ArticleBrain : a journal of neurology2013
Co-induction of the heat shock response ameliorates disease progression in a mouse model of human spinal and bulbar muscular atrophy: implications for therapy.
Article in Brain : a journal of neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 64 citations in OpenAlex.
- Breaking the proteasome balance: α-synuclein and the ubiquitin-proteasome system.Frontiers in cell and developmental biology · 2026Review
- Amplifying the Heat Shock Response Ameliorates ALS and FTD Pathology in Mouse and Human Models.Molecular neurobiology · 2023Article
- HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023Review
- Heat increases full-length SMN splicing: promise for splice-augmenting therapies for SMA.Human genetics · 2022Article
- Biosensors for Studying Neuronal Proteostasis.Frontiers in molecular neuroscience · 2022Review
- Hsc70-4 aggravates PolyQ-mediated neurodegeneration by modulating NF-κB mediated immune response inFrontiers in molecular neuroscience · 2022Article
- Proteostatic imbalance and protein spreading in amyotrophic lateral sclerosis.The EMBO journal · 2021Review
- Linking epigenetic dysregulation, mitochondrial impairment, and metabolic dysfunction in SBMA motor neurons.JCI insight · 2020Article
- Deterioration of muscle force and contractile characteristics are early pathological events in spinal and bulbar muscular atrophy mice.Disease models & mechanisms · 2020Article
- Clinical manifestations and AR gene mutations in Kennedy's disease.Functional & integrative genomics · 2019Article
- Gene expression analysis reveals early dysregulation of disease pathways and links Chmp7 to pathogenesis of spinal and bulbar muscular atrophy.Scientific reports · 2019Article
- Heat Shock Proteins and Autophagy Pathways in Neuroprotection: from Molecular Bases to Pharmacological Interventions.International journal of molecular sciences · 2018Review
- The heat shock response in neurons and astroglia and its role in neurodegenerative diseases.Molecular neurodegeneration · 2017Review
- Components of a mammalian protein disaggregation/refolding machine are targeted to nuclear speckles following thermal stress in differentiated human neuronal cells.Cell stress & chaperones · 2017Article
- Cellular Chaperones As Therapeutic Targets in ALS to Restore Protein Homeostasis and Improve Cellular Function.Frontiers in molecular neuroscience · 2017Review
- Lysosome and endoplasmic reticulum quality control pathways in Niemann-Pick type C disease.Brain research · 2016Review
- Heat shock protein-based therapy as a potential candidate for treating the sphingolipidoses.Science translational medicine · 2016Article
- 215th ENMC International Workshop VCP-related multi-system proteinopathy (IBMPFD) 13-15 November 2015, Heemskerk, The Netherlands.Neuromuscular disorders : NMD · 2016Article
- A small-molecule Nrf1 and Nrf2 activator mitigates polyglutamine toxicity in spinal and bulbar muscular atrophy.Human molecular genetics · 2016Article
- MiR-206 Attenuates Denervation-Induced Skeletal Muscle Atrophy in Rats Through Regulation of Satellite Cell Differentiation via TGF-β1, Smad3, and HDAC4 Signaling.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Spinal and bulbar muscular atrophy, also known as Kennedy's disease, is an adult-onset hereditary neurodegenerative disorder caused by an expansion of the polyglutamine repeat in the first exon in the androgen receptor gene. Pathologically, the disease is defined by selective loss of spinal and bulbar motor neurons causing bulbar, facial and limb weakness. Although the precise disease pathophysiology is largely unknown, it appears to be related to abnormal accumulation of the pathogenic androgen receptor protein within the nucleus, leading to disruption of cellular processes. Using a mouse model of spinal and bulbar muscular atrophy that exhibits many of the characteristic features of the human disease, in vivo physiological assessment of muscle function revealed that mice with the pathogenic expansion of the androgen receptor develop a motor deficit characterized by a reduction in muscle force, abnormal muscle contractile characteristics, loss of functional motor units and motor neuron degeneration. We have previously shown that treatment with arimoclomol, a co-inducer of the heat shock stress response, delays disease progression in the mutant superoxide dismutase 1 mouse model of amyotrophic lateral sclerosis, a fatal motor neuron disease. We therefore evaluated the therapeutic potential of arimoclomol in mice with spinal and bulbar muscular atrophy. Arimoclomol was administered orally, in drinking water, from symptom onset and the effects established at 18 months of age, a late stage of disease. Arimoclomol significantly improved hindlimb muscle force and contractile characteristics, rescued motor units and, importantly, improved motor neuron survival and upregulated the expression of the vascular endothelial growth factor which possess neurotrophic activity. These results provide evidence that upregulation of the heat shock response by treatment with arimoclomol may have therapeutic potential in the treatment of spinal and bulbar muscular atrophy and may also be a possible approach for the treatment of other neurodegenerative diseases.
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