Lost in translation: treatment trials in the SOD1 mouse and in human ALS.
about
Improving basic and translational science by accounting for litter-to-litter variation in animal modelsMuscle atrophy and motor neuron degeneration in human NEDL1 transgenic miceCan animal models of disease reliably inform human studies?Examining the Predictive Validity of NIH Peer Review ScoresIdentification of new epilepsy treatments: issues in preclinical methodologyLaunching invasive, first-in-human trials against Parkinson's disease: ethical considerationsNeuroinflammation in motor neuron diseaseQuality of Animal Experiments in Anti-Angiogenic Cancer Drug Development--A Systematic ReviewMind the gap: models in multiple species needed for therapeutic development in Huntington's diseaseInduced pluripotent stem cells from ALS patients for disease modelingTherapeutic neuroprotective agents for amyotrophic lateral sclerosisTranslational spinal cord injury research: preclinical guidelines and challengesTempol moderately extends survival in a hSOD1(G93A) ALS rat model by inhibiting neuronal cell loss, oxidative damage and levels of non-native hSOD1(G93A) formsEmerging from the bottleneck: benefits of the comparative approach to modern neuroscienceA comprehensive library of familial human amyotrophic lateral sclerosis induced pluripotent stem cellsACTH (Acthar Gel) Reduces Toxic SOD1 Protein Linked to Amyotrophic Lateral Sclerosis in Transgenic Mice: A Novel ObservationBromocriptine Mesylate Attenuates Amyotrophic Lateral Sclerosis: A Phase 2a, Randomized, Double-Blind, Placebo-Controlled Research in Japanese PatientsThe mdx mouse model as a surrogate for Duchenne muscular dystrophyComprehensive behavioral testing in the R6/2 mouse model of Huntington's disease shows no benefit from CoQ10 or minocyclineA comprehensive assessment of the SOD1G93A low-copy transgenic mouse, which models human amyotrophic lateral sclerosis.Genome-wide association analysis reveals a SOD1 mutation in canine degenerative myelopathy that resembles amyotrophic lateral sclerosis.Evaluation of animal models of neurobehavioral disorders.Gene expression profiling for human iPS-derived motor neurons from sporadic ALS patients reveals a strong association between mitochondrial functions and neurodegeneration.An in vitro screening cascade to identify neuroprotective antioxidants in ALSNoninvasive model of sciatic nerve conduction in healthy and septic mice: reliability and normative data.Control of neuroinflammation as a therapeutic strategy for amyotrophic lateral sclerosis and other neurodegenerative disordersIdentification of compounds protective against G93A-SOD1 toxicity for the treatment of amyotrophic lateral sclerosis.Loss of Ranbp2 in motoneurons causes disruption of nucleocytoplasmic and chemokine signaling, proteostasis of hnRNPH3 and Mmp28, and development of amyotrophic lateral sclerosis-like syndromesUbiquilin modifies TDP-43 toxicity in a Drosophila model of amyotrophic lateral sclerosis (ALS).Spinal but not cortical microglia acquire an atypical phenotype with high VEGF, galectin-3 and osteopontin, and blunted inflammatory responses in ALS rats.Potential involvement of intracellular pH in a mouse model of amyotrophic lateral sclerosis.Optimised and rapid pre-clinical screening in the SOD1(G93A) transgenic mouse model of amyotrophic lateral sclerosis (ALS).Reduction in hSOD1 copy number significantly impacts ALS phenotype presentation in G37R (line 29) mice: implications for the assessment of putative therapeutic agentsHuman skeletal muscle stem cell antiinflammatory activity ameliorates clinical outcome in amyotrophic lateral sclerosis models.Catalytic antioxidants and neurodegenerationSuperoxide dismutase mimics: chemistry, pharmacology, and therapeutic potentialPharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trialsEarly detection of motor dysfunction in the SOD1G93A mouse model of Amyotrophic Lateral Sclerosis (ALS) using home cage running wheels.The rho kinase inhibitor Y-27632 improves motor performance in male SOD1(G93A) mice.Unlike physical exercise, modified environment increases the lifespan of SOD1G93A mice however both conditions induce cellular changes.
P2860
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P2860
Lost in translation: treatment trials in the SOD1 mouse and in human ALS.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
Lost in translation: treatment trials in the SOD1 mouse and in human ALS.
@ast
Lost in translation: treatment trials in the SOD1 mouse and in human ALS.
@en
type
label
Lost in translation: treatment trials in the SOD1 mouse and in human ALS.
@ast
Lost in translation: treatment trials in the SOD1 mouse and in human ALS.
@en
prefLabel
Lost in translation: treatment trials in the SOD1 mouse and in human ALS.
@ast
Lost in translation: treatment trials in the SOD1 mouse and in human ALS.
@en
P1476
Lost in translation: treatment trials in the SOD1 mouse and in human ALS.
@en
P356
10.1016/J.NBD.2006.12.015
P577
2007-01-03T00:00:00Z