Central to our hypothesis of improved condition through upregulation of the signaling pathways Akt and MAPK, full length IGF-1 has been shown to have a broader therapeutic capacity than the tri-peptide form as:
Neuronal cultures show higher phosphorylation of Akt and MAPK when exposed to similar doses of rhIGF1 (full length) and (1-3)IGF-1 (Corvin et al., 2012).
Can increase the transcription of BDNF as opposed to the (1-3)IGF-1 (Park et al., 2011)
(1-3)IGF-1 pharmacokinetic is much faster than full length IGF-1. (1-3)IGF-1 peaks in few minutes and is cleared from circulatory system and (although we don’t have data on this) CSF much faster (Baker et al., 2005). Although it seems that (1-3)IGF-1 stays longer in brain tissue than in plasma, we can always argue that full length IGF-1 is in fact cleaved once it trespass the BBB, so I think we have an interesting (thus the importance of conducting the study) question. With the full length we can maintain the levels of IGF-1 for a longer period and eventually, once it passes the BBB stays as long as (1-3)IGF-1.
We already mentioned this but I guess is worth highlighting again that full length IGF-1 has been already approved for the prescription in neurological disorders including muscular dystrophy, multiple sclerosis, amyotrophic lateral sclerosis (ALS), and dementia (Rosenbloom, 2009). In some of the papers below (1-3) IGF1 is proposed as a neuroprotective drug but I haven’t read any clinical paper using it in humans. Baker, A.M., Batchelor, D.C., Thomas, G.B., Wen, J.Y., Rafiee, M., Lin, H., and Guan, J. (2005). Central penetration and stability of N-terminal tripeptide of insulin-like growth factor-I, glycine-proline-glutamate in adult rat. Neuropeptides 39, 81-87. Corvin, A.P., Molinos, I., Little, G., Donohoe, G., Gill, M., Morris, D.W., and Tropea, D. (2012). Insulin-like growth factor 1 (IGF1) and its active peptide (1-3)IGF1 enhance the expression of synaptic markers in neuronal...
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