Evidence map›Paper›PMID 23393146›Full record

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.

Bilal Malik, Niranjanan Nirmalananthan, Anna L Gray, Albert R La Spada, Michael G Hanna, Linda Greensmith

Open access · bronzeAbstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.3field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
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  5. Biosensors for Studying Neuronal Proteostasis.Frontiers in molecular neuroscience · 2022
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Bilal MalikSobell Department of Motor Neuroscience, MRC Centre for Neuromuscular Diseases, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK. l.greensmith@ucl.ac.uk
Niranjanan Nirmalananthan
Anna L Gray
Albert R La Spada
Michael G Hanna
Linda Greensmith
National Hospital for Neurology and Neurosurgery · GBUniversity College London · GBRady Children's Hospital-San Diego · US

Funding

MODELS OF SBMA MOTOR NEURON DEGENERATIONR01NS041648 · NINDS · UNIVERSITY OF WASHINGTON · PI LA SPADA, ALBERT R · 2001 to 2014
$4.5M
Medical Research Council G0601943Medical Research Council MR/K000608/1NINDS NIH HHS R01 NS041648NINDS NIH HHS R01 NS41648
6 · The paper itself

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.

Indexed as

AnimalsBlotting, WesternDisease Models, AnimalDisease ProgressionHeat-Shock ProteinsHeat-Shock ResponseHydroxylaminesMaleMiceMuscular Disorders, AtrophicNeuroprotective AgentsReal-Time Polymerase Chain ReactionarimoclomolHeat-Shock ProteinsHydroxylaminesNeuroprotective Agents

Identifiers

PMID23393146
PMCPMC3624668
OpenAlexW2127832322

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.