Studies on Neuroprotective Potential of IGF-1 DES Peptide

Insulin-like growth factor-1 DES (a splicing variation) seems to be a shortened and endogenous protein. Studies suggest that IGF-1 DES peptide may induce hypertrophy and hyperplasia in various cell types. Extensive research suggests it may be more effective than regular IGF-1 potentially from an increased bioavailability.

IGF-1 DES inflammation and neurological diseases are now the focus of active research. One important theory under exploration is that IGF-1 DES may possibly support healthy synapses in the brain and neurological system. In addition, it may possibly stimulate the regeneration of muscle and connective tissues, like all forms of IGF-1, which may aid in repairing and preserving these tissues.

IGF-1 DES Peptide: What is it?

The investigations indicate that the N-terminal tripeptide Gly-Pro-Glu is absent in IGF-1 DES, making it a shortened protein version. The cellular effects of IGF-1 DES seem to be more powerful than those of IGF-1, potentially as it is not considered to be bound to IGF-1 binding proteins. Because of this, it is hypothesized that IGF-1 DES may be around ten times more effective than IGF-1 in stimulating muscle growth and cell division.

Recently, IGF-1 DES has been under investigation within the context of several neurological and neurodevelopmental problems. [i] Research has suggested that IGF-1 and its analogs may affect neuronal synapse health. The IGF-1 DES and the IGF-1 may exhibit some capacity to alleviate symptoms and enhance many behavioral features of autism, speculated strictly through animal models.

IGF-1 DES Peptide: Mechanism of Action 

IGF-1 hormone peptides are categorized as insulin-binding proteins because of their potential to interact with IGF-1 receptors. Recent studies [ii] have offered insight into the potential channels by which IGF-1 DES may exert its effects.

IGF-1 DES Peptide and Neuroprotection

The IGF-1 DES peptide appears to significantly impact the development of new synapses, suggesting it may be involved in fundamental cognitive processes like learning and memory. Studies suggest that IGF-1 is important in establishing and maintaining functional synapses. Recent studies suggest that IGF-1 is essential for maintaining adequate amounts of the presynaptic protein synapsin-1, which controls neurotransmitter release. Additionally, IGF-1 seems to be involved in the post-synaptic protein PSD-95, which is thought to be in charge of preserving synaptic structure.

Rett syndrome and chromosome 22 deletion syndrome are two disorders that have been documented to respond well to IGF-1 and its analogs. Researchers speculate that it "has suggested reversing the decrease in the number of excitatory synapses and the density of neurons that characterize these illnesses in animal studies"; therefore, it is being presented as an experimental compound in further studies.

Research on the potential impact of IGF-1 on neurological disorders such as MS, ALS, PD, and AD has been found to have conflicting results. IGF-1 research in ALS suggested promising signs of slowing the disease's course, boosting muscular strength, and improving respiratory function. However, it seems that IGF-1 had little effect on MS, potentially because the disease affects the cells surrounding neurons rather than directly killing them. Although other studies of IGF-1 for PD have not yet been published, speculative data in animal models have suggested promise in preserving dopaminergic neurons and enhancing behavior.

IGF-1 DES Peptide and Autism

The possible role of IGF-1 in various neurological disorders, including autism, has been posited by limited scientific research. Brain-derived IGF-1 levels seem to be lower in younger autistic models compared to age-matched controls. Since "the action of IGF-1 is (reportedly) most pronounced in the developing brain," this finding implies that reduced concentrations of IGF-1 in the brain, especially during early developmental stages, may disturb normal neurodevelopment and contribute to the pathophysiology of autism. 

A five-day study of IGF-1 DES in a mouse model suggested potential impacts as a result of the peptide in terms of the rodents' social behavior, recognition of novel objects, contextual fear conditioning, reduction of repetitive/compulsive behavior, grooming, and memory. [vi]  Autism is thought to originate from disruptions in synapse formation. Autism is a neurodevelopmental disorder that bears pathological characteristics with other disorders such as fragile X syndrome, tuberous sclerosis, and Angelman syndrome.

IGF-1 DES Peptide and the Brain

Research suggests analogs like IGF-1 DES may be more potent than the original IGF-1 molecule as IGF-1 appears to undergo extensive changes in the brain, perhaps generating shorter versions. It seems that the capacity of these modified molecules, especially IGF-1 DES, to traverse the blood-brain barrier has been improved. Researchers have hypothesized that IGF-1 and its analogs may have the capacity to reduce neuronal death and offer neuroprotection against neurodegenerative diseases. [vii]

Research on rats has suggested that IGF-1 DES may also improve synaptic transmission and benefit cognition. As endogenous IGF-1 levels naturally decrease over time, this may elucidate future research in learning and memory functions. Studies suggest that excitatory post-synaptic potentials may be significantly boosted by 40% when IGF-1 DES is presented. [viii]

Purchasing research peptides for study is permissible but human consumption and personal use is strictly prohibited by law.

References

[i] Ballard FJ, Wallace JC, Francis GL, Read LC, Tomas FM. Des (1-3)IGF-I: a truncated form of insulin-like growth factor-I. Int J Biochem Cell Biol. 1996 Oct;28(10):1085-7. doi: 10.1016/1357-2725(96)00056-8. PMID: 8930132. https://pubmed.ncbi.nlm.nih.gov/8930132/

[ii] Melinda M. Ramsey et al, Functional Characterization of Des-IGF-1 Action at Excitatory Synapses in the CA1 Region of Rat Hippocampus, 01 Jul 2005. https://journals.physiology.org/doi/full/10.1152/jn.00768.2004

[iii] Canitano R. New experimental treatments for core social domain in autism spectrum disorders. Front Pediatr. 2014 Jun 20;2:61. doi: 10.3389/fped.2014.00061. PMID: 24999471; PMCID: PMC4064155. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4064155/

[iv] Costales J, Kolevzon A. The therapeutic potential of insulin-like growth factor-1 in central nervous system disorders. Neurosci Biobehav Rev. 2016 Apr;63:207-22. doi: 10.1016/j.neubiorev.2016.01.001. Epub 2016 Jan 15. PMID: 26780584; PMCID: PMC4790729. https://pubmed.ncbi.nlm.nih.gov/26780584/

[v] Riikonen R. Insulin-Like Growth Factors in the Pathogenesis of Neurological Diseases in Children. Int J Mol Sci. 2017 Sep 26;18(10):2056. doi: 10.3390/ijms18102056. PMID: 28954393; PMCID: PMC5666738. https://pubmed.ncbi.nlm.nih.gov/28954393/

[vi] Adam B. Steinmetz et al., Insulin-Like Growth Factor II Targets the mTOR Pathway to Reverse Autism-Like Phenotypes in Mice, Journal of Neuroscience 24 January 2018, 38 (4) 1015-1029; DOI: https://doi.org/10.1523/JNEUROSCI.2010-17.2017

[vii] Ebrahimi-Fakhari D, Sahin M. Autism and the synapse: emerging mechanisms and mechanism-based therapies. Curr Opin Neurol. 2015 Apr;28(2):91-102. https://pubmed.ncbi.nlm.nih.gov/25695134/

[viii] Górecki DC, Beresewicz M, Zabłocka B. Neuroprotective effects of short peptides derived from the Insulin-like growth factor 1. Neurochem Int. 2007 Dec;51(8):451-8. doi: 10.1016/j.neuint.2007.04.030. Epub 2007 May 16. PMID: 17582656. https://pubmed.ncbi.nlm.nih.gov/17582656/

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