[FONT="]IGF 1 lr3 as we know is a fantastic growth factor for bodybuilders and athletes of all kinds. Used for Building quality lean muscle mass, as well as for its ability to keep you lean by way of signa;ling the body to burn fat for energy. We have also read and posted many studies here at MuscleChemistry regarding Insulin-like growth factor 1 healing power and regenerative capabilities on tendons and cartlidge and it promotes collagen synthesis as well. But lately I have been reading a ton on IGF 1 treatment for Central Nervous System Disorders.
So Enjoy:
The therapeutic potential of IGF-1 was found to be relevant to the treatment of several CNS disorders, most notably Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Alzheimer’s Disease, Parkinson’s Disease, and autism spectrum disorder. Table 1 categorizes the human clinical trials in specific CNS diseases.
[h=3]Table 1[/h]Clinical Trials with IGF-1 in CNS DisordersOverview of clinical trials using IGF-1 as a therapeutic agent in CNS disorders to date
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The extensive investigation of the effect of IGF-1 during development and the continued discovery of its diverse roles throughout the CNS exemplifies the presence of common underlying pathways responsible for neuronal development. Although many different genetic mutations and disrupted pathways lead to syndromes associated with ASD, there is significant overlap in their molecular and electrophysiological deficits. Specific deficits in synaptic function and plasticity in glutamate signaling have been consistently documented in various forms of ASD using mouse and human neuronal models and have been rescued with IGF-1. The link between synapse dysfunction and ASD suggest that treatment with IGF-1 may also have implications for ASD associated with disruptions in common underlying pathways. Preliminary studies in children with PMS and Rett syndrome have been successful, and IGF-1 may also be a promising therapeutic candidate in other single gene causes of ASD and perhaps in idiopathic ASD; a trial is underway with IGF-1 in ASD defined broadly (ClinicalTrials.gov Identifier: NCT01970345). Although definitive studies are needed, pilot data suggest the promise of IGF-1 in neurodevelopmental disorders associated with ASD.
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[FONT="][h=3]Highlights[/h]
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So Enjoy:
The therapeutic potential of IGF-1 was found to be relevant to the treatment of several CNS disorders, most notably Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Alzheimer’s Disease, Parkinson’s Disease, and autism spectrum disorder. Table 1 categorizes the human clinical trials in specific CNS diseases.
[h=3]Table 1[/h]Clinical Trials with IGF-1 in CNS DisordersOverview of clinical trials using IGF-1 as a therapeutic agent in CNS disorders to date
Intervention | Author and Year | Sample Size | Study Design | Duration of Treatment | Primary Outcome Measure | Outcome | |
---|---|---|---|---|---|---|---|
Multiple Sclerosis | rhIGF-1 | (J. A. Frank et al., 2002) | 7 | Open-label crossover | 6 months | Contrast enhancing lesion frequency on MRI | Negative |
Amyotrophic Lateral Sclerosis | rhIGF-1 | (Nagano, Shiote, et al., 2005) | 9 | Double- blind, randomized clinical | 9 months | Norris Scales | Positive |
Amyotrophic Lateral Sclerosis | rhIGF-1 | (Lai et al., 1997) | 141 | Double blind, placebo controlled, parallel group | 9 months | Appel Amyotrophic Lateral Sclerosis rating scale | Positive |
Amyotrophic Lateral Sclerosis | rhIGF-1 | (Borasio et al., 1998) | 183 | Double blind, placebo controlled, parallel group | 9 months | Appel Amyotrophic Lateral Sclerosis rating scale | Negative |
Amyotrophic Lateral Sclerosis | rhIGF-1 | (Sorenson et al., 2008) | 330 | Double blind, placebo controlled, parallel group | 2 years | Rate of change in the averaged manual muscle testing score (MMT) | Negative |
Alzheimer’s Dementia | MK-677 | (Sevigny et al., 2008) | 563 | Double blind, placebo controlled, parallel group | 12 months | Clinician’s Interview Based Impression of Change with caregiver input (CIBIC-plus) | Negative |
Phelan- McDermid syndrome | rhIGF-1 | (Kolevzon et al., 2014) | 9 | Double blind, placebo controlled, crossover | 3 months | Aberrant Behavior Checklist-Social Withdrawal subscale | Positive |
Rett syndrome | rhIGF-1 | (Khwaja et al., 2014) | 9 (MAD) 12 (OLE) | Unblind multiple ascending dose and open label extension | 4 week MAD 20 week OLE | Multiple Cardiorespiratory measures | Positive |
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Abbreviations: MK-677 = ibutamoren mesylate; MAD = multiple ascending dose; OLE = open-label extensionThe extensive investigation of the effect of IGF-1 during development and the continued discovery of its diverse roles throughout the CNS exemplifies the presence of common underlying pathways responsible for neuronal development. Although many different genetic mutations and disrupted pathways lead to syndromes associated with ASD, there is significant overlap in their molecular and electrophysiological deficits. Specific deficits in synaptic function and plasticity in glutamate signaling have been consistently documented in various forms of ASD using mouse and human neuronal models and have been rescued with IGF-1. The link between synapse dysfunction and ASD suggest that treatment with IGF-1 may also have implications for ASD associated with disruptions in common underlying pathways. Preliminary studies in children with PMS and Rett syndrome have been successful, and IGF-1 may also be a promising therapeutic candidate in other single gene causes of ASD and perhaps in idiopathic ASD; a trial is underway with IGF-1 in ASD defined broadly (ClinicalTrials.gov Identifier: NCT01970345). Although definitive studies are needed, pilot data suggest the promise of IGF-1 in neurodevelopmental disorders associated with ASD.
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[FONT="][h=3]Highlights[/h]
- IGF-1 is necessary for proper development of the central nervous system
- IGF-1 dysregulation leads to neuronal dysfunction and severe developmental disorders
- IGF-1 may be a safe and potentially effective treatment for several CNS disorders
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