IGF-1 and its Cognitive Effect
IGF-1 (Insulin-Like Growth Factor-1) is a peptide that is a mediator for growth hormone. Unbeknownst to many, IGF-1 is also classified as a neurotrophic factor, meaning it supports neuron growth and functional adaptation. Reviews in medical literature show that IGF-1 is involved in brain development and long-term neural adaptability, particularly in regions that are responsible for learning and memory. (Dyer et al., Neuroscience, 2016) (Aberg et al., Endocrinology, 2006)
In animal models, IGF-1 has been shown to influence experience-dependent plasticity, meaning the brain’s ability to reorganize itself in response to environmental input. One study demonstrated that IGF-1 administration could restore plasticity in the adult visual cortex, it was able to reopen an adaptive capacity that normally declines after developmental periods (Maya-Vetencourt et al., PNAS, 2012)
Can Synthetic IGF-1 Replicate this Effect?
IGF-1 LR3, a synthetic analogue of IGF-1, is modified to resist IGF-binding proteins, which extends its lifespan compared to native IGF-1. Despite IGF-1 LR3 being a synthetic analogue of IGF-1, it still binds to the same receptors native IGF-1 binds to, meaning it activates the same pathways responsible for brain plasticity and synaptic remodeling
One of the biggest objections to systemic IGF-1 analogs is the blood-brain barrier. But this objection weakens once you look at the literature on intranasal neuropeptide delivery. Intranasal administration has been shown to allow peptides to reach the brain via cranial pathways, bypassing the blood-brain barrier altogether. Intranasal IGF-1 itself has been studied for neuroprotection and CNS targeting in animal research. (Thorne et al., Neuroscience, 2004).
From that point, extending the logic to IGF-1 LR3 is not a wild leap. If intranasal IGF-1 reaches the brain and activates IGF1R, and if LR3 activates the same receptor with higher stability, then nasal LR3 should theoretically engage the same pathways as native IGF-1, as well as it potentially being more consistent. It's been established that IGF-1 signaling at synapses can be locally regulated and activity-dependent, meaning enhanced availability at the receptor level could bias the brain toward plastic reorganization.
IGF-1 (Insulin-Like Growth Factor-1) is a peptide that is a mediator for growth hormone. Unbeknownst to many, IGF-1 is also classified as a neurotrophic factor, meaning it supports neuron growth and functional adaptation. Reviews in medical literature show that IGF-1 is involved in brain development and long-term neural adaptability, particularly in regions that are responsible for learning and memory. (Dyer et al., Neuroscience, 2016) (Aberg et al., Endocrinology, 2006)
In animal models, IGF-1 has been shown to influence experience-dependent plasticity, meaning the brain’s ability to reorganize itself in response to environmental input. One study demonstrated that IGF-1 administration could restore plasticity in the adult visual cortex, it was able to reopen an adaptive capacity that normally declines after developmental periods (Maya-Vetencourt et al., PNAS, 2012)
Can Synthetic IGF-1 Replicate this Effect?
IGF-1 LR3, a synthetic analogue of IGF-1, is modified to resist IGF-binding proteins, which extends its lifespan compared to native IGF-1. Despite IGF-1 LR3 being a synthetic analogue of IGF-1, it still binds to the same receptors native IGF-1 binds to, meaning it activates the same pathways responsible for brain plasticity and synaptic remodeling
One of the biggest objections to systemic IGF-1 analogs is the blood-brain barrier. But this objection weakens once you look at the literature on intranasal neuropeptide delivery. Intranasal administration has been shown to allow peptides to reach the brain via cranial pathways, bypassing the blood-brain barrier altogether. Intranasal IGF-1 itself has been studied for neuroprotection and CNS targeting in animal research. (Thorne et al., Neuroscience, 2004).
From that point, extending the logic to IGF-1 LR3 is not a wild leap. If intranasal IGF-1 reaches the brain and activates IGF1R, and if LR3 activates the same receptor with higher stability, then nasal LR3 should theoretically engage the same pathways as native IGF-1, as well as it potentially being more consistent. It's been established that IGF-1 signaling at synapses can be locally regulated and activity-dependent, meaning enhanced availability at the receptor level could bias the brain toward plastic reorganization.
