ArticleExperimental neurology2007
The lack of effect of specific overexpression of IGF-1 in the central nervous system or skeletal muscle on pathophysiology in the G93A SOD-1 mouse model of ALS.
Article in Experimental neurology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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
20 citing papers in PubMed, 37 citations in OpenAlex.
- A randomized, double blind, placebo-controlled trial of pioglitazone in combination with riluzole in amyotrophic lateral sclerosis.PloS one · 2012Trial
- Subcutaneous IGF-1 is not beneficial in 2-year ALS trial.Neurology · 2008Trial
- The evidence for old age motor neuron death: A scoping review.Physiological reports · 2026Article
- Application of Neurotrophic Factors as a Therapeutic Approach for Neurodegenerative Diseases.Experimental neurobiology · 2025Review
- Androgen receptor antagonism accelerates disease onset in the SOD1British journal of pharmacology · 2019Article
- Astrocyte-Mediated Neuromodulatory Regulation in Preclinical ALS: A Metadata Analysis.Frontiers in cellular neuroscience · 2018Article
- Potential new complication in drug therapy development for amyotrophic lateral sclerosis.Expert review of neurotherapeutics · 2016Review
- Article
- The Role of Skeletal Muscle in Amyotrophic Lateral Sclerosis.Brain pathology (Zurich, Switzerland) · 2016Review
- The Paradoxical Signals of Two TrkC Receptor Isoforms Supports a Rationale for Novel Therapeutic Strategies in ALS.PloS one · 2016Article
- Progressive impairment of CaV1.1 function in the skeletal muscle of mice expressing a mutant type 1 Cu/Zn superoxide dismutase (G93A) linked to amyotrophic lateral sclerosis.Skeletal muscle · 2016Article
- Mechanisms of Muscle Denervation in Aging: Insights from a Mouse Model of Amyotrophic Lateral Sclerosis.Aging and disease · 2015Review
- Expression and regulation of excitation-contraction coupling proteins in aging skeletal muscle.Current aging science · 2011Review
- Motor neuron trophic factors: therapeutic use in ALS?Brain research reviews · 2011Review
- AAV4-mediated expression of IGF-1 and VEGF within cellular components of the ventricular system improves survival outcome in familial ALS mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2010Article
- Tetanus toxin C-fragment: the courier and the cure?Toxins · 2010Review
- Motor neuron-immune interactions: the vicious circle of ALS.Journal of neural transmission (Vienna, Austria : 1996) · 2010Review
- Neurotrophic growth factors for the treatment of amyotrophic lateral sclerosis: where do we stand?Frontiers in neuroscience · 2010Article
- Insulin-like growth factor-I for the treatment of amyotrophic lateral sclerosis.Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases · 2009Review
- Insulin-like growth factors in the peripheral nervous system.Endocrinology · 2008Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The ability of insulin like growth factor 1 (IGF-1) to prevent the pathophysiology associated with amyotrophic lateral sclerosis (ALS) is currently being explored with animal models and in clinical trials with patients. Several studies have reported positive effects of IGF-1 in reducing motor neuron death, delaying the onset of motor performance decline, and increasing life span, in SOD-1 mouse models of ALS and in one clinical trial. However, a second clinical trial produced no positive results raising questions about the therapeutic efficacy of IGF-1. To investigate the effect of specific and sustained IGF-1 expression in skeletal muscle or central nervous system on motor performance, life span, and motor neuron survival, human-IGF-1 transgenic mice were crossed with the G93A SOD-1 mutant model of ALS. No significant differences were found in onset of motor performance decline, life span, or motor neuron survival in the spinal cord, between SOD+/IGF-1+ and SOD+/IGF-1- hybrid mice. IGF-1 concentration levels, measured by radioimmunoassay, were found to be highly increased throughout life in the central nervous system (CNS) and skeletal muscle of IGF-1 transgenic hybrid mice. Additionally, increased CNS weight in SOD+ mice crossbred with CNS IGF-1 transgenic mice demonstrates that IGF-1 overexpression is biologically active even after the disease is fully developed. Taken together, these results raise questions concerning the therapeutic value of IGF-1 and indicate that further studies are needed to examine the relationship between methods of IGF-1 administration and its potential therapeutic value.
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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.