In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease? - Wikidata - wikimedia - TriplyDB

In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?

In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?

http://www.wikidata.org/entity/Q36976137

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Selective and brain-permeable polo-like kinase-2 (Plk-2) inhibitors that reduce α-synuclein phosphorylation in rat brain Gene-environment interactions: key to unraveling the mystery of Parkinson's disease Metabolites of purine nucleoside phosphorylase (NP) in serum have the potential to delineate pancreatic adenocarcinoma Pale body-like inclusion formation and neurodegeneration following depletion of 26S proteasomes in mouse brain neurones are independent of α-synuclein The cybrid model of sporadic Parkinson's disease.Vocalization deficits in mice over-expressing alpha-synuclein, a model of pre-manifest Parkinson's disease.Gamma-synucleinopathy: neurodegeneration associated with overexpression of the mouse protein.Axon degeneration and PGC-1α-mediated protection in a zebrafish model of α-synuclein toxicity Hippocampal α-synuclein and interneurons in Parkinson's disease: Data from human and mouse models.Strengths and limitations of genetic mouse models of Parkinson's disease.Bacterial artificial chromosome transgenic mice expressing a truncated mutant parkin exhibit age-dependent hypokinetic motor deficits, dopaminergic neuron degeneration, and accumulation of proteinase K-resistant alpha-synuclein.Extensive enteric nervous system abnormalities in mice transgenic for artificial chromosomes containing Parkinson disease-associated alpha-synuclein gene mutations precede central nervous system changes.Parkinson's disease: insights from pathways.Pros and cons of a prion-like pathogenesis in Parkinson's disease Versatile somatic gene transfer for modeling neurodegenerative diseases.25-Hydroxyvitamin D depletion does not exacerbate MPTP-induced dopamine neuron damage in mice.A53T human α-synuclein overexpression in transgenic mice induces pervasive mitochondria macroautophagy defects preceding dopamine neuron degeneration Abnormal colonic motility in mice overexpressing human wild-type alpha-synuclein.Olfactory deficits in mice overexpressing human wildtype alpha-synuclein.Animal models of Parkinson's disease: a source of novel treatments and clues to the cause of the disease.Fractalkine over expression suppresses α-synuclein-mediated neurodegeneration Targeted Overexpression of α-Synuclein by rAAV2/1 Vectors Induces Progressive Nigrostriatal Degeneration and Increases Vulnerability to MPTP in Mouse Analysis of striatal transcriptome in mice overexpressing human wild-type alpha-synuclein supports synaptic dysfunction and suggests mechanisms of neuroprotection for striatal neurons Nigral overexpression of alpha-synuclein in the absence of parkin enhances alpha-synuclein phosphorylation but does not modulate dopaminergic neurodegeneration.Adenosine A2A receptor gene disruption protects in an α-synuclein model of Parkinson's disease.α-Synuclein overexpressing transgenic mice show internal organ pathology and autonomic deficits Conditional expression of Parkinson's disease-related mutant α-synuclein in the midbrain dopaminergic neurons causes progressive neurodegeneration and degradation of transcription factor nuclear receptor related 1 Inhibition by Multifunctional Magnetic Nanoparticles Loaded with Alpha-Synuclein RNAi Plasmid in a Parkinson's Disease Model Elevated tonic extracellular dopamine concentration and altered dopamine modulation of synaptic activity precede dopamine loss in the striatum of mice overexpressing human α-synuclein Distinct roles in vivo for the ubiquitin-proteasome system and the autophagy-lysosomal pathway in the degradation of α-synuclein.TRPV1 on astrocytes rescues nigral dopamine neurons in Parkinson's disease via CNTF.MsrA knockout mouse exhibits abnormal behavior and brain dopamine levels Animal models of Parkinson's disease progression Gene therapy for misfolding protein diseases of the central nervous system.Alpha-synuclein overexpression in mice alters synaptic communication in the corticostriatal pathway.alpha-Synuclein: a therapeutic target for Parkinson's disease?Cathepsin D expression level affects alpha-synuclein processing, aggregation, and toxicity in vivo.Conditional transgenic mice expressing C-terminally truncated human alpha-synuclein (alphaSyn119) exhibit reduced striatal dopamine without loss of nigrostriatal pathway dopaminergic neurons.Region-specific deficits in dopamine, but not norepinephrine, signaling in a novel A30P α-synuclein BAC transgenic mouse.Genetic animal models of Parkinson's disease.

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P2860

In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?

http://www.wikidata.org/entity/Q36976137

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In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?

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In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?

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In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?

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J.EXPNEUROL.2007.08.006

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Experimental Neurology

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In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?

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P2860

Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis

Mutation in the alpha-synuclein gene identified in families with Parkinson's disease

Parkinson's disease: mechanisms and models

Genetic mouse models of parkinsonism: strengths and limitations.

Evaluation of epidemiologic and animal data associating pesticides with Parkinson's disease.

Modeling CNS neurodegeneration by overexpression of disease-causing proteins using viral vectors.

Dopaminergic neuron loss and up-regulation of chaperone protein mRNA induced by targeted over-expression of alpha-synuclein in mouse substantia nigra.

Aggregation promoting C-terminal truncation of alpha-synuclein is a normal cellular process and is enhanced by the familial Parkinson's disease-linked mutations

Toxin-induced models of Parkinson's disease.

beta-amyloid peptides enhance alpha-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease.

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22-27

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Parkinson's disease

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