ReviewProgress in neurobiology2012
Developing treatment for spinal and bulbar muscular atrophy.
Review in Progress in neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- EQ-5D and SF-6D health utility scores in patients with spinal and bulbar muscular atrophy.The European journal of health economics : HEPAC : health economics in prevention and care · 2023Article
- The French national protocol for Kennedy's disease (SBMA): consensus diagnostic and management recommendations.Orphanet journal of rare diseases · 2020Article
- The Role of Sex and Sex Hormones in Neurodegenerative Diseases.Endocrine reviews · 2020Review
- Autophagy induction by trehalose: Molecular mechanisms and therapeutic impacts.Journal of cellular physiology · 2018Review
- The metabolic and endocrine characteristics in spinal and bulbar muscular atrophy.Journal of neurology · 2018Article
- Clinical Trials in Spinal and Bulbar Muscular Atrophy-Past, Present, and Future.Journal of molecular neuroscience : MN · 2016Review
- The Role of the Protein Quality Control System in SBMA.Journal of molecular neuroscience : MN · 2016Review
- Synergic prodegradative activity of Bicalutamide and trehalose on the mutant androgen receptor responsible for spinal and bulbar muscular atrophy.Human molecular genetics · 2015Article
- Clinical and genetic diversity of SMN1-negative proximal spinal muscular atrophies.Brain : a journal of neurology · 2014Review
- Muscle matters in Kennedy's disease.Neuron · 2014Article
- Clearance of the mutant androgen receptor in motoneuronal models of spinal and bulbar muscular atrophy.Neurobiology of aging · 2013Article
- A role for androgen reduction treatment in Kennedy disease?Muscle & nerve · 2013Article
- Mechanisms mediating spinal and bulbar muscular atrophy: investigations into polyglutamine-expanded androgen receptor function and dysfunction.Frontiers in neurology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Spinal and bulbar muscular atrophy is unique among the polyglutamine diseases in that the toxicity of the mutant protein, the androgen receptor, is ligand-dependent. In cell culture and animal models the mutant androgen receptor causes protein aggregation and alterations in transcriptional regulation, axonal transport, and mitochondrial function. Various therapeutic approaches have shown efficacy in mouse models, including androgen reduction and agents that alter the processing and degradation of the mutant androgen receptor protein, such as HSP90 inhibitors, IGF-1, and ASC-J9. Clinical trials of androgen-reducing agents have shown indications of efficacy but not proof of clinically meaningful benefit to date. This trial experience has set the stage for future clinical studies of other agents that have been found to be beneficial in transgenic animal models.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.