Late stage treatment with arimoclomol delays disease progression and prevents protein aggregation in the SOD1 mouse model of ALS
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Therapeutic neuroprotective agents for amyotrophic lateral sclerosisHeat shock transcription factor 1 as a therapeutic target in neurodegenerative diseasesDeficiency of the zinc finger protein ZFP106 causes motor and sensory neurodegeneration.Targeting protein homeostasis in sporadic inclusion body myositis.Molecular chaperone mediated late-stage neuroprotection in the SOD1(G93A) mouse model of amyotrophic lateral sclerosisCo-induction of the heat shock response ameliorates disease progression in a mouse model of human spinal and bulbar muscular atrophy: implications for therapyPlasma neurofilament heavy chain levels correlate to markers of late stage disease progression and treatment response in SOD1(G93A) mice that model ALSNonlethal dose of silver nanoparticles attenuates TNF-α-induced hepatic epithelial cell death through HSP70 overexpression.A comprehensive assessment of the SOD1G93A low-copy transgenic mouse, which models human amyotrophic lateral sclerosis.Overexpression of human wild-type FUS causes progressive motor neuron degeneration in an age- and dose-dependent fashion.A novel SOD1-ALS mutation separates central and peripheral effects of mutant SOD1 toxicityProtein Homeostasis in Amyotrophic Lateral Sclerosis: Therapeutic Opportunities?One universal common endpoint in mouse models of amyotrophic lateral sclerosis.Potential therapeutic drugs and methods for the treatment of amyotrophic lateral sclerosis.Heat shock protein-based therapy as a potential candidate for treating the sphingolipidoses.The novel hydroxylamine derivative NG-094 suppresses polyglutamine protein toxicity in Caenorhabditis elegans.A novel small molecule HSP90 inhibitor, NXD30001, differentially induces heat shock proteins in nervous tissue in culture and in vivoArimoclomol: a potential therapy under development for ALS.Substantially elevating the levels of αB-crystallin in spinal motor neurons of mutant SOD1 mice does not significantly delay paralysis or attenuate mutant protein aggregation.Molecular chaperones in Parkinson's disease--present and futureAmyotrophic lateral sclerosis: update and new developments.Lysosomal membrane permeability stimulates protein aggregate formation in neurons of a lysosomal diseaseRegulation of superoxide dismutase genes: implications in disease.The role of molecular chaperones in human misfolding diseases.A nonsense mutation in mouse Tardbp affects TDP43 alternative splicing activity and causes limb-clasping and body tone defects.Heat shock proteins: keys to healthy ageing?Molecular chaperones as rational drug targets for Parkinson's disease therapeutics.Evidence-based drug treatment in amyotrophic lateral sclerosis and upcoming clinical trials.Emerging drugs for treating skeletal muscle injury and promoting muscle repair.Molecular chaperones and associated cellular clearance mechanisms against toxic protein conformers in Parkinson's disease.SOD1 and TDP-43 animal models of amyotrophic lateral sclerosis: recent advances in understanding disease toward the development of clinical treatments.Emerging drugs for amyotrophic lateral sclerosis.Drug targets from genetics: α-synuclein.Clinical utility of neuroprotective agents in neurodegenerative diseases: current status of drug development for Alzheimer's, Parkinson's and Huntington's diseases, and amyotrophic lateral sclerosis.Moving forward in clinical trials for ALS: motor neurons lead the way please.Barcoding heat shock proteins to human diseases: looking beyond the heat shock responseThe ER mitochondria calcium cycle and ER stress response as therapeutic targets in amyotrophic lateral sclerosis.Molecular chaperones and neuronal proteostasis.A retrospective review of the progress in amyotrophic lateral sclerosis drug discovery over the last decade and a look at the latest strategies.Eukaryotic aggresomes: from a model of conformational diseases to an emerging type of immobilized biocatalyzers.
P2860
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P2860
Late stage treatment with arimoclomol delays disease progression and prevents protein aggregation in the SOD1 mouse model of ALS
description
2008 nî lūn-bûn
@nan
2008 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
name
Late stage treatment with arim ...... in the SOD1 mouse model of ALS
@ast
Late stage treatment with arim ...... in the SOD1 mouse model of ALS
@en
Late stage treatment with arim ...... in the SOD1 mouse model of ALS
@nl
type
label
Late stage treatment with arim ...... in the SOD1 mouse model of ALS
@ast
Late stage treatment with arim ...... in the SOD1 mouse model of ALS
@en
Late stage treatment with arim ...... in the SOD1 mouse model of ALS
@nl
prefLabel
Late stage treatment with arim ...... in the SOD1 mouse model of ALS
@ast
Late stage treatment with arim ...... in the SOD1 mouse model of ALS
@en
Late stage treatment with arim ...... in the SOD1 mouse model of ALS
@nl
P2093
P2860
P3181
P1476
Late stage treatment with arim ...... in the SOD1 mouse model of ALS
@en
P2093
Bernadett Kalmar
Boris Margulis
Linda Greensmith
Michael E Cheetham
Sergey Novoselov
P2860
P304
P3181
P356
10.1111/J.1471-4159.2008.05595.X
P407
P577
2008-10-01T00:00:00Z