In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?
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Selective and brain-permeable polo-like kinase-2 (Plk-2) inhibitors that reduce α-synuclein phosphorylation in rat brainGene-environment interactions: key to unraveling the mystery of Parkinson's diseaseMetabolites of purine nucleoside phosphorylase (NP) in serum have the potential to delineate pancreatic adenocarcinomaPale body-like inclusion formation and neurodegeneration following depletion of 26S proteasomes in mouse brain neurones are independent of α-synucleinThe 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 toxicityHippocampal 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 diseaseVersatile 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 degenerationAbnormal 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 neurodegenerationTargeted Overexpression of α-Synuclein by rAAV2/1 Vectors Induces Progressive Nigrostriatal Degeneration and Increases Vulnerability to MPTP in MouseAnalysis of striatal transcriptome in mice overexpressing human wild-type alpha-synuclein supports synaptic dysfunction and suggests mechanisms of neuroprotection for striatal neuronsNigral 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 deficitsConditional 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 1Inhibition by Multifunctional Magnetic Nanoparticles Loaded with Alpha-Synuclein RNAi Plasmid in a Parkinson's Disease ModelElevated tonic extracellular dopamine concentration and altered dopamine modulation of synaptic activity precede dopamine loss in the striatum of mice overexpressing human α-synucleinDistinct 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 levelsAnimal models of Parkinson's disease progressionGene 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.
P2860
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P2860
In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?
@en
type
label
In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?
@en
prefLabel
In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?
@en
P2860
P921
P1476
In vivo alpha-synuclein overexpression in rodents: a useful model of Parkinson's disease?
@en
P2860
P356
10.1016/J.EXPNEUROL.2007.08.006
P407
P577
2007-08-23T00:00:00Z