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

Morpholino-mediated SOD1 reduction ameliorates an amyotrophic lateral sclerosis disease phenotype

16 Feb 2016

Abstract excerpt

Neurotoxicity due to the accumulation of mutant proteins is thought to drive pathogenesis in neurodegenerative diseases. Mutations in superoxide dismutase 1 (SOD1) are linked to familial amyotrophic lateral sclerosis (fALS); these mutations result in progressive motor neuron death through one or more acquired toxicities. Interestingly, SOD1 is not only responsible for fALS but may also play a significant role in...

Read the complete abstract on PubMed

Topics

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

Share to Amyotrophic Lateral Sclerosis Research
Share to biodegradable polymer synthesis and properties
Share to Neurogenetic and Muscular Disorders Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 26878886
DOI: 10.1038/srep21301

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Morpholino-mediated SOD1 reduction ameliorates an amyotrophic lateral sclerosis disease phenotypePMID 26878886Read ↗

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

Antisense oligonucleotides extend survival and reverse decrement in muscle response in ALS modelsSemantic proximity Read ↗

Antisense oligonucleotide therapy for neurodegenerative diseaseSemantic proximity Read ↗

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

Human Motor Neurons With SOD1-G93A Mutation Generated From CRISPR/Cas9 Gene-Edited iPSCs Develop Pathological Features of Amyotrophic Lateral SclerosisSemantic proximity Read ↗

Recent Progress of Antisense Oligonucleotide Therapy for Superoxide Dismutase 1-mutated Amyotrophic Lateral Sclerosis: Focus on TofersenSemantic proximity Read ↗

Amyotrophic lateral sclerosis model derived from human embryonic stem cells overexpressing mutant superoxide dismutase 1.Semantic proximity Read ↗

Mutant SOD1 knockdown in all cell types ameliorates disease in G85R SOD1 mice with a limited additional effect over knockdown restricted to motor neurons.Semantic proximity Read ↗

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

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

Recent Progress of Antisense Oligonucleotide Therapy for Superoxide-Dismutase-1-Mutated Amyotrophic Lateral Sclerosis: Focus on Tofersen.Semantic proximity Read ↗

Cell-penetrating peptide-conjugated Morpholino rescues SMA in a symptomatic preclinical model.Semantic proximity Read ↗

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