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Article

Copper-ATSM as a Treatment for ALS: Support from Mutant SOD1 Models and Beyond

4 Nov 2020

Abstract excerpt

The blood–brain barrier permeant, copper-containing compound, CuII(atsm), has successfully progressed from fundamental research outcomes in the laboratory through to phase 2/3 clinical assessment in patients with the highly aggressive and fatal neurodegenerative condition of amyotrophic lateral sclerosis (ALS). The most compelling outcomes to date to indicate potential for disease-modification have come from...

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PMID: 33158182
DOI: 10.3390/life10110271

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Copper-ATSM as a Treatment for ALS: Support from Mutant SOD1 Models and BeyondPMID 33158182Read ↗

CuII(atsm) improves the neurological phenotype and survival of SOD1G93A mice and selectively increases enzymatically active SOD1 in the spinal cord.Semantic proximity Read ↗

Disrupted copper availability in sporadic ALS: Implications for Cu <sup>II</sup> (atsm) as a treatment optionSemantic proximity Read ↗

Copper Homeostasis as a Therapeutic Target in Amyotrophic Lateral Sclerosis with SOD1 Mutations.Semantic proximity Read ↗

Cells Overexpressing ALS-Associated SOD1 Variants Are Differentially Susceptible to CuATSM-Associated Toxicity.Semantic proximity Read ↗

Transgenics, toxicity and therapeutics in rodent models of mutant SOD1-mediated familial ALS.Semantic proximity Read ↗

CuATSM improves motor function and extends survival but is not tolerated at a high dose in SOD1G93A mice with a C57BL/6 backgroundSemantic proximity Read ↗

Dysregulation of intracellular copper homeostasis is common to transgenic mice expressing human mutant superoxide dismutase-1s regardless of their copper-binding abilities.Semantic proximity Read ↗

Unraveling the Complexity of Amyotrophic Lateral Sclerosis: Recent Advances from the Transgenic Mutant SOD1 MiceSemantic proximity Read ↗

A copper chaperone-mimetic polytherapy for SOD1-associated amyotrophic lateral sclerosis.Semantic proximity Read ↗

Overexpression of metallothionein-I, a copper-regulating protein, attenuates intracellular copper dyshomeostasis and extends lifespan in a mouse model of amyotrophic lateral sclerosis caused by mutant superoxide dismutase-1.Semantic proximity Read ↗

Oral treatment with Cu(II)(atsm) increases mutant SOD1 in vivo but protects motor neurons and improves the phenotype of a transgenic mouse model of amyotrophic lateral sclerosis.Semantic proximity Read ↗

Transgenic mouse models of amyotrophic lateral sclerosis.Semantic proximity Read ↗

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