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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Tracking extranigral degeneration in animal models of Parkinson’s disease: Quest for effective therapeutic strategies</title><author><name sortKey="Knaryan, Varduhi H" sort="Knaryan, Varduhi H" uniqKey="Knaryan V" first="Varduhi H." last="Knaryan">Varduhi H. Knaryan</name><affiliation><nlm:aff id="A1"> Department of Neurosciences, Medical University of South Carolina, Charleston, South Carolina, USA</nlm:aff></affiliation></author><author><name sortKey="Samantaray, Supriti" sort="Samantaray, Supriti" uniqKey="Samantaray S" first="Supriti" last="Samantaray">Supriti Samantaray</name><affiliation><nlm:aff id="A1"> Department of Neurosciences, Medical University of South Carolina, Charleston, South Carolina, USA</nlm:aff></affiliation></author><author><name sortKey="Le Gal, Charlene" sort="Le Gal, Charlene" uniqKey="Le Gal C" first="Charlene" last="Le Gal">Charlene Le Gal</name><affiliation><nlm:aff id="A2"> Inter-University Exchange Student from Université de Poitiers, France</nlm:aff></affiliation></author><author><name sortKey="Ray, Swapan K" sort="Ray, Swapan K" uniqKey="Ray S" first="Swapan K." last="Ray">Swapan K. Ray</name><affiliation><nlm:aff id="A3"> Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, Columbia, South Carolina, USA</nlm:aff></affiliation></author><author><name sortKey="Banik, Naren L" sort="Banik, Naren L" uniqKey="Banik N" first="Naren L." last="Banik">Naren L. Banik</name><affiliation><nlm:aff id="A1"> Department of Neurosciences, Medical University of South Carolina, Charleston, South Carolina, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">21615738</idno><idno type="pmc">3135734</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3135734</idno><idno type="RBID">PMC:3135734</idno><idno type="doi">10.1111/j.1471-4159.2011.07320.x</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">000614</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000614</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Tracking extranigral degeneration in animal models of Parkinson’s disease: Quest for effective therapeutic strategies</title><author><name sortKey="Knaryan, Varduhi H" sort="Knaryan, Varduhi H" uniqKey="Knaryan V" first="Varduhi H." last="Knaryan">Varduhi H. Knaryan</name><affiliation><nlm:aff id="A1"> Department of Neurosciences, Medical University of South Carolina, Charleston, South Carolina, USA</nlm:aff></affiliation></author><author><name sortKey="Samantaray, Supriti" sort="Samantaray, Supriti" uniqKey="Samantaray S" first="Supriti" last="Samantaray">Supriti Samantaray</name><affiliation><nlm:aff id="A1"> Department of Neurosciences, Medical University of South Carolina, Charleston, South Carolina, USA</nlm:aff></affiliation></author><author><name sortKey="Le Gal, Charlene" sort="Le Gal, Charlene" uniqKey="Le Gal C" first="Charlene" last="Le Gal">Charlene Le Gal</name><affiliation><nlm:aff id="A2"> Inter-University Exchange Student from Université de Poitiers, France</nlm:aff></affiliation></author><author><name sortKey="Ray, Swapan K" sort="Ray, Swapan K" uniqKey="Ray S" first="Swapan K." last="Ray">Swapan K. Ray</name><affiliation><nlm:aff id="A3"> Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, Columbia, South Carolina, USA</nlm:aff></affiliation></author><author><name sortKey="Banik, Naren L" sort="Banik, Naren L" uniqKey="Banik N" first="Naren L." last="Banik">Naren L. Banik</name><affiliation><nlm:aff id="A1"> Department of Neurosciences, Medical University of South Carolina, Charleston, South Carolina, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Neurochemistry</title><idno type="ISSN">0022-3042</idno><idno type="eISSN">1471-4159</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Sporadic Parkinson’s disease (PD) is now interpreted as a complex nervous system disorder in which the projection neurons are predominantly damaged. Such an interpretation is based on mapping of Lewy body (LB) and Lewy neurite (LN) pathology. Symptoms of the human disease are much widespread, which span from preclinical nonmotor symptoms and clinical motor symptoms to cognitive discrepancies often seen in advanced stages. Existing symptomatic treatments further complicate with overt drug-irresponsive symptoms. PD is better understood by assimilation of extranigral degenerative pathways with nigrostriatal degenerative mechanisms. The term ‘extranigral’ appeared first in ‘90s’ to more rigorously define the nigral pathology by process of elimination. However, as clinicians progressively identified PD symptoms unresponsive to the gold standard drug L-DOPA, definitions of PD symptoms were redefined. Nonmotor symptoms prodromal to motor symptoms just as preclinical to clinical, and conjointly emerged the concept of nigral versus extranigral degeneration in PD. While nigrostriatal degeneration is responsible for the neurobiological substrates of extrapyramydal motor features, extranigral degeneration corroborates a vast majority of other changes in discrete central, peripheral, and enteric nervous system nuclei which together account for global symptoms of the human disease. As an extranigral site, spinal cord has also been implicated in PD progression. Interconnected to the upper central nervous system structures with descending and ascending pathways, spinal neurons participate in movement and sensory circuits, controlling movement and reflexes. Several clinical and <italic>in vivo</italic> studies have demonstrated signs of parkinsonism-related degenerative processes in spinal cord, which led to recent consideration of spinal cord as an area of potential therapeutic applications. In nutshell, the review explores how the existing animal models can actually reflect the human disease in order to facilitate PD research. Evolution of extranigral degeneration studies has been succinctly revisited, followed by a survey on animal models in light of recent findings in clinical PD. Together, it may help to develop effective therapeutic strategies.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">2985190R</journal-id><journal-id journal-id-type="pubmed-jr-id">5004</journal-id><journal-id journal-id-type="nlm-ta">J Neurochem</journal-id><journal-id journal-id-type="iso-abbrev">J. Neurochem.</journal-id><journal-title-group><journal-title>Journal of Neurochemistry</journal-title></journal-title-group><issn pub-type="ppub">0022-3042</issn><issn pub-type="epub">1471-4159</issn></journal-meta><article-meta><article-id pub-id-type="pmid">21615738</article-id><article-id pub-id-type="pmc">3135734</article-id><article-id pub-id-type="doi">10.1111/j.1471-4159.2011.07320.x</article-id><article-id pub-id-type="manuscript">NIHMS299615</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Tracking extranigral degeneration in animal models of Parkinson’s disease: Quest for effective therapeutic strategies</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Knaryan</surname><given-names>Varduhi H.</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref rid="FN2" ref-type="author-notes">a</xref></contrib><contrib contrib-type="author"><name><surname>Samantaray</surname><given-names>Supriti</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref rid="FN2" ref-type="author-notes">a</xref></contrib><contrib contrib-type="author"><name><surname>Le Gal</surname><given-names>Charlene</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Ray</surname><given-names>Swapan K.</given-names></name><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Banik</surname><given-names>Naren L.</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref rid="FN1" ref-type="author-notes">*</xref></contrib></contrib-group><aff id="A1"><label>1</label> Department of Neurosciences, Medical University of South Carolina, Charleston, South Carolina, USA</aff><aff id="A2"><label>2</label> Inter-University Exchange Student from Université de Poitiers, France</aff><aff id="A3"><label>3</label> Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, Columbia, South Carolina, USA</aff><author-notes><corresp id="FN1"><label>*</label>Address for correspondence: Naren L. Banik, Ph.D., Division of Neurology, Department of Neurosciences, Medical University of South Carolina, 96 Jonathan Lucas Street, Suite 309, Charleston, SC 29425, USA. Voice: 1-843-792-7594, fax: 1-843-792-8626, <email>baniknl@musc.edu</email></corresp><fn id="FN2" fn-type="equal"><label>a</label><p>V. Knaryan and S. Samantaray contributed equally.</p></fn></author-notes><pub-date pub-type="nihms-submitted"><day>3</day><month>6</month><year>2011</year></pub-date><pub-date pub-type="epub"><day>17</day><month>6</month><year>2011</year></pub-date><pub-date pub-type="ppub"><month>8</month><year>2011</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>8</month><year>2012</year></pub-date><volume>118</volume><issue>3</issue><fpage>326</fpage><lpage>338</lpage><abstract><p id="P1">Sporadic Parkinson’s disease (PD) is now interpreted as a complex nervous system disorder in which the projection neurons are predominantly damaged. Such an interpretation is based on mapping of Lewy body (LB) and Lewy neurite (LN) pathology. Symptoms of the human disease are much widespread, which span from preclinical nonmotor symptoms and clinical motor symptoms to cognitive discrepancies often seen in advanced stages. Existing symptomatic treatments further complicate with overt drug-irresponsive symptoms. PD is better understood by assimilation of extranigral degenerative pathways with nigrostriatal degenerative mechanisms. The term ‘extranigral’ appeared first in ‘90s’ to more rigorously define the nigral pathology by process of elimination. However, as clinicians progressively identified PD symptoms unresponsive to the gold standard drug L-DOPA, definitions of PD symptoms were redefined. Nonmotor symptoms prodromal to motor symptoms just as preclinical to clinical, and conjointly emerged the concept of nigral versus extranigral degeneration in PD. While nigrostriatal degeneration is responsible for the neurobiological substrates of extrapyramydal motor features, extranigral degeneration corroborates a vast majority of other changes in discrete central, peripheral, and enteric nervous system nuclei which together account for global symptoms of the human disease. As an extranigral site, spinal cord has also been implicated in PD progression. Interconnected to the upper central nervous system structures with descending and ascending pathways, spinal neurons participate in movement and sensory circuits, controlling movement and reflexes. Several clinical and <italic>in vivo</italic> studies have demonstrated signs of parkinsonism-related degenerative processes in spinal cord, which led to recent consideration of spinal cord as an area of potential therapeutic applications. In nutshell, the review explores how the existing animal models can actually reflect the human disease in order to facilitate PD research. Evolution of extranigral degeneration studies has been succinctly revisited, followed by a survey on animal models in light of recent findings in clinical PD. Together, it may help to develop effective therapeutic strategies.</p></abstract><kwd-group><kwd>Parkinson’s disease</kwd><kwd>animal models</kwd><kwd>extranigral degeneration</kwd><kwd>spinal cord degeneration</kwd></kwd-group><funding-group><award-group><funding-source country="United States">National Institute of Neurological Disorders and Stroke : NINDS</funding-source><award-id>R01 NS062327-01A2 || NS</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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