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

Chronic treatment with lithium does not improve neuromuscular phenotype in a mouse model of severe spinal muscular atrophy.

Neuroscience - 10 Oct 2013

Dachs E, Piedrafita L, Hereu M, Esquerda J E, Calderó J

Abstract excerpt

Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disorder caused by defective levels of the survival motor neuron (SMN) protein. SMA causes spinal motoneuron (MN) loss, and progressive muscle weakness and paralysis. Currently, there is no effective therapy to cure this disease. Although different strategies focused on increasing the expression of functional SMN protein have been assayed,...

Read the complete abstract on PubMed

Topics

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

Share to Glycogen Synthase Kinase 3
Share to Glycogen Synthase Kinase 3 beta

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Lithium Chloride

Share to Oncogene Protein v-akt

Share to Postural Balance

Share to Psychomotor Performance

Share to Reflex

Share to Survival of Motor Neuron 1 Protein

Source

Identifiers

PMID: 23876328
DOI: 10.1016/j.neuroscience.2013.07.026

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

Chronic treatment with lithium does not improve neuromuscular phenotype in a mouse model of severe spinal muscular atrophy.PMID 23876328Read ↗

Inhibition of autophagy delays motoneuron degeneration and extends lifespan in a mouse model of spinal muscular atrophy.Semantic proximity Read ↗

A screen for regulators of survival of motor neuron protein levels.Semantic proximity Read ↗

Suppression of the necroptotic cell death pathways improves survival in Smn2B/− miceSemantic proximity Read ↗

Genetic inhibition of JNK3 ameliorates spinal muscular atrophySemantic proximity Read ↗

Treatment with lithium carbonate does not improve disease progression in two different strains of SOD1 mutant mice.Semantic proximity Read ↗

Increasing expression and decreasing degradation of SMN ameliorate the spinal muscular atrophy phenotype in mice.Semantic proximity Read ↗

IPLEX administration improves motor neuron survival and ameliorates motor functions in a severe mouse model of spinal muscular atrophy.Semantic proximity Read ↗

Loganin possesses neuroprotective properties, restores SMN protein and activates protein synthesis positive regulator Akt/mTOR in experimental models of spinal muscular atrophy.Semantic proximity Read ↗

Combined lithium and valproate treatment delays disease onset, reduces neurological deficits and prolongs survival in an amyotrophic lateral sclerosis mouse model.Semantic proximity Read ↗

The neuroprotective drug riluzole acts via small conductance Ca2+-activated K+ channels to ameliorate defects in spinal muscular atrophy models.Semantic proximity Read ↗

Abolishing Trp53-dependent apoptosis does not benefit spinal muscular atrophy model mice.Semantic proximity Read ↗

Abolishing Bax-Dependent Apoptosis Shows Beneficial Effects on Spinal Muscular Atrophy Model MiceSemantic proximity Read ↗

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