</ce:given-name><ce:surname>O'Brien</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>c</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Ronald C.</ce:given-name><ce:surname>Petersen</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Emre</ce:given-name><ce:surname>Kokmen</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Physiology and Biophysics, Mayo Clinic Rochester, Rochester, MN 55905, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Department Laboratory Medicine and Pathology, Mayo Clinic Rochester, Rochester, MN 55905, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF4"><ce:label>d</ce:label><ce:textfn>Department of Neurology, Mayo Clinic Jacksonville; Jacksonville, FL, USA</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Corresponding author. Tel.: +1 (507) 284-9231; Fax: +1 (507) 284-2203.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="9" month="5" year="1995"></ce:date-received><ce:date-revised day="19" month="9" year="1995"></ce:date-revised><ce:date-accepted day="27" month="9" year="1995"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Prior studies have documented functional and pathological compromise of the peripheral sympathetic nervous system in patients with Parkinson's disease, suggesting the possibility of reduced catecholamine release into the circulation. We measured free plasma catechols in early and untreated patients with Parkinson's disease, but found no evidence of reduced concentrations, compared to control subjects or a group of patients with probable Alzheimer's disease. Rather, there was a significant elevation of plasma norepinephrine within the Parkinson's disease group. Furthermore, 6 of 15 untreated Parkinson's disease patients (40%) displayed markedly elevated plasma concentrations of the catecholamine MAO metabolites, DOPAC or DOPEG. Despite this finding, platelet MAO-B activity measured in these and all other Parkinson's disease patients fell well within the range of the control subjects, and was also statistically similar to the group with Alzheimer's type dementia. Plasma dopa levels were similar in all groups, whereas the majority of patients in the three groups had plasma free dopamine and epinephrine concentrations below the limits of detection. These trends toward increased, rather than decreased, circulating catechol concentrations suggest that peripheral sympathetic nervous system catecholamine production and release is not severely compromised in patients with early Parkinson's disease. In addition, we were unable to confirm certain previous reports of elevated MAO-B activity in patients with Parkinson's or Alzheimer's diseases.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Catecholamine</ce:text></ce:keyword><ce:keyword><ce:text>Monoamine oxidase</ce:text></ce:keyword><ce:keyword><ce:text>Parkinson's disease</ce:text></ce:keyword><ce:keyword><ce:text>Alzheimer's disease</ce:text></ce:keyword><ce:keyword><ce:text>DOPAC</ce:text></ce:keyword><ce:keyword><ce:text>DOPEG</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Plasma catechols and monoamine oxidase metabolites in untreated Parkinson's and Alzheimer's diseases</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Plasma catechols and monoamine oxidase metabolites in untreated Parkinson's and Alzheimer's diseases</title></titleInfo><name type="personal"><namePart type="given">J.Eric</namePart><namePart type="family">Ahlskog</namePart><affiliation>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</affiliation><description>Corresponding author. Tel.: +1 (507) 284-9231; Fax: +1 (507) 284-2203.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ryan J.</namePart><namePart type="family">Uitti</namePart><affiliation>Department of Neurology, Mayo Clinic Jacksonville; Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gertrude M.</namePart><namePart type="family">Tyce</namePart><affiliation>Department of Physiology and Biophysics, Mayo Clinic Rochester, Rochester, MN 55905, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John F.</namePart><namePart type="family">O'Brien</namePart><affiliation>Department Laboratory Medicine and Pathology, Mayo Clinic Rochester, Rochester, MN 55905, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ronald C.</namePart><namePart type="family">Petersen</namePart><affiliation>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Emre</namePart><namePart type="family">Kokmen</namePart><affiliation>Department of Neurology, Mayo Clinic Rochester, Rochester, MI 55905, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1995</dateIssued><dateValid encoding="w3cdtf">1995-09-27</dateValid><dateModified encoding="w3cdtf">1995-09-19</dateModified><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Prior studies have documented functional and pathological compromise of the peripheral sympathetic nervous system in patients with Parkinson's disease, suggesting the possibility of reduced catecholamine release into the circulation. We measured free plasma catechols in early and untreated patients with Parkinson's disease, but found no evidence of reduced concentrations, compared to control subjects or a group of patients with probable Alzheimer's disease. Rather, there was a significant elevation of plasma norepinephrine within the Parkinson's disease group. Furthermore, 6 of 15 untreated Parkinson's disease patients (40%) displayed markedly elevated plasma concentrations of the catecholamine MAO metabolites, DOPAC or DOPEG. Despite this finding, platelet MAO-B activity measured in these and all other Parkinson's disease patients fell well within the range of the control subjects, and was also statistically similar to the group with Alzheimer's type dementia. Plasma dopa levels were similar in all groups, whereas the majority of patients in the three groups had plasma free dopamine and epinephrine concentrations below the limits of detection. These trends toward increased, rather than decreased, circulating catechol concentrations suggest that peripheral sympathetic nervous system catecholamine production and release is not severely compromised in patients with early Parkinson's disease. In addition, we were unable to confirm certain previous reports of elevated MAO-B activity in patients with Parkinson's or Alzheimer's diseases.</abstract><note type="content">Section title: Research article</note><subject><genre>Article category</genre><topic>Clinical section</topic></subject><subject><genre>Keywords</genre><topic>Catecholamine</topic><topic>Monoamine oxidase</topic><topic>Parkinson's disease</topic><topic>Alzheimer's disease</topic><topic>DOPAC</topic><topic>DOPEG</topic></subject><relatedItem type="host"><titleInfo><title>Journal of the Neurological Sciences</title></titleInfo><titleInfo type="abbreviated"><title>JNS</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">199603</dateIssued></originInfo><identifier type="ISSN">0022-510X</identifier><identifier type="PII">S0022-510X(00)X0005-6</identifier><part><date>199603</date><detail type="volume"><number>136</number><caption>vol.</caption></detail><detail type="issue"><number>1–2</number><caption>no.</caption></detail><extent unit="issue pages"><start>1</start><end>202</end></extent><extent unit="pages"><start>162</start><end>168</end></extent></part></relatedItem><identifier type="istex">F164C656FA89DA0907A2F1EBDEA8FAB39E920533</identifier><identifier type="DOI">10.1016/0022-510X(95)00318-V</identifier><identifier type="PII">0022-510X(95)00318-V</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/F164C656FA89DA0907A2F1EBDEA8FAB39E920533/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROIMAGING</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments></istex></record>Pour manipuler ce document sous Unix (Dilib)
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