Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

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

Nature medicine - 1 Apr 2005

Raoul Cédric, Abbas-Terki Toufik, Bensadoun Jean-Charles, Guillot Sandrine, Haase Georg, Szulc Jolanta, Henderson Christopher E, Aebischer Patrick

Abstract excerpt

Mutations in Cu/Zn superoxide dismutase (encoded by SOD1), one of the causes of familial amyotrophic lateral sclerosis (ALS), lead to progressive death of motoneurons through a gain-of-function mechanism. RNA interference (RNAi) mediated by viral vectors allows for long-term reduction in gene expression and represents an attractive therapeutic approach for genetic diseases characterized by acquired toxic...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amyotrophic Lateral Sclerosis
Share to Disease Progression

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genetic Vectors

Share to Lentivirus

Share to Mice, Transgenic

Share to RNA Interference

Share to RNA, Small Interfering

Share to Superoxide Dismutase

Source

Identifiers

PMID: 15768028
DOI: 10.1038/nm1207

Genes

SOD1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Lentiviral-mediated silencing of SOD1 through RNA interference retards disease onset and progression in a mouse model of ALS.PMID 15768028Read ↗

Silencing mutant SOD1 using RNAi protects against neurodegeneration and extends survival in an ALS model.Semantic proximity Read ↗

Therapeutic gene silencing delivered by a chemically modified small interfering RNA against mutant SOD1 slows amyotrophic lateral sclerosis progression.Semantic proximity Read ↗

Allele-specific RNAi selectively silences mutant SOD1 and achieves significant therapeutic benefit in vivo.Semantic proximity Read ↗

Silence superoxide dismutase 1 (SOD1): a promising therapeutic target for amyotrophic lateral sclerosis (ALS).Semantic proximity Read ↗

Therapeutic AAV9-mediated Suppression of Mutant SOD1 Slows Disease Progression and Extends Survival in Models of Inherited ALSSemantic proximity Read ↗

SOD1 silencing in motoneurons or glia rescues neuromuscular function in <scp>ALS</scp> miceSemantic proximity Read ↗

Silencing strategies for therapy of SOD1-mediated ALS.Semantic proximity Read ↗

RNA interference and amyotrophic lateral sclerosis.Semantic proximity Read ↗

Preemptive SOD1 Silencing via Neonatal Intramuscular AAV Therapy Modifies Disease Trajectory in an ALS Mouse ModelSemantic proximity Read ↗

Selective silencing by RNAi of a dominant allele that causes amyotrophic lateral sclerosis.Semantic proximity Read ↗

Adeno‐associated virus–delivered artificial microRNA extends survival and delays paralysis in an amyotrophic lateral sclerosis mouse modelSemantic proximity Read ↗

In vivo genome editing improves motor function and extends survival in a mouse model of ALS.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.