about
Recent progress in the discovery of small molecules for the treatment of amyotrophic lateral sclerosis (ALS)ALS Patient Stem Cells for Unveiling Disease Signatures of Motoneuron Susceptibility: Perspectives on the Deadly Mitochondria, ER Stress and Calcium TriadCRISPR/Cas9: a powerful genetic engineering tool for establishing large animal models of neurodegenerative diseasesiPSC-Based Models to Unravel Key Pathogenetic Processes Underlying Motor Neuron Disease DevelopmentMicroglia centered pathogenesis in ALS: insights in cell interconnectivityMonoaminergic control of spinal locomotor networks in SOD1G93A newborn mice.The Wobbler mouse model of amyotrophic lateral sclerosis (ALS) displays hippocampal hyperexcitability, and reduced number of interneurons, but no presynaptic vesicle release impairments.Elevated mRNA-levels of distinct mitochondrial and plasma membrane Ca(2+) transporters in individual hypoglossal motor neurons of endstage SOD1 transgenic mice.Significant expansion of the REST/NRSF cistrome in human versus mouse embryonic stem cells: potential implications for neural developmentAstroglia acquires a toxic neuroinflammatory role in response to the cerebrospinal fluid from amyotrophic lateral sclerosis patientsCa2+ entry pathways in mouse spinal motor neurons in culture following in vitro exposure to methylmercury.Selective mitochondrial Ca2+ uptake deficit in disease endstage vulnerable motoneurons of the SOD1G93A mouse model of amyotrophic lateral sclerosis.Inflammatory and non-inflammatory monocytes as novel prognostic biomarkers of survival in SOD1G93A mouse model of Amyotrophic Lateral Sclerosis.Host genetic background influences diverse neurological responses to viral infection in mice.Intramuscular Injections Along the Motor End Plates: A Minimally Invasive Approach to Shuttle Tracers Directly into Motor NeuronsLinks between electrophysiological and molecular pathology of amyotrophic lateral sclerosis.Etiogenic factors present in the cerebrospinal fluid from amyotrophic lateral sclerosis patients induce predominantly pro-inflammatory responses in microglia.CRISPR/Cas9 Technology as an Emerging Tool for Targeting Amyotrophic Lateral Sclerosis (ALS).Senataxin mutations elicit motor neuron degeneration phenotypes and yield TDP-43 mislocalization in ALS4 mice and human patients
P2860
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P2860
description
2011 nî lūn-bûn
@nan
2011 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Genetic rodent models of amyotrophic lateral sclerosis
@ast
Genetic rodent models of amyotrophic lateral sclerosis
@en
Genetic rodent models of amyotrophic lateral sclerosis
@nl
type
label
Genetic rodent models of amyotrophic lateral sclerosis
@ast
Genetic rodent models of amyotrophic lateral sclerosis
@en
Genetic rodent models of amyotrophic lateral sclerosis
@nl
prefLabel
Genetic rodent models of amyotrophic lateral sclerosis
@ast
Genetic rodent models of amyotrophic lateral sclerosis
@en
Genetic rodent models of amyotrophic lateral sclerosis
@nl
P2860
P356
P1476
Genetic rodent models of amyotrophic lateral sclerosis
@en
P2093
L Van Den Bosch
P2860
P304
P356
10.1155/2011/348765
P577
2011-01-02T00:00:00Z