pd – -Translation – Keybot Dictionary

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Show textShow cached sourceOpen source URL	PD is a common neurodegenerative disease that greatly reduces quality of life and costs the United States around 23 billion dollars a year. Until now, researchers have encountered difficulty in reproducing PD pathology in animals because of an incomplete understanding of the disease.
Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine actu.epfl.ch as primary domain	La MP est une maladie neurodégénérative courante qui porte sensiblement atteinte à la qualité de la vie de l’être humain et coûte quelque 23 milliards de dollars par an au système de santé américain. Jusqu’ici, les chercheurs avaient du mal à reproduire la pathologie parkinsonienne chez les animaux en raison d’une compréhension incomplète de la maladie.

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Show textShow cached sourceOpen source URL	PD is a common neurodegenerative disease that greatly reduces quality of life and costs the United States around 23 billion dollars a year. Until now, researchers have encountered difficulty in reproducing PD pathology in animals because of an incomplete understanding of the disease.
Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine actu.epfl.ch as primary domain	La MP est une maladie neurodégénérative courante qui porte sensiblement atteinte à la qualité de la vie de l’être humain et coûte quelque 23 milliards de dollars par an au système de santé américain. Jusqu’ici, les chercheurs avaient du mal à reproduire la pathologie parkinsonienne chez les animaux en raison d’une compréhension incomplète de la maladie.

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Recently, a mutation of the gene coding for LRRK2, a large enzyme in the brain, has emerged as the most prevalent genetic cause of PD (genetics are implicated in about 10 percent of all PD cases). When the enzyme is mutated, it becomes hyperactive, causing the death of vulnerable neurons and leading to a reduction in levels of the brain neurotransmistter dopamine.

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Récemment, il est apparu qu’une mutation du gène codant pour la LRRK2, une enzyme cérébrale de grande taille, était la cause génétique prévalente de la MP (les facteurs génétiques sont impliqués dans environ 10 pour cent des cas de la maladie). En cas de mutation, cette enzyme devient hyperactive et entraîne la mort de neurones vulnérables, ce qui diminue le niveau de dopamine, un neurotransmetteur du cerveau. Cette baisse de la dopamine finit par déclencher les symptômes caractéristiques de la MP, tels que les tremblements, l’instabilité, les troubles de mouvement et, à terme, la démence.

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Evidence is steadily mounting that genetic factors play an important role in many cases of Parkinson’s disease (PD). In a study published February 2, 2011, online in the Journal of Neuroscience, researchers from the Ecole Polytechnique Fédérale de Lausanne (EPFL) in Switzerland report a new mammalian model for studying a specific gene mutation commonly found in PD sufferers, opening the door to new drugs to fight the malady.

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De plus en plus d’indices tendent à montrer que les facteurs génétiques jouent un rôle important dans de nombreux cas de maladie de Parkinson (MP). Dans une étude en ligne publiée le 2 février 2011 par le Journal of Neuroscience, des chercheurs de l’Ecole Polytechnique Fédérale de Lausanne (EPFL) présentent un nouveau modèle animal pour l’étude d’une mutation génétique spécifique que l’on rencontre fréquemment chez les personnes souffrant de MP. Cette avancée ouvre la voie à la mise au point de médicaments innovants qui faciliteront la lutte contre cette maladie.

  A New Model for Studyin...  

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Evidence is steadily mounting that genetic factors play an important role in many cases of Parkinson’s disease (PD). In a study published February 2, 2011, online in the Journal of Neuroscience, researchers from the Ecole Polytechnique Fédérale de Lausanne (EPFL) in Switzerland report a new mammalian model for studying a specific gene mutation commonly found in PD sufferers, opening the door to new drugs to fight the malady.

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De plus en plus d’indices tendent à montrer que les facteurs génétiques jouent un rôle important dans de nombreux cas de maladie de Parkinson (MP). Dans une étude en ligne publiée le 2 février 2011 par le Journal of Neuroscience, des chercheurs de l’Ecole Polytechnique Fédérale de Lausanne (EPFL) présentent un nouveau modèle animal pour l’étude d’une mutation génétique spécifique que l’on rencontre fréquemment chez les personnes souffrant de MP. Cette avancée ouvre la voie à la mise au point de médicaments innovants qui faciliteront la lutte contre cette maladie.

  A New Model for Studyin...  

Show textShow cached sourceOpen source URL

Recently, a mutation of the gene coding for LRRK2, a large enzyme in the brain, has emerged as the most prevalent genetic cause of PD (genetics are implicated in about 10 percent of all PD cases). When the enzyme is mutated, it becomes hyperactive, causing the death of vulnerable neurons and leading to a reduction in levels of the brain neurotransmistter dopamine.

Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine actu.epfl.ch as primary domain

Récemment, il est apparu qu’une mutation du gène codant pour la LRRK2, une enzyme cérébrale de grande taille, était la cause génétique prévalente de la MP (les facteurs génétiques sont impliqués dans environ 10 pour cent des cas de la maladie). En cas de mutation, cette enzyme devient hyperactive et entraîne la mort de neurones vulnérables, ce qui diminue le niveau de dopamine, un neurotransmetteur du cerveau. Cette baisse de la dopamine finit par déclencher les symptômes caractéristiques de la MP, tels que les tremblements, l’instabilité, les troubles de mouvement et, à terme, la démence.

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Armed with the LRRK2 model, new pharmaceuticals that inhibit the hyper-activity of the enzyme could one day prevent the destructive chain of events that leads to neurodegeneration and devastation in many with PD.

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Le nouveau modèle mammalien élaboré par l’EPFL ne manquera pas de profiter à la recherche future sur la MP. Le fait que la LRRK2 soit une enzyme – une protéine catalytique impliquée dans des réactions chimiques – la rend accessible aux médicaments et donc particulièrement intéressante pour les chercheurs qui tentent d’identifier des stratégies neuroprotectrices ou des traitements pharmaceutiques capables de ralentir, voire d’interrompre la progression de la maladie en protégeant les neurones vulnérables. Armés du modèle LRRK2, de nouveaux produits pharmaceutiques inhibant l’hyperactivité de l’enzyme pourraient un jour prévenir la chaîne d’événements destructrice qui aboutit à la neurodégénérescence et aux ravages que subissent de nombreux patients atteints de MP.

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Now, with funding from the Michael J. Fox Foundation for Parkinson's Research, Aebischer and his team in the Neurodegenerative Studies Laboratory at EPFL, have successfully introduced mutant LRRK2 enzyme into one hemisphere of a rat brain, resulting in the same PD manifestations that occur in humans in one side of the rodent’s body.

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Grâce à un financement de la Fondation Michael J. Fox pour la recherche sur la maladie de Parkinson, Patrick Aebischer et son équipe du Laboratoire d’études sur la neurodégénérescence de l’EPFL ont réussi à introduire l’enzyme LRRK2 mutée dans l’hémisphère cérébral d’un rat et à provoquer, d’un côté de son corps, les mêmes manifestations parkinsoniennes que celles survenant chez l’être humain. Pour obtenir ce résultat, les chercheurs ont passé deux années à produire, puis à optimiser un vecteur viral permettant de transporter, vers le cerveau du rongeur, l’ADN codant de l’enzyme mutée. Etant donné la complexité et la taille de la LRRK2, la conception d’un vecteur capable de transporter son code génétique extrêmement long n’a pas été une mince affaire.

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Mutations in the genes encoding LRRK2 and α-synuclein cause autosomal dominant forms of familial Parkinson's disease (PD). Fibrillar forms of α-synuclein are a major component of Lewy bodies, the intracytoplasmic proteinaceous inclusions that are a pathological hallmark of idiopathic and certain familial forms of PD.

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Mutations in the genes encoding LRRK2 and α-synuclein cause autosomal dominant forms of familial Parkinson's disease (PD). Fibrillar forms of α-synuclein are a major component of Lewy bodies, the intracytoplasmic proteinaceous inclusions that are a pathological hallmark of idiopathic and certain familial forms of PD. LRRK2 mutations cause late-onset familial PD with a clinical, neurochemical and, for the most part, neuropathological phenotype that is indistinguishable from idiopathic PD. Importantly, α-synuclein-positive Lewy bodies are the most common pathology identified in the brains of PD subjects harboring LRRK2 mutations. These observations may suggest that LRRK2 functions in a common pathway with α-synuclein to regulate its aggregation. To explore the potential pathophysiological interaction between LRRK2 and α-synuclein in vivo, the group of Prof. Darren Moore(Laboratory of Molecular Neurodegenerative Research) modulated LRRK2 expression in a well-established human A53T α-synuclein transgenic mouse model with transgene expression driven by the hindbrain-selective prion protein promoter. They failed to provide support for a pathophysiological interaction of LRRK2 and α-synuclein in vivo, at least within neurons of the mouse hindbrain.

  New insightes in the pa...  

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Mutations in the genes encoding LRRK2 and α-synuclein cause autosomal dominant forms of familial Parkinson's disease (PD). Fibrillar forms of α-synuclein are a major component of Lewy bodies, the intracytoplasmic proteinaceous inclusions that are a pathological hallmark of idiopathic and certain familial forms of PD.

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Mutations in the genes encoding LRRK2 and α-synuclein cause autosomal dominant forms of familial Parkinson's disease (PD). Fibrillar forms of α-synuclein are a major component of Lewy bodies, the intracytoplasmic proteinaceous inclusions that are a pathological hallmark of idiopathic and certain familial forms of PD. LRRK2 mutations cause late-onset familial PD with a clinical, neurochemical and, for the most part, neuropathological phenotype that is indistinguishable from idiopathic PD. Importantly, α-synuclein-positive Lewy bodies are the most common pathology identified in the brains of PD subjects harboring LRRK2 mutations. These observations may suggest that LRRK2 functions in a common pathway with α-synuclein to regulate its aggregation. To explore the potential pathophysiological interaction between LRRK2 and α-synuclein in vivo, the group of Prof. Darren Moore(Laboratory of Molecular Neurodegenerative Research) modulated LRRK2 expression in a well-established human A53T α-synuclein transgenic mouse model with transgene expression driven by the hindbrain-selective prion protein promoter. They failed to provide support for a pathophysiological interaction of LRRK2 and α-synuclein in vivo, at least within neurons of the mouse hindbrain.

  New insightes in the pa...  

Show textShow cached sourceOpen source URL

Mutations in the genes encoding LRRK2 and α-synuclein cause autosomal dominant forms of familial Parkinson's disease (PD). Fibrillar forms of α-synuclein are a major component of Lewy bodies, the intracytoplasmic proteinaceous inclusions that are a pathological hallmark of idiopathic and certain familial forms of PD.

Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine actu.epfl.ch as primary domain

Mutations in the genes encoding LRRK2 and α-synuclein cause autosomal dominant forms of familial Parkinson's disease (PD). Fibrillar forms of α-synuclein are a major component of Lewy bodies, the intracytoplasmic proteinaceous inclusions that are a pathological hallmark of idiopathic and certain familial forms of PD. LRRK2 mutations cause late-onset familial PD with a clinical, neurochemical and, for the most part, neuropathological phenotype that is indistinguishable from idiopathic PD. Importantly, α-synuclein-positive Lewy bodies are the most common pathology identified in the brains of PD subjects harboring LRRK2 mutations. These observations may suggest that LRRK2 functions in a common pathway with α-synuclein to regulate its aggregation. To explore the potential pathophysiological interaction between LRRK2 and α-synuclein in vivo, the group of Prof. Darren Moore(Laboratory of Molecular Neurodegenerative Research) modulated LRRK2 expression in a well-established human A53T α-synuclein transgenic mouse model with transgene expression driven by the hindbrain-selective prion protein promoter. They failed to provide support for a pathophysiological interaction of LRRK2 and α-synuclein in vivo, at least within neurons of the mouse hindbrain.

  New insightes in the pa...  

Show textShow cached sourceOpen source URL

Mutations in the genes encoding LRRK2 and α-synuclein cause autosomal dominant forms of familial Parkinson's disease (PD). Fibrillar forms of α-synuclein are a major component of Lewy bodies, the intracytoplasmic proteinaceous inclusions that are a pathological hallmark of idiopathic and certain familial forms of PD.

Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine actu.epfl.ch as primary domain

Mutations in the genes encoding LRRK2 and α-synuclein cause autosomal dominant forms of familial Parkinson's disease (PD). Fibrillar forms of α-synuclein are a major component of Lewy bodies, the intracytoplasmic proteinaceous inclusions that are a pathological hallmark of idiopathic and certain familial forms of PD. LRRK2 mutations cause late-onset familial PD with a clinical, neurochemical and, for the most part, neuropathological phenotype that is indistinguishable from idiopathic PD. Importantly, α-synuclein-positive Lewy bodies are the most common pathology identified in the brains of PD subjects harboring LRRK2 mutations. These observations may suggest that LRRK2 functions in a common pathway with α-synuclein to regulate its aggregation. To explore the potential pathophysiological interaction between LRRK2 and α-synuclein in vivo, the group of Prof. Darren Moore(Laboratory of Molecular Neurodegenerative Research) modulated LRRK2 expression in a well-established human A53T α-synuclein transgenic mouse model with transgene expression driven by the hindbrain-selective prion protein promoter. They failed to provide support for a pathophysiological interaction of LRRK2 and α-synuclein in vivo, at least within neurons of the mouse hindbrain.

  New insightes in the pa...  

Show textShow cached sourceOpen source URL

Mutations in the genes encoding LRRK2 and α-synuclein cause autosomal dominant forms of familial Parkinson's disease (PD). Fibrillar forms of α-synuclein are a major component of Lewy bodies, the intracytoplasmic proteinaceous inclusions that are a pathological hallmark of idiopathic and certain familial forms of PD.

Compare text pagesCompare HTM pagesOpen source URLOpen target URLDefine actu.epfl.ch as primary domain

Mutations in the genes encoding LRRK2 and α-synuclein cause autosomal dominant forms of familial Parkinson's disease (PD). Fibrillar forms of α-synuclein are a major component of Lewy bodies, the intracytoplasmic proteinaceous inclusions that are a pathological hallmark of idiopathic and certain familial forms of PD. LRRK2 mutations cause late-onset familial PD with a clinical, neurochemical and, for the most part, neuropathological phenotype that is indistinguishable from idiopathic PD. Importantly, α-synuclein-positive Lewy bodies are the most common pathology identified in the brains of PD subjects harboring LRRK2 mutations. These observations may suggest that LRRK2 functions in a common pathway with α-synuclein to regulate its aggregation. To explore the potential pathophysiological interaction between LRRK2 and α-synuclein in vivo, the group of Prof. Darren Moore(Laboratory of Molecular Neurodegenerative Research) modulated LRRK2 expression in a well-established human A53T α-synuclein transgenic mouse model with transgene expression driven by the hindbrain-selective prion protein promoter. They failed to provide support for a pathophysiological interaction of LRRK2 and α-synuclein in vivo, at least within neurons of the mouse hindbrain.