Parkinson's syndrome and Parkinson's disease in mitochondrial disorders.
Identifieur interne : 001403 ( PubMed/Curation ); précédent : 001402; suivant : 001404Parkinson's syndrome and Parkinson's disease in mitochondrial disorders.
Auteurs : Josef Finsterer [Autriche]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2011.
English descriptors
- KwdEn :
- DNA, Mitochondrial (genetics), Humans, Mitochondrial Diseases (complications), Mitochondrial Diseases (genetics), Mitochondrial Diseases (therapy), Mutation (genetics), Parkinson Disease (etiology), Parkinson Disease (genetics), Parkinson Disease (pathology), Parkinson Disease (therapy), Parkinsonian Disorders (etiology), Parkinsonian Disorders (genetics), Parkinsonian Disorders (pathology), Parkinsonian Disorders (therapy).
- MESH :
- chemical , genetics : DNA, Mitochondrial.
- complications : Mitochondrial Diseases.
- etiology : Parkinson Disease, Parkinsonian Disorders.
- genetics : Mitochondrial Diseases, Mutation, Parkinson Disease, Parkinsonian Disorders.
- pathology : Parkinson Disease, Parkinsonian Disorders.
- therapy : Mitochondrial Diseases, Parkinson Disease, Parkinsonian Disorders.
- Humans.
Abstract
In the majority of cases, mitochondrial disorders are multisystem conditions that most frequently affect the skeletal muscle, followed by the central nervous system. One of the clinical manifestations of central nervous system involvement is Parkinson's syndrome (PS). Evidence for an association of mitochondrial defects with PS comes from mitochondrial disorder patients who have developed Parkinson's syndrome and from Parkinson's syndrome patients who have developed a mitochondrial disorder. In addition, there are a number of patients with Parkinson's syndrome or Parkinson's disease (PD) who later develop subclinical immunohistological or biochemical indications of mitochondrial defects or accumulates mitochondrial DNA mutations within various cerebral regions. There are also Parkinson's syndrome patients who present with elevated cerebrospinal-fluid lactate by magnetic resonance spectroscopy. Furthermore, it has been shown that mutations in genes causing PD, such as PINK1, parkin, DJ1, alpha-synuclein, and LRRK2, also cause mitochondrial dysfunction, which is one of the reasons why they are called mitochondrial nigropathies. Parkinson's syndrome in patients with a mitochondrial disorder may also result from oxidative stress or exogenous toxins. Treatment of mitochondrial Parkinson's syndrome is not at variance with the treatment of Parkinson's syndrome due to other causes, but because of the multisystem nature of mitochondrial disorders, mitochondrial Parkinson's syndrome requires additional therapeutic support.
DOI: 10.1002/mds.23651
PubMed: 21384429
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One of the clinical manifestations of central nervous system involvement is Parkinson's syndrome (PS). Evidence for an association of mitochondrial defects with PS comes from mitochondrial disorder patients who have developed Parkinson's syndrome and from Parkinson's syndrome patients who have developed a mitochondrial disorder. In addition, there are a number of patients with Parkinson's syndrome or Parkinson's disease (PD) who later develop subclinical immunohistological or biochemical indications of mitochondrial defects or accumulates mitochondrial DNA mutations within various cerebral regions. There are also Parkinson's syndrome patients who present with elevated cerebrospinal-fluid lactate by magnetic resonance spectroscopy. Furthermore, it has been shown that mutations in genes causing PD, such as PINK1, parkin, DJ1, alpha-synuclein, and LRRK2, also cause mitochondrial dysfunction, which is one of the reasons why they are called mitochondrial nigropathies. Parkinson's syndrome in patients with a mitochondrial disorder may also result from oxidative stress or exogenous toxins. Treatment of mitochondrial Parkinson's syndrome is not at variance with the treatment of Parkinson's syndrome due to other causes, but because of the multisystem nature of mitochondrial disorders, mitochondrial Parkinson's syndrome requires additional therapeutic support.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">21384429</PMID><DateCreated><Year>2011</Year><Month>04</Month><Day>26</Day></DateCreated><DateCompleted><Year>2011</Year><Month>08</Month><Day>24</Day></DateCompleted><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>26</Volume><Issue>5</Issue><PubDate><Year>2011</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. 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In addition, there are a number of patients with Parkinson's syndrome or Parkinson's disease (PD) who later develop subclinical immunohistological or biochemical indications of mitochondrial defects or accumulates mitochondrial DNA mutations within various cerebral regions. There are also Parkinson's syndrome patients who present with elevated cerebrospinal-fluid lactate by magnetic resonance spectroscopy. Furthermore, it has been shown that mutations in genes causing PD, such as PINK1, parkin, DJ1, alpha-synuclein, and LRRK2, also cause mitochondrial dysfunction, which is one of the reasons why they are called mitochondrial nigropathies. Parkinson's syndrome in patients with a mitochondrial disorder may also result from oxidative stress or exogenous toxins. Treatment of mitochondrial Parkinson's syndrome is not at variance with the treatment of Parkinson's syndrome due to other causes, but because of the multisystem nature of mitochondrial disorders, mitochondrial Parkinson's syndrome requires additional therapeutic support.</AbstractText><CopyrightInformation>Copyright © 2011 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Finsterer</LastName><ForeName>Josef</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Krankenanstalt Rudolfstiftung, Vienna, Danube University, Krems, Austria. fifigs1@yahoo.de</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>03</Month><Day>07</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004272">DNA, Mitochondrial</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004272">DNA, Mitochondrial</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D028361">Mitochondrial Diseases</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000628">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009154">Mutation</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000628">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020734">Parkinsonian Disorders</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000628">therapy</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2010</Year><Month>8</Month><Day>2</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2010</Year><Month>12</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2011</Year><Month>1</Month><Day>3</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2011</Year><Month>3</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>3</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>3</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>8</Month><Day>25</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.23651</ArticleId><ArticleId IdType="pubmed">21384429</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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