Parkinson's disease: from causes to mechanisms.
Identifieur interne : 002F25 ( Main/Merge ); précédent : 002F24; suivant : 002F26Parkinson's disease: from causes to mechanisms.
Auteurs : Olga Corti [France] ; Cornelia Hampe ; Frédéric Darios ; Pablo Ibanez ; Merle Ruberg ; Alexis BriceSource :
- Comptes rendus biologies [ 1631-0691 ] ; 2005.
English descriptors
- KwdEn :
- Corpus Striatum (physiopathology), Dopamine (physiology), Humans, Mitochondria (pathology), Mitochondria (physiology), Nerve Tissue Proteins (genetics), Parkinson Disease (etiology), Parkinson Disease (genetics), Parkinson Disease (physiopathology), Substantia Nigra (physiopathology), Synucleins, Ubiquitin-Protein Ligases (genetics).
- MESH :
- chemical , genetics : Nerve Tissue Proteins, Ubiquitin-Protein Ligases.
- chemical , physiology : Dopamine.
- etiology : Parkinson Disease.
- genetics : Parkinson Disease.
- pathology : Mitochondria.
- physiology : Mitochondria.
- physiopathology : Corpus Striatum, Parkinson Disease, Substantia Nigra.
- Humans, Synucleins.
Abstract
Parkinson's disease (PD) is a common age-related, progressive neurodegenerative disease of unknown etiology. Environmental factors have long been suspected to participate in the pathogenesis of PD due to the existence of neurotoxins that preferentially damage the dopaminergic nigrostriatal pathway. In the past few years, novel insights into the degenerative process have been provided by the discovery of genes responsible for rare monogenic parkinsonian syndromes. Compelling evidence is accumulating, suggesting that the products of several of these genes can interact with environmental toxins and intervene in molecular pathways controlling the functional integrity of mitochondria.
PubMed: 15770999
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pubmed:15770999Le document en format XML
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scheme="KwdEn" xml:lang="en"><term>Corpus Striatum (physiopathology)</term><term>Dopamine (physiology)</term><term>Humans</term><term>Mitochondria (pathology)</term><term>Mitochondria (physiology)</term><term>Nerve Tissue Proteins (genetics)</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (physiopathology)</term><term>Substantia Nigra (physiopathology)</term><term>Synucleins</term><term>Ubiquitin-Protein Ligases (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Nerve Tissue Proteins</term><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Synucleins</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a common age-related, progressive neurodegenerative disease of unknown etiology. Environmental factors have long been suspected to participate in the pathogenesis of PD due to the existence of neurotoxins that preferentially damage the dopaminergic nigrostriatal pathway. In the past few years, novel insights into the degenerative process have been provided by the discovery of genes responsible for rare monogenic parkinsonian syndromes. Compelling evidence is accumulating, suggesting that the products of several of these genes can interact with environmental toxins and intervene in molecular pathways controlling the functional integrity of mitochondria.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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