Neurodegeneration in Parkinson's disease: genetics enlightens physiopathology.
Identifieur interne : 000C35 ( PubMed/Corpus ); précédent : 000C34; suivant : 000C36Neurodegeneration in Parkinson's disease: genetics enlightens physiopathology.
Auteurs : Olga Corti ; Margot Fournier ; Alexis BriceSource :
- Journal of neural transmission. Supplementum [ 0303-6995 ] ; 2009.
English descriptors
- KwdEn :
- Dopamine (metabolism), Humans, Mitochondrial Diseases (physiopathology), Mutation (genetics), Nerve Degeneration (etiology), Nerve Degeneration (genetics), Nerve Degeneration (pathology), Neurons (pathology), Oxidative Stress (physiology), Parkinson Disease (complications), Parkinson Disease (genetics), Protein Kinases (genetics), Ubiquitin-Protein Ligases (genetics), alpha-Synuclein (metabolism).
- MESH :
- chemical , genetics : Protein Kinases, Ubiquitin-Protein Ligases.
- chemical , metabolism : Dopamine, alpha-Synuclein.
- complications : Parkinson Disease.
- etiology : Nerve Degeneration.
- genetics : Mutation, Nerve Degeneration, Parkinson Disease.
- pathology : Nerve Degeneration, Neurons.
- physiology : Oxidative Stress.
- physiopathology : Mitochondrial Diseases.
- Humans.
Abstract
Parkinson's disease (PD) is a severe neurodegenerative disorder of complex etiology and enigmatic physiopathology. In the past decade, the identification of genes involved in rare familial Parkinsonian syndromes has brought hope that understanding the functions of their products will provide insight into the molecular mechanisms responsible for neurodegeneration. The knowledge accumulated thus far has delineated two putative, potentially interconnected, disease-causing pathways: alpha-synuclein accumulation may be central to Parkinsonism due to alpha-synuclein gene defects, but possibly also to sporadic PD and other genetic forms presenting with Lewy bodies; altered mitochondrial physiology may be pivotal to Parkinsonian syndromes caused by parkin, PINK1, and possibly DJ-1 gene mutations. Adding new pieces to this fragmentary picture to determine to what extent sporadic PD and Parkinsonism due to distinct genetic causes share common pathogenic mechanisms remains a major challenge toward the development of future therapeutic strategies for these disabling disorders.
PubMed: 20411780
Links to Exploration step
pubmed:20411780Le document en format XML
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Supplementum</title><idno type="ISSN">0303-6995</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dopamine (metabolism)</term><term>Humans</term><term>Mitochondrial Diseases (physiopathology)</term><term>Mutation (genetics)</term><term>Nerve Degeneration (etiology)</term><term>Nerve Degeneration (genetics)</term><term>Nerve Degeneration (pathology)</term><term>Neurons (pathology)</term><term>Oxidative Stress (physiology)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (genetics)</term><term>Protein Kinases (genetics)</term><term>Ubiquitin-Protein Ligases (genetics)</term><term>alpha-Synuclein (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Protein Kinases</term><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Nerve Degeneration</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Mitochondrial Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a severe neurodegenerative disorder of complex etiology and enigmatic physiopathology. In the past decade, the identification of genes involved in rare familial Parkinsonian syndromes has brought hope that understanding the functions of their products will provide insight into the molecular mechanisms responsible for neurodegeneration. The knowledge accumulated thus far has delineated two putative, potentially interconnected, disease-causing pathways: alpha-synuclein accumulation may be central to Parkinsonism due to alpha-synuclein gene defects, but possibly also to sporadic PD and other genetic forms presenting with Lewy bodies; altered mitochondrial physiology may be pivotal to Parkinsonian syndromes caused by parkin, PINK1, and possibly DJ-1 gene mutations. Adding new pieces to this fragmentary picture to determine to what extent sporadic PD and Parkinsonism due to distinct genetic causes share common pathogenic mechanisms remains a major challenge toward the development of future therapeutic strategies for these disabling disorders.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20411780</PMID><DateCreated><Year>2010</Year><Month>04</Month><Day>23</Day></DateCreated><DateCompleted><Year>2010</Year><Month>05</Month><Day>14</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0303-6995</ISSN><JournalIssue CitedMedium="Print"><Issue>73</Issue><PubDate><Year>2009</Year></PubDate></JournalIssue><Title>Journal of neural transmission. Supplementum</Title><ISOAbbreviation>J. Neural Transm. Suppl.</ISOAbbreviation></Journal><ArticleTitle>Neurodegeneration in Parkinson's disease: genetics enlightens physiopathology.</ArticleTitle><Pagination><MedlinePgn>215-21</MedlinePgn></Pagination><Abstract><AbstractText>Parkinson's disease (PD) is a severe neurodegenerative disorder of complex etiology and enigmatic physiopathology. In the past decade, the identification of genes involved in rare familial Parkinsonian syndromes has brought hope that understanding the functions of their products will provide insight into the molecular mechanisms responsible for neurodegeneration. The knowledge accumulated thus far has delineated two putative, potentially interconnected, disease-causing pathways: alpha-synuclein accumulation may be central to Parkinsonism due to alpha-synuclein gene defects, but possibly also to sporadic PD and other genetic forms presenting with Lewy bodies; altered mitochondrial physiology may be pivotal to Parkinsonian syndromes caused by parkin, PINK1, and possibly DJ-1 gene mutations. 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