Mechano-growth factor, an IGF-I splice variant, rescues motoneurons and improves muscle function in SOD1(G93A) mice.
Riddoch-Contreras. Joanna J; Yang. Shi-Yu SY; Dick. James R T JR; Goldspink. Geoffrey G; Orrell. Richard W RW; Greensmith. Linda L
Key Findings
- MGF gene delivery improved hindlimb strength in ALS mice
- Both IGF‑I and MGF increased motor unit and motoneuron survival
- MGF led to significantly more surviving motoneurons than IGF‑I
Practical Outcomes
- The results hint that MGF might be a stronger neuroprotective agent than IGF‑I, but because the study used gene therapy in mice, it doesn’t give a clear, safe protocol for human use. Biohackers should view this as early‑stage evidence and wait for human safety and dosing data before trying MGF for neuro‑protection.
Summary
A study in ALS‑model mice showed that delivering the IGF‑I splice variant mechano‑growth factor (MGF) to leg muscles helped keep motor neurons alive and improved muscle strength, doing even better than regular IGF‑I. The work used a DNA plasmid to make the muscles produce MGF, not a simple peptide injection, and was done in mice, not people.
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by motoneuron degeneration. Although viral delivery of IGF-I has shown therapeutic efficacy in the SOD1(G93A) mouse model of ALS, clinical trials of IGF-I in ALS patients have led to conflicting results. Here we examine the effects of an IGF-I splice variant, mechano-growth factor (MGF) which has previously been shown to have greater neuroprotective effects than IGF-I in a number of models of neurodegeneration. A mammalian expression plasmid containing either MGF or, for comparison, the IGF-I cDNA sequence was delivered to the hindlimb muscles of SOD1(G93A) mice at 70 days of age, at symptom onset. Treatment with either IGF-I or MGF resulted in a significant improvement in hindlimb muscle strength, and an increase in motor unit and motoneuron survival. Significantly more motoneurons survived in MGF treated mice.
Study Information
pubmed
2008
2008-11-07T00:00:00.000Z
10.1016/j.expneurol.2008.10.014
50
43