Oxidation versus aggregation - how do SOD1 mutants cause ALS?

Article Abstract:

An overview is presented of genetic and cell biology research on the mechanism by which amyotrophic lateral sclerosis is induced by mutant superoxide dismutase 1 (SOD1). Possible mechanisms include protein degradation, protein folding and oxidative chemistry.

Physiological aspects, Oxidation, Physiological, Physiological oxidation, Cell aggregation

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Lentiviral-mediated silencing of SOD1 through RNA interference retards disease onset and progression in a mouse model of ALS

Article Abstract:

The ability of lentiviral vectors encoding super-oxide dismutase (SOD1) short hairpin RNA species (shRNA) to protect against mutant SOD1 toxicity both in vitro and vivo are investigated. An shRNA is developed to provide potent silencing of all forms of human SOD1, so as to be potentially applicable to the majority of mutant proteins.

Science & research, Research, RNA interference

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Silencing mutant SOD1 using RNAi protects against neurodegenration and extends survival in an ALS model

Article Abstract:

A lentiviral vector is generated to mediate expression of RNAi molecules specifically targeting the human superoxide dismutase (SOD1) gene (SOD1). Injection of this vector into various muscle groups of mice engineered to overexpress a mutated form of human SOD1 resulted in an efficient and specific reduction of SOD1 expression and improved survival of vulnerable motor neurons in the brainstem and spinal cord.

Nervous system, Superoxide dismutase, Neurodegenerative diseases

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