Transgenic Small Interfering RNA Halts Amyotrophic Lateral Sclerosis in a Mouse Model
نویسندگان
چکیده
منابع مشابه
Informatics-assisted protein profiling in a transgenic mouse model of amyotrophic lateral sclerosis.
One of the causes of amyotrophic lateral sclerosis (ALS) is due to mutations in Cu,Zn-superoxide dismutase (SOD1). The mutant protein exhibits a toxic gain of function that adversely affects the function of neurons in the spinal cord, brain stem, and motor cortex. A proteomic analysis of protein expression in a widely used mouse model of ALS was undertaken to identify differences in protein exp...
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BACKGROUND AND PURPOSE N-methyl-D-aspartate (NMDA)-mediated neurotoxicity and oxidative stress have been implicated in the etiology of amyotrophic lateral sclerosis (ALS). Memantine is a low-affinity, noncompetitive NMDA receptor antagonist that may protect against motor neuron degeneration. METHODS Thirty transgenic mice expressing the G93A SOD1 mutation were randomly divided into control, l...
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One of the causes of amyotrophic lateral sclerosis (ALS) is due to mutations in Cu,Zn-superoxide dismutase (SOD1). The mutant protein exhibits a toxic gain of function that adversely affects the function of neurons in the spinal cord, brain stem, and motor cortex. A proteomic analysis of protein expression in a widely used mouse model of ALS was undertaken to identify differences in protein exp...
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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the selective degeneration of motor neurons. Mutations of the Cu,Zn superoxide dismutase (SOD1) account for 20% of the familial cases of ALS. Transgenic mice overexpressing the mutated human SOD1 enzyme develop phenotypic and pathological symptoms resembling ALS in humans. Previous studies showed that, in this t...
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ژورنال
عنوان ژورنال: Journal of Biological Chemistry
سال: 2005
ISSN: 0021-9258
DOI: 10.1074/jbc.m507685200