Functional brain imaging of cognitive dysfunction in Parkinson's disease
Identifieur interne : 000A01 ( Main/Corpus ); précédent : 000A00; suivant : 000A02Functional brain imaging of cognitive dysfunction in Parkinson's disease
Auteurs : Shigeki Hirano ; Hitoshi Shinotoh ; David EidelbergSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 2012-10.
Abstract
Multiple factors are involved in the development of cognitive impairment in Parkinson's disease (PD) and related disorders. Notably, several underlying factors, such as monoaminergic dysfunction, Lewy body pathology, Alzheimer disease-like pathology and cerebrovascular disease are implied in the PD pathophysiology of cognitive impairment. The mesocortical dopaminergic system is associated with executive functions which are frequently affected in PD and are influenced by local levodopa concentration, dopamine metabolism and baseline performance status. The ventral striatum and frontal cortex are associated with impulse control disorders reported in PD patients treated with dopamine replacement therapy. Cholinergic impairment in PD plays a cardinal role in the development of dementia. Acetylcholinesterase positron emission tomography demonstrates that posterior brain areas are related to cognitive decline in PD patients. Amyloid radiotracer illustrates that patients with PD with severe cognitive impairment were prone to accompanied cortical amyloid deposition. Metabolism/perfusion change associated with cognitive impairment in PD, so-called PD related cognitive pattern, is characterised by reduced frontoparietal activity and is an effective way to differentiate and monitor cognitive function of individual PD patients. Cognitive impairment in PD cannot be explained by a single mechanism and is entangled by multiple factors. Imaging studies can unravel each pathological domain, further shed light on the interrelation between different pathomechanisms, not only in PD but also in other dementia related disorders, and thereby integrate its interpretation to apply to therapeutics in individual patients.
Url:
DOI: 10.1136/jnnp-2011-301818
Links to Exploration step
ISTEX:63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Functional brain imaging of cognitive dysfunction in Parkinson's disease</title><author><name sortKey="Hirano, Shigeki" sort="Hirano, Shigeki" uniqKey="Hirano S" first="Shigeki" last="Hirano">Shigeki Hirano</name><affiliation><mods:affiliation>Department of Neurology, Chiba University School of Medicine, Chiba, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Molecular Neuroimaging Program, Molecular Imaging Centre, National Institute of Radiological Sciences, Chiba, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: s_hirano@chiba-u.jp</mods:affiliation></affiliation></author><author><name sortKey="Shinotoh, Hitoshi" sort="Shinotoh, Hitoshi" uniqKey="Shinotoh H" first="Hitoshi" last="Shinotoh">Hitoshi Shinotoh</name><affiliation><mods:affiliation>Molecular Neuroimaging Program, Molecular Imaging Centre, National Institute of Radiological Sciences, Chiba, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Asahi Hospital for Neurological Diseases, Chiba, Japan</mods:affiliation></affiliation></author><author><name sortKey="Eidelberg, David" sort="Eidelberg, David" uniqKey="Eidelberg D" first="David" last="Eidelberg">David Eidelberg</name><affiliation><mods:affiliation>The Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, New York, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Departments of Neurology and Medicine, North Shore University Hospital, New York University School of Medicine, New York, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9</idno><date when="2012" year="2012">2012</date><idno type="doi">10.1136/jnnp-2011-301818</idno><idno type="url">https://api.istex.fr/document/63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000A01</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Functional brain imaging of cognitive dysfunction in Parkinson's disease</title><author><name sortKey="Hirano, Shigeki" sort="Hirano, Shigeki" uniqKey="Hirano S" first="Shigeki" last="Hirano">Shigeki Hirano</name><affiliation><mods:affiliation>Department of Neurology, Chiba University School of Medicine, Chiba, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Molecular Neuroimaging Program, Molecular Imaging Centre, National Institute of Radiological Sciences, Chiba, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: s_hirano@chiba-u.jp</mods:affiliation></affiliation></author><author><name sortKey="Shinotoh, Hitoshi" sort="Shinotoh, Hitoshi" uniqKey="Shinotoh H" first="Hitoshi" last="Shinotoh">Hitoshi Shinotoh</name><affiliation><mods:affiliation>Molecular Neuroimaging Program, Molecular Imaging Centre, National Institute of Radiological Sciences, Chiba, Japan</mods:affiliation></affiliation><affiliation><mods:affiliation>Asahi Hospital for Neurological Diseases, Chiba, Japan</mods:affiliation></affiliation></author><author><name sortKey="Eidelberg, David" sort="Eidelberg, David" uniqKey="Eidelberg D" first="David" last="Eidelberg">David Eidelberg</name><affiliation><mods:affiliation>The Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, New York, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Departments of Neurology and Medicine, North Shore University Hospital, New York University School of Medicine, New York, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="ISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2012-10">2012-10</date><biblScope unit="volume">83</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="963">963</biblScope></imprint><idno type="ISSN">0022-3050</idno></series><idno type="istex">63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9</idno><idno type="DOI">10.1136/jnnp-2011-301818</idno><idno type="href">jnnp-83-963.pdf</idno><idno type="ArticleID">jnnp-2011-301818</idno><idno type="PMID">22807560</idno><idno type="local">jnnp;83/10/963</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3050</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Multiple factors are involved in the development of cognitive impairment in Parkinson's disease (PD) and related disorders. Notably, several underlying factors, such as monoaminergic dysfunction, Lewy body pathology, Alzheimer disease-like pathology and cerebrovascular disease are implied in the PD pathophysiology of cognitive impairment. The mesocortical dopaminergic system is associated with executive functions which are frequently affected in PD and are influenced by local levodopa concentration, dopamine metabolism and baseline performance status. The ventral striatum and frontal cortex are associated with impulse control disorders reported in PD patients treated with dopamine replacement therapy. Cholinergic impairment in PD plays a cardinal role in the development of dementia. Acetylcholinesterase positron emission tomography demonstrates that posterior brain areas are related to cognitive decline in PD patients. Amyloid radiotracer illustrates that patients with PD with severe cognitive impairment were prone to accompanied cortical amyloid deposition. Metabolism/perfusion change associated with cognitive impairment in PD, so-called PD related cognitive pattern, is characterised by reduced frontoparietal activity and is an effective way to differentiate and monitor cognitive function of individual PD patients. Cognitive impairment in PD cannot be explained by a single mechanism and is entangled by multiple factors. Imaging studies can unravel each pathological domain, further shed light on the interrelation between different pathomechanisms, not only in PD but also in other dementia related disorders, and thereby integrate its interpretation to apply to therapeutics in individual patients.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>Shigeki Hirano</name><affiliations><json:string>Department of Neurology, Chiba University School of Medicine, Chiba, Japan</json:string><json:string>Molecular Neuroimaging Program, Molecular Imaging Centre, National Institute of Radiological Sciences, Chiba, Japan</json:string><json:string>E-mail: s_hirano@chiba-u.jp</json:string></affiliations></json:item><json:item><name>Hitoshi Shinotoh</name><affiliations><json:string>Molecular Neuroimaging Program, Molecular Imaging Centre, National Institute of Radiological Sciences, Chiba, Japan</json:string><json:string>Asahi Hospital for Neurological Diseases, Chiba, Japan</json:string></affiliations></json:item><json:item><name>David Eidelberg</name><affiliations><json:string>The Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, New York, USA</json:string><json:string>Departments of Neurology and Medicine, North Shore University Hospital, New York University School of Medicine, New York, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Movement disorders</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Multiple factors are involved in the development of cognitive impairment in Parkinson's disease (PD) and related disorders. Notably, several underlying factors, such as monoaminergic dysfunction, Lewy body pathology, Alzheimer disease-like pathology and cerebrovascular disease are implied in the PD pathophysiology of cognitive impairment. The mesocortical dopaminergic system is associated with executive functions which are frequently affected in PD and are influenced by local levodopa concentration, dopamine metabolism and baseline performance status. The ventral striatum and frontal cortex are associated with impulse control disorders reported in PD patients treated with dopamine replacement therapy. Cholinergic impairment in PD plays a cardinal role in the development of dementia. Acetylcholinesterase positron emission tomography demonstrates that posterior brain areas are related to cognitive decline in PD patients. Amyloid radiotracer illustrates that patients with PD with severe cognitive impairment were prone to accompanied cortical amyloid deposition. Metabolism/perfusion change associated with cognitive impairment in PD, so-called PD related cognitive pattern, is characterised by reduced frontoparietal activity and is an effective way to differentiate and monitor cognitive function of individual PD patients. Cognitive impairment in PD cannot be explained by a single mechanism and is entangled by multiple factors. Imaging studies can unravel each pathological domain, further shed light on the interrelation between different pathomechanisms, not only in PD but also in other dementia related disorders, and thereby integrate its interpretation to apply to therapeutics in individual patients.</abstract><qualityIndicators><score>8.26</score><pdfVersion>1.4</pdfVersion><pdfPageSize>595.276 x 793.701 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>1</keywordCount><abstractCharCount>1724</abstractCharCount><pdfWordCount>5346</pdfWordCount><pdfCharCount>38539</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>230</abstractWordCount></qualityIndicators><title>Functional brain imaging of cognitive dysfunction in Parkinson's disease</title><pmid><json:string>22807560</json:string></pmid><genre><json:string>review-article</json:string></genre><host><volume>83</volume><pages><first>963</first></pages><issn><json:string>0022-3050</json:string></issn><issue>10</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1468-330X</json:string></eissn><title>Journal of Neurology, Neurosurgery & Psychiatry</title></host><publicationDate>2012</publicationDate><copyrightDate>2012</copyrightDate><doi><json:string>10.1136/jnnp-2011-301818</json:string></doi><id>63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Functional brain imaging of cognitive dysfunction in Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>BMJ Publishing Group Ltd</publisher><availability><p>BMJ</p></availability><date>2012-07-17</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Functional brain imaging of cognitive dysfunction in Parkinson's disease</title><author corresp="yes"><persName><forename type="first">Shigeki</forename><surname>Hirano</surname></persName><email>s_hirano@chiba-u.jp</email><affiliation>Department of Neurology, Chiba University School of Medicine, Chiba, Japan</affiliation><affiliation>Molecular Neuroimaging Program, Molecular Imaging Centre, National Institute of Radiological Sciences, Chiba, Japan</affiliation></author><author><persName><forename type="first">Hitoshi</forename><surname>Shinotoh</surname></persName><affiliation>Molecular Neuroimaging Program, Molecular Imaging Centre, National Institute of Radiological Sciences, Chiba, Japan</affiliation><affiliation>Asahi Hospital for Neurological Diseases, Chiba, Japan</affiliation></author><author><persName><forename type="first">David</forename><surname>Eidelberg</surname></persName><affiliation>The Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, New York, USA</affiliation><affiliation>Departments of Neurology and Medicine, North Shore University Hospital, New York University School of Medicine, New York, USA</affiliation></author></analytic><monogr><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="pISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2012-10"></date><biblScope unit="volume">83</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="963">963</biblScope></imprint></monogr><idno type="istex">63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9</idno><idno type="DOI">10.1136/jnnp-2011-301818</idno><idno type="href">jnnp-83-963.pdf</idno><idno type="ArticleID">jnnp-2011-301818</idno><idno type="PMID">22807560</idno><idno type="local">jnnp;83/10/963</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2012-07-17</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Multiple factors are involved in the development of cognitive impairment in Parkinson's disease (PD) and related disorders. Notably, several underlying factors, such as monoaminergic dysfunction, Lewy body pathology, Alzheimer disease-like pathology and cerebrovascular disease are implied in the PD pathophysiology of cognitive impairment. The mesocortical dopaminergic system is associated with executive functions which are frequently affected in PD and are influenced by local levodopa concentration, dopamine metabolism and baseline performance status. The ventral striatum and frontal cortex are associated with impulse control disorders reported in PD patients treated with dopamine replacement therapy. Cholinergic impairment in PD plays a cardinal role in the development of dementia. Acetylcholinesterase positron emission tomography demonstrates that posterior brain areas are related to cognitive decline in PD patients. Amyloid radiotracer illustrates that patients with PD with severe cognitive impairment were prone to accompanied cortical amyloid deposition. Metabolism/perfusion change associated with cognitive impairment in PD, so-called PD related cognitive pattern, is characterised by reduced frontoparietal activity and is an effective way to differentiate and monitor cognitive function of individual PD patients. Cognitive impairment in PD cannot be explained by a single mechanism and is entangled by multiple factors. Imaging studies can unravel each pathological domain, further shed light on the interrelation between different pathomechanisms, not only in PD but also in other dementia related disorders, and thereby integrate its interpretation to apply to therapeutics in individual patients.</p></abstract></profileDesc><revisionDesc><change when="2012-07-17">Created</change><change when="2012-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus bmj" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="no"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Archiving and Interchange DTD v2.3 20070202//EN" URI="archivearticle.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="review-article"><front><journal-meta><journal-id journal-id-type="hwp">jnnp</journal-id><journal-id journal-id-type="nlm-ta">J Neurol Neurosurg Psychiatry</journal-id><journal-id journal-id-type="publisher-id">jnnp</journal-id><journal-title>Journal of Neurology, Neurosurgery & Psychiatry</journal-title><abbrev-journal-title abbrev-type="publisher">J Neurol Neurosurg Psychiatry</abbrev-journal-title><abbrev-journal-title>J Neurol Neurosurg Psychiatry</abbrev-journal-title><issn pub-type="ppub">0022-3050</issn><issn pub-type="epub">1468-330X</issn><publisher><publisher-name>BMJ Publishing Group Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">jnnp-2011-301818</article-id><article-id pub-id-type="doi">10.1136/jnnp-2011-301818</article-id><article-id pub-id-type="other">jnnp;83/10/963</article-id><article-id pub-id-type="other">jnnp;jnnp-2011-301818</article-id><article-id pub-id-type="pmid">22807560</article-id><article-id pub-id-type="other">963</article-id><article-id pub-id-type="other">jnnp-2011-301818</article-id><article-categories><subj-group subj-group-type="heading"><subject>Movement disorders</subject></subj-group><series-title>Review</series-title></article-categories><title-group><article-title>Functional brain imaging of cognitive dysfunction in Parkinson's disease</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Hirano</surname><given-names>Shigeki</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Shinotoh</surname><given-names>Hitoshi</given-names></name><xref ref-type="aff" rid="aff2">2</xref><xref ref-type="aff" rid="aff3">3</xref></contrib><contrib contrib-type="author"><name><surname>Eidelberg</surname><given-names>David</given-names></name><xref ref-type="aff" rid="aff4">4</xref><xref ref-type="aff" rid="aff5">5</xref></contrib></contrib-group><aff id="aff1"><label>1</label>Department of Neurology, Chiba University School of Medicine, Chiba, Japan</aff><aff id="aff2"><label>2</label>Molecular Neuroimaging Program, Molecular Imaging Centre, National Institute of Radiological Sciences, Chiba, Japan</aff><aff id="aff3"><label>3</label>Asahi Hospital for Neurological Diseases, Chiba, Japan</aff><aff id="aff4"><label>4</label>The Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, New York, USA</aff><aff id="aff5"><label>5</label>Departments of Neurology and Medicine, North Shore University Hospital, New York University School of Medicine, New York, USA</aff><author-notes><corresp><label>Correspondence to</label> Dr S Hirano, Department of Neurology, Chiba University School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba-shi, Chiba 260-8670, Japan; <email>s_hirano@chiba-u.jp</email></corresp></author-notes><pub-date pub-type="epub-original"><day>17</day><month>7</month><year>2012</year></pub-date><pub-date pub-type="ppub"><month>10</month><year>2012</year></pub-date><pub-date pub-type="epub"><day>17</day><month>7</month><year>2012</year></pub-date><volume>83</volume><volume-id pub-id-type="other">83</volume-id><volume-id pub-id-type="other">83</volume-id><issue>10</issue><issue-id pub-id-type="other">jnnp;83/10</issue-id><issue-id pub-id-type="other">10</issue-id><issue-id pub-id-type="other">83/10</issue-id><fpage>963</fpage><history><date date-type="received"><day>4</day><month>4</month><year>2012</year></date><date date-type="rev-recd"><day>13</day><month>6</month><year>2012</year></date><date date-type="accepted"><day>14</day><month>6</month><year>2012</year></date></history><permissions><copyright-statement>© 2012, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</copyright-statement><copyright-year>2012</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="jnnp-83-963.pdf"></self-uri><abstract><p>Multiple factors are involved in the development of cognitive impairment in Parkinson's disease (PD) and related disorders. Notably, several underlying factors, such as monoaminergic dysfunction, Lewy body pathology, Alzheimer disease-like pathology and cerebrovascular disease are implied in the PD pathophysiology of cognitive impairment. The mesocortical dopaminergic system is associated with executive functions which are frequently affected in PD and are influenced by local levodopa concentration, dopamine metabolism and baseline performance status. The ventral striatum and frontal cortex are associated with impulse control disorders reported in PD patients treated with dopamine replacement therapy. Cholinergic impairment in PD plays a cardinal role in the development of dementia. Acetylcholinesterase positron emission tomography demonstrates that posterior brain areas are related to cognitive decline in PD patients. Amyloid radiotracer illustrates that patients with PD with severe cognitive impairment were prone to accompanied cortical amyloid deposition. Metabolism/perfusion change associated with cognitive impairment in PD, so-called PD related cognitive pattern, is characterised by reduced frontoparietal activity and is an effective way to differentiate and monitor cognitive function of individual PD patients. Cognitive impairment in PD cannot be explained by a single mechanism and is entangled by multiple factors. Imaging studies can unravel each pathological domain, further shed light on the interrelation between different pathomechanisms, not only in PD but also in other dementia related disorders, and thereby integrate its interpretation to apply to therapeutics in individual patients.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><partName>Review</partName><title>Functional brain imaging of cognitive dysfunction in Parkinson's disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><partName>Review</partName><title>Functional brain imaging of cognitive dysfunction in Parkinson's disease</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">Shigeki</namePart><namePart type="family">Hirano</namePart><affiliation>Department of Neurology, Chiba University School of Medicine, Chiba, Japan</affiliation><affiliation>Molecular Neuroimaging Program, Molecular Imaging Centre, National Institute of Radiological Sciences, Chiba, Japan</affiliation><affiliation>E-mail: s_hirano@chiba-u.jp</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hitoshi</namePart><namePart type="family">Shinotoh</namePart><affiliation>Molecular Neuroimaging Program, Molecular Imaging Centre, National Institute of Radiological Sciences, Chiba, Japan</affiliation><affiliation>Asahi Hospital for Neurological Diseases, Chiba, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David</namePart><namePart type="family">Eidelberg</namePart><affiliation>The Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, New York, USA</affiliation><affiliation>Departments of Neurology and Medicine, North Shore University Hospital, New York University School of Medicine, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="review-article"></genre><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">2012-10</dateIssued><dateCreated encoding="w3cdtf">2012-07-17</dateCreated><copyrightDate encoding="w3cdtf">2012</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>Multiple factors are involved in the development of cognitive impairment in Parkinson's disease (PD) and related disorders. Notably, several underlying factors, such as monoaminergic dysfunction, Lewy body pathology, Alzheimer disease-like pathology and cerebrovascular disease are implied in the PD pathophysiology of cognitive impairment. The mesocortical dopaminergic system is associated with executive functions which are frequently affected in PD and are influenced by local levodopa concentration, dopamine metabolism and baseline performance status. The ventral striatum and frontal cortex are associated with impulse control disorders reported in PD patients treated with dopamine replacement therapy. Cholinergic impairment in PD plays a cardinal role in the development of dementia. Acetylcholinesterase positron emission tomography demonstrates that posterior brain areas are related to cognitive decline in PD patients. Amyloid radiotracer illustrates that patients with PD with severe cognitive impairment were prone to accompanied cortical amyloid deposition. Metabolism/perfusion change associated with cognitive impairment in PD, so-called PD related cognitive pattern, is characterised by reduced frontoparietal activity and is an effective way to differentiate and monitor cognitive function of individual PD patients. Cognitive impairment in PD cannot be explained by a single mechanism and is entangled by multiple factors. Imaging studies can unravel each pathological domain, further shed light on the interrelation between different pathomechanisms, not only in PD but also in other dementia related disorders, and thereby integrate its interpretation to apply to therapeutics in individual patients.</abstract><relatedItem type="host"><titleInfo><title>Journal of Neurology, Neurosurgery & Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol Neurosurg Psychiatry</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0022-3050</identifier><identifier type="eISSN">1468-330X</identifier><identifier type="PublisherID">jnnp</identifier><identifier type="PublisherID-hwp">jnnp</identifier><identifier type="PublisherID-nlm-ta">J Neurol Neurosurg Psychiatry</identifier><part><date>2012</date><detail type="volume"><caption>vol.</caption><number>83</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>963</start></extent></part></relatedItem><identifier type="istex">63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9</identifier><identifier type="DOI">10.1136/jnnp-2011-301818</identifier><identifier type="href">jnnp-83-963.pdf</identifier><identifier type="ArticleID">jnnp-2011-301818</identifier><identifier type="PMID">22807560</identifier><identifier type="local">jnnp;83/10/963</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2012, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</accessCondition><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9/annexes/jpeg</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000A01 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000A01 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:63DB34BE8DEF2BB0A76BBF27EE59739676EFF1E9
|texte= Functional brain imaging of cognitive dysfunction in Parkinson's disease
}}
| This area was generated with Dilib version V0.6.23. |  |