FG Loop Peptide (FGL)

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Potential Benefits of FG Loop Peptide
What is FG Loop Peptide?
How FG Loop Peptide Works
Chemical Structure of FG Loop Peptide
Research on FG Loop Peptide
Associated Side Effects of FG Loop Peptide
References

Potential Benefits of FG Loop Peptide

Treats stroke and traumatic brain injuries [1-12]
Improves cognitive function [13-25]
Wards off depression [26-30]
Fights inflammation [31-35]

What is FG Loop Peptide?

FG loop peptide (FGL) is derived from the neural cell adhesion molecule (NCAM). NCAM is a glycoprotein (a protein that has sugar attached to it) and is found on the surface of nerve cells (neurons) and glial cells (protect neurons). Research shows that NCAM activates FGL which in turn stimulates the production of new projections of developing neurons. FGL also plays an integral role in the formation of synapses between neurons and the proliferation of stem cells – both of these important mechanisms enhance cognitive capacities and protect against stroke and other chronic, debilitating brain diseases.

How FG Loop Peptide Works?

FG loop peptide works by mobilizing the neural stem cells, which have the potential to give rise to offspring cells that grow and develop into neurons (nerve cells) and glial cells. They provide a protective covering to the cells and enhance the transmission of signals, thus improving regenerative capacity and cognitive function.

Chemical Structure of FG Loop Peptide

Research on FG Loop Peptide

Treats Stroke and Traumatic Brain Injuries

FGL can help treat brain damage associated with stroke. There’s an overwhelming body of clinical evidence supporting the regenerative properties of this powerful peptide:

A 2008 study published in the Neuroscience Letters found that adolescent rats with a traumatic brain injury that were treated with FGL had reduced inflammatory markers and regulators of programmed cell death (apoptosis). [1]
A 2014 study published in the Stem Cells and Reviews showed that exposure of neural stem cells (generate neurons of the central nervous system) to various concentrations of FGL enhanced the proliferation of the stem cells and that injection of FGL in adult rats increased the mobilization of stem cells in different areas of the brain, suggesting that the treatment can be a potential therapeutic option for demyelinating neurological disorders (any condition that damages the protective covering of nerve fibers in the brain). [2]
A 2018 study published in the Neurochemical Research that reviewed various preclinical studies on FGL found that the peptide has successfully treated neurological disorders including stroke, traumatic brain injury, and Alzheimer’s disease. [3]
In primary rat neurons, FGL induced growth and survival of brain neurons. [4]
A cell study found that FGL treatment protected mouse brain cells against lipopolysaccharide-induced changes by reducing the levels of inflammatory markers. [5]
In oxygen-deprived rat brain neurons, 24-hour pretreatment with a single injection of FGL significantly protected the neurons against death, suggesting that the peptide can protect against stroke. [6]
In a rat model of Alzheimer’s disease, systemic treatment with FGL alleviated the loss of brain neurons. [7]
A 2016 study published in the Journal of Neuroimmune Pharmacology found that FGL promotes the regenerative capacity of brain neurons by amplifying remyelination (formation of protective covering around neurons) and modulating inflammation. [8]
A cell study also found that FGL promotes the growth and recovery of brain neurons by activating the fibroblast growth factor receptor (FGFR). [9-10]
In mice, repeated administration of FGL enhanced the survival of the newly born neurons. [11]
In an animal model of stroke, nose-to-brain delivery of FGL prevented brain damage induced by low oxygen levels. [12]

Improves Cognitive Function

Because FGL plays an integral role in the formation of synapses between neurons and proliferation of stem cells, administration of this peptide can help improve different cognitive skills:

A cell study found that FGL improved cognitive health by promoting the formation of new brain neurons (neurogenesis). [13]
In newborn rats, the administration of FGL through the nose promoted early sensorimotor development and enhanced social memory retention. [14]
In rats, FGL treatment ameliorated the working memory deficits induced by phencyclidine. [15]
In aged rat brains, FGL treatment ameliorated different processes related to brain aging. [16]
When injected at a dose of 8 mg/kg, FGL induced positive changes in the structure of neurons in aged rats. [17]
In rats, injection of FGL significantly reduced Abeta25-35-induced cognitive impairment. [18]
A cell study found that treatment of rat brain cells with FGL prevented the death of brain neurons. [19]
A study also found that FGL has the ability to stimulate the growth of brain neurons. [20]
In wild-type rats, FGL treatment improved memory by enhancing the transmission of nerve signals. [21]
Studies in animal models of chronic stress have shown that FGL enhances memory by protecting brain neurons. [22-23]
A study found that FGL protected against neuroinflammation. [24]
FGL has also been found to prevent age-related structural changes in synapses. [25]

Wards Off Depression

There’s also a good deal of evidence supporting the antidepressant properties of FGL, suggesting that this peptide can help correct depressive symptoms and improve quality of life:

In mice, acute or repeated administration of FGL reversed depression-like behaviors. [26]
A study found that the levels of neural cell adhesion molecules were decreased in patients with depression, suggesting that FGL treatment has the potential to treat depressive symptoms. [27]
By improving the function of synapses, FGL can provide a long-term antidepressant effect. [28]
In mice, partial reduction in neural cell adhesion molecule induced depression-related behavior. [29]
A study found that FGL exerts its antidepressant effects by promoting the growth of new neurons, the development of dendritic spines, and synaptic adaptations. [30]

Fights Inflammation

Evidence also suggests that this NCAM can help fight a wide array of inflammatory conditions through its potent anti-inflammatory properties:

A 2010 study published in the Neurobiology of Aging found that administration of FGL in aged rats significantly reduced the increase in pro-inflammatory interleukin-1beta (IL-1beta). [31]
A 2009 study published in the Journal of Neurochemistry reported that FGL exerts its anti-inflammatory properties via IGF-1, interferon-gamma, and interferon‐γ modulation. [32-33]
A 2017 study published in the Journal of Translational Medicine found that FGL and other anti-inflammatory peptides have the potential to treat various inflammatory diseases such as Alzheimer’s disease and rheumatoid arthritis. [34]
A 2006 study published in the Journal of Immunology found that FGL fights inflammation by regulating the development of the immune system cell alpha beta T cells. [35]

Associated Side Effects of FG Loop Peptide

FG loop peptide side effects are very uncommon. There have been some side effects associated with the use of this drug wherein the patient had one of the issues listed below at some point while being on FG loop peptide. However, these side effects weren’t confirmed to be associated with the treatment and could have been a coincidence and not related to the use of FG loop peptide. Despite this, it was listed as a side effect associated with FG loop peptide even though these associated side effects are very uncommon.

Side effects associated with FG loop peptide may include the following:

Dizziness
Headache
Vomiting

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Reference

Pedersen MV, Helweg-larsen RB, Nielsen FC, Berezin V, Bock E, Penkowa M. The synthetic NCAM-derived peptide, FGL, modulates the transcriptional response to traumatic brain injury. NeurosciLett. 2008;437(2):148-53.

The synthetic NCAM-derived peptide, FGL, modulates the transcriptional response to traumatic brain injury

The study by Pedersen et al. explored the effects of FGL, a peptide derived from the neural cell adhesion molecule (NCAM), on the transcriptional response to traumatic brain injury. FGL was found to modulate gene expression related to brain injury, suggesting its potential therapeutic role in neuroprotection and recovery. The findings indicate that FGL influences the molecular pathways associated with brain injury repair mechanisms.

For more detailed report https://www.sciencedirect.com/science/article/pii/S0304394008003509
Klein R, Blaschke S, Neumaier B, et al. The synthetic NCAM mimetic peptide FGL mobilizes neural stem cells in vitro and in vivo. Stem Cell Rev Rep. 2014;10(4):539-47.

The synthetic NCAM mimetic peptide FGL mobilizes neural stem cells in vitro and in vivo

The study by Klein et al. demonstrated that the synthetic peptide FGL, mimicking the neural cell adhesion molecule (NCAM), can activate neural stem cells both in vitro and in vivo. This activation suggests potential for FGL in enhancing neural regeneration and repair mechanisms, pointing towards its application in treating neurological conditions by promoting stem cell mobilization. This research contributes to the understanding of stem cell biology and opens new avenues for therapeutic strategies in regenerative medicine.

For more detailed report https://link.springer.com/article/10.1007/s12015-014-9512-5
Chu C, Gao Y, Lan X, Thomas A, Li S. NCAM Mimetic Peptides: Potential Therapeutic Target for Neurological Disorders. Neurochem Res. 2018;43(9):1714-1722.

NCAM Mimetic Peptides: Potential Therapeutic Target for Neurological Disorders

The study by Chu et al. reviews the potential of NCAM mimetic peptides as therapeutic targets for neurological disorders. These peptides mimic the neural cell adhesion molecule (NCAM), playing crucial roles in neural development, regeneration, and synaptic plasticity. Their therapeutic potential lies in their capacity to modulate neuronal functions and processes, offering promising avenues for treating a range of neurological conditions. This research underscores the significance of NCAM in neurochemistry and its potential in developing new treatments for neurological diseases.

For more detailed report https://link.springer.com/article/10.1007/s11064-018-2594-8
Neiiendam JL, Kohler LB, Christensen C, et al. An NCAM-derived FGF-receptor agonist, the FGL-peptide, induces neurite outgrowth and neuronal survival in primary rat neurons. J Neurochem. 2004;91(4):920-35.

An NCAM-derived FGF-receptor agonist, the FGL-peptide, induces neurite outgrowth and neuronal survival in primary rat neurons

The study by Neiiendam et al. demonstrates that the FGL-peptide, derived from NCAM, acts as an agonist for FGF-receptors, promoting neurite outgrowth and enhancing neuronal survival in primary rat neurons. This research highlights the therapeutic potential of NCAM mimetic peptides in neuroregeneration and neuroprotection, offering promising insights for developing treatments for neurological disorders. For more details, refer to the publication in the Journal of Neurochemistry.

For more detailed report https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1471-4159.2004.02779.x
Cox FF, Berezin V, Bock E, Lynch MA. The neural cell adhesion molecule-derived peptide, FGL, attenuates lipopolysaccharide-induced changes in glia in a CD200-dependent manner. Neuroscience. 2013;235:141-8.

The neural cell adhesion molecule-derived peptide, FGL, attenuates lipopolysaccharide-induced changes in glia in a CD200-dependent manner

The study by Cox FF et al. found that the peptide FGL, derived from the neural cell adhesion molecule (NCAM), can mitigate the effects of lipopolysaccharide (LPS)-induced changes in glial cells via a CD200-dependent mechanism. This suggests FGL’s potential role in neuroinflammation, highlighting its therapeutic prospects in conditions associated with glial activation and inflammation.

For more detailed report https://www.sciencedirect.com/science/article/pii/S0306452212012183
Skibo GG, Lushnikova IV, Voronin KY, et al. A synthetic NCAM-derived peptide, FGL, protects hippocampal neurons from ischemic insult both in vitro and in vivo. Eur J Neurosci. 2005;22(7):1589-96.

A synthetic NCAM-derived peptide, FGL, protects hippocampal neurons from ischemic insult both in vitro and in vivo

The study by Skibo GG et al. demonstrates that FGL, a peptide derived from NCAM, offers protection to hippocampal neurons from ischemic damage both in vitro and in vivo. This finding underlines the potential of FGL as a neuroprotective agent in conditions involving ischemic injury, suggesting its utility in developing treatments for stroke and other ischemia-related neurological conditions.

For more detailed report https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1460-9568.2005.04345.x
Corbett NJ, Gabbott PL, Klementiev B, et al. Amyloid-beta induced CA1 pyramidal cell loss in young adult rats is alleviated by systemic treatment with FGL, a neural cell adhesion molecule-derived mimetic peptide. PLoS ONE. 2013;8(8):e71479.

Amyloid-beta induced CA1 pyramidal cell loss in young adult rats is alleviated by systemic treatment with FGL, a neural cell adhesion molecule-derived mimetic peptide

The study by Corbett NJ et al. found that systemic treatment with FGL, a mimetic peptide derived from the neural cell adhesion molecule, alleviates amyloid-beta induced loss of CA1 pyramidal cells in young adult rats. This suggests FGL’s potential as a therapeutic agent against early neuronal damage associated with amyloid-beta, which is relevant for conditions like Alzheimer’s disease.

For more detailed report https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0071479
Klein R, Mahlberg N, Ohren M, et al. The Neural Cell Adhesion Molecule-Derived (NCAM)-Peptide FG Loop (FGL) Mobilizes Endogenous Neural Stem Cells and Promotes Endogenous Regenerative Capacity after Stroke. J NeuroimmunePharmacol. 2016;11(4):708-720.

The Neural Cell Adhesion Molecule-Derived (NCAM)-Peptide FG Loop (FGL) Mobilizes Endogenous Neural Stem Cells and Promotes Endogenous Regenerative Capacity after Stroke

The study by Klein R et al. demonstrates that the NCAM-derived peptide FGL can activate endogenous neural stem cells and enhance regenerative capacity following a stroke. This suggests FGL’s potential in promoting neural recovery and improving outcomes after neurological injuries by leveraging the body’s own stem cells for regeneration.

For more detailed report https://link.springer.com/article/10.1007/s11481-016-9694-5
Chen Y, Li S, Berezin V, Bock E. The fibroblast growth factor receptor (FGFR) agonist FGF1 and the neural cell adhesion molecule-derived peptide FGL activate FGFR substrate 2alpha differently. J Neurosci Res. 2010;88(9):1882-9.

The fibroblast growth factor receptor (FGFR) agonist FGF1 and the neural cell adhesion molecule-derived peptide FGL activate FGFR substrate 2alpha differently

The study by Chen Y et al. explored how the fibroblast growth factor receptor (FGFR) agonist FGF1 and the NCAM-derived peptide FGL activate FGFR substrate 2alpha in different ways. This research highlights the distinct mechanisms by which FGF1 and FGL influence FGFR signaling, suggesting potential for tailored therapeutic strategies targeting FGFR-related pathways in neurological conditions.

For more detailed report https://onlinelibrary.wiley.com/doi/abs/10.1002/jnr.22374
Aonurm-helm A, Berezin V, Bock E, Zharkovsky A. NCAM-mimetic, FGL peptide, restores disrupted fibroblast growth factor receptor (FGFR) phosphorylation and FGFR mediated signaling in neural cell adhesion molecule (NCAM)-deficient mice. Brain Res. 2010;1309:1-8.

NCAM-mimetic, FGL peptide, restores disrupted fibroblast growth factor receptor (FGFR) phosphorylation and FGFR mediated signaling in neural cell adhesion molecule (NCAM)-deficient mice

The study by Aonurm-Helm et al. demonstrates that the NCAM-mimetic peptide FGL can restore disrupted fibroblast growth factor receptor (FGFR) phosphorylation and FGFR-mediated signaling in NCAM-deficient mice. This research indicates the potential of FGL to compensate for NCAM deficits, emphasizing its role in maintaining FGFR signaling pathways crucial for neural function and development.

For more detailed report https://www.sciencedirect.com/science/article/pii/S0006899309023956
Aonurm-helm A, Jurgenson M, Zharkovsky T, et al. Depression-like behaviour in neural cell adhesion molecule (NCAM)-deficient mice and its reversal by an NCAM-derived peptide, FGL. Eur J Neurosci. 2008;28(8):1618-28.

Depression-like behaviour in neural cell adhesion molecule (NCAM)-deficient mice and its reversal by an NCAM-derived peptide, FGL

The study by Aonurm-Helm et al. found that NCAM-deficient mice exhibit depression-like behavior, which can be reversed by the NCAM-derived peptide, FGL. This suggests that FGL has potential therapeutic value for treating depression by targeting NCAM-related pathways, highlighting the importance of NCAM in mood regulation and the potential of peptide-based interventions.

For more detailed report https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1460-9568.2008.06471.x
Kim YS, Sung DK, Kim H, Kong WH, Kim YE, Hahn SK. Nose-to-brain delivery of hyaluronate – FG loop peptide conjugate for non-invasive hypoxic-ischemic encephalopathy therapy. J Control Release. 2019;307:76-89.

Nose-to-brain delivery of hyaluronate – FG loop peptide conjugate for non-invasive hypoxic-ischemic encephalopathy therapy

The study by Kim YS et al. explores a non-invasive therapy for hypoxic-ischemic encephalopathy using a nose-to-brain delivery system of a hyaluronate-FG loop peptide conjugate. This innovative approach aims to target brain injury directly through the nasal passage, offering a promising treatment strategy for conditions that previously had limited non-invasive therapeutic options.

For more detailed report https://www.sciencedirect.com/science/article/pii/S0168365919303426
Dallérac G, Zerwas M, Novikova T, et al. The neural cell adhesion molecule-derived peptide FGL facilitates long-term plasticity in the dentate gyrus in vivo. Learn Mem. 2011;18(5):306-13.

The neural cell adhesion molecule-derived peptide FGL facilitates long-term plasticity in the dentate gyrus in vivo

The study by Dallérac et al. demonstrated that the NCAM-derived peptide FGL enhances long-term plasticity in the dentate gyrus in vivo, indicating its potential role in supporting memory and learning processes. This research suggests that FGL could be a valuable tool for improving cognitive functions through its effect on neural plasticity.

For more detailed report http://learnmem.cshlp.org/content/18/5/306.short
Secher T, Novitskaia V, Berezin V, Bock E, Glenthøj B, Klementiev B. A neural cell adhesion molecule-derived fibroblast growth factor receptor agonist, the FGL-peptide, promotes early postnatal sensorimotor development and enhances social memory retention. Neuroscience. 2006;141(3):1289-99.

A neural cell adhesion molecule-derived fibroblast growth factor receptor agonist, the FGL-peptide, promotes early postnatal sensorimotor development and enhances social memory retention

The study by Secher T et al. explored the effects of the FGL-peptide, derived from the neural cell adhesion molecule, on early postnatal sensorimotor development and social memory retention. This NCAM-derived fibroblast growth factor receptor agonist was found to promote sensorimotor development in the early postnatal period and enhance the retention of social memories, suggesting its potential therapeutic applications in developmental and cognitive disorders.

For more detailed report https://www.sciencedirect.com/science/article/pii/S0306452206006075
Secher T, Berezin V, Bock E, Glenthøj B. Effect of an NCAM mimetic peptide FGL on impairment in spatial learning and memory after neonatal phencyclidine treatment in rats. Behav Brain Res. 2009;199(2):288-97.

Effect of an NCAM mimetic peptide FGL on impairment in spatial learning and memory after neonatal phencyclidine treatment in rats

The study by Secher T et al. investigated the effects of FGL, an NCAM mimetic peptide, on spatial learning and memory impairments induced by neonatal phencyclidine treatment in rats. The findings suggest that FGL treatment can mitigate the cognitive deficits associated with early phencyclidine exposure, highlighting its potential therapeutic value for neurodevelopmental disorders.

For more detailed report https://www.sciencedirect.com/science/article/pii/S0166432808006748
Ojo B, Rezaie P, Gabbott PL, et al. A neural cell adhesion molecule-derived peptide, FGL, attenuates glial cell activation in the aged hippocampus. Exp Neurol. 2011;232(2):318-28.

A neural cell adhesion molecule-derived peptide, FGL, attenuates glial cell activation in the aged hippocampus

The study by Ojo B et al. examined the effects of FGL, a peptide derived from the neural cell adhesion molecule, on glial cell activation in the aged hippocampus. Their findings suggest that FGL can reduce glial cell activation, which is often associated with neuroinflammation and cognitive decline in aging. This points to FGL’s potential for mitigating age-related neuroinflammatory processes and preserving cognitive function.

For more detailed report https://www.sciencedirect.com/science/article/pii/S0014488611003335
Popov VI, Medvedev NI, Kraev IV, et al. A cell adhesion molecule mimetic, FGL peptide, induces alterations in synapse and dendritic spine structure in the dentate gyrus of aged rats: a three-dimensional ultrastructural study. Eur J Neurosci. 2008;27(2):301-14.

A cell adhesion molecule mimetic, FGL peptide, induces alterations in synapse and dendritic spine structure in the dentate gyrus of aged rats: a three-dimensional ultrastructural study

The study by Popov VI et al. explored the effects of the FGL peptide, a mimetic of the cell adhesion molecule, on synapse and dendritic spine structure in the dentate gyrus of aged rats. The research revealed that FGL induces structural alterations, highlighting its potential for influencing neural connectivity and plasticity in aging. This three-dimensional ultrastructural study contributes to understanding how interventions can modulate neural architecture in the aged brain.

For more detailed report https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1460-9568.2007.06004.x
Klementiev B, Novikova T, Novitskaya V, et al. A neural cell adhesion molecule-derived peptide reduces neuropathological signs and cognitive impairment induced by Abeta25-35. Neuroscience. 2007;145(1):209-24.

A neural cell adhesion molecule-derived peptide reduces neuropathological signs and cognitive impairment induced by Abeta25-35

The study by Klementiev B et al. investigated the effects of a neural cell adhesion molecule-derived peptide on neuropathological signs and cognitive impairment induced by Abeta25-35, a fragment of beta-amyloid associated with Alzheimer’s disease. The research showed that the peptide reduced neuropathological signs and cognitive deficits, suggesting its potential as a therapeutic intervention for Alzheimer’s disease-related pathology and cognitive impairment.

For more detailed report https://www.sciencedirect.com/science/article/pii/S0306452206016563
Dityatev A, Dityateva G, Schachner M. Synaptic strength as a function of post- versus presynaptic expression of the neural cell adhesion molecule NCAM. Neuron. 2000;26(1):207-17.

Synaptic strength as a function of post-versus presynaptic expression of the neural cell adhesion molecule NCAM

The study by Dityatev et al. investigated synaptic strength in relation to the post- versus presynaptic expression of the neural cell adhesion molecule NCAM. The research explored how the presence of NCAM in either the post- or presynaptic neuron influences synaptic function. This study contributes to our understanding of the role of NCAM in synaptic plasticity and its impact on the strength of neuronal connections.

For more detailed report https://www.cell.com/fulltext/S0896-6273(00)81151-4
Kiselyov VV, Skladchikova G, Hinsby AM, et al. Structural basis for a direct interaction between FGFR1 and NCAM and evidence for a regulatory role of ATP. Structure. 2003;11(6):691-701.

Structural basis for a direct interaction between FGFR1 and NCAM and evidence for a regulatory role of ATP

The study by Kiselyov VV et al. investigated the structural basis for the direct interaction between FGFR1 (Fibroblast Growth Factor Receptor 1) and NCAM (Neural Cell Adhesion Molecule) and provided evidence for the regulatory role of ATP in this interaction. The research elucidated the molecular mechanisms underlying the interaction between these two important molecules and highlighted the influence of ATP in regulating their binding. This study contributes to our understanding of cell adhesion and signaling processes involving FGFR1 and NCAM.

For more detailed report https://www.cell.com/structure/pdf/S0969-2126(03)00096-0.pdf
Cambon K, Hansen SM, Venero C, Herrero AI, Skibo G, Berezin V, Bock E, Sandi C. A synthetic neural cell adhesion molecule mimetic peptide promotes synaptogenesis, enhances presynaptic function, and facilitates memory consolidation. J Neurosci. 2004 Apr 28;24(17):4197-204.

A synthetic neural cell adhesion molecule mimetic peptide promotes synaptogenesis, enhances presynaptic function, and facilitates memory consolidation

The study by Cambon K et al. investigated the effects of a synthetic neural cell adhesion molecule (NCAM) mimetic peptide on synaptic processes and memory consolidation. The research demonstrated that this peptide promotes synaptogenesis, enhances presynaptic function, and facilitates memory consolidation. These findings suggest the potential therapeutic value of NCAM mimetic peptides in enhancing synaptic plasticity and memory formation.

For more detailed report https://www.jneurosci.org/content/24/17/4197.short
Borcel E, Pérez-Alvarez L, Herrero AI, Brionne T, Varea E, Berezin V, Bock E, Sandi C, Venero C. Chronic stress in adulthood followed by intermittent stress impairs spatial memory and the survival of newborn hippocampal cells in aging animals: prevention by FGL, a peptide mimetic of neural cell adhesion molecule. BehavPharmacol. 2008 Feb;19(1):41-9.

Chronic stress in adulthood followed by intermittent stress impairs spatial memory and the survival of newborn hippocampal cells in aging animals: prevention by FGL, a peptide mimetic of neural cell adhesion molecule

The study by Borcel E et al. investigated the impact of chronic stress in adulthood followed by intermittent stress on spatial memory and the survival of newborn hippocampal cells in aging animals. This research found that this stress paradigm impairs both spatial memory and the survival of new hippocampal cells. However, these detrimental effects were prevented by FGL, a peptide mimetic of the neural cell adhesion molecule (NCAM). This suggests that FGL may have protective effects against the negative consequences of chronic and intermittent stress on cognitive function and neurogenesis.

For more detailed report https://journals.lww.com/behaviouralpharm/fulltext/2008/02000/chronic_stress_in_adulthood_followed_by.5.aspx
Bisaz R, Schachner M, Sandi C. Causal evidence for the involvement of the neural cell adhesion molecule, NCAM, in chronic stress-induced cognitive impairments. Hippocampus. 2011 Jan;21(1):56-71.

Causal evidence for the involvement of the neural cell adhesion molecule, NCAM, in chronic stress-induced cognitive impairments

The study by Bisaz R et al. provides causal evidence for the involvement of the neural cell adhesion molecule (NCAM) in chronic stress-induced cognitive impairments. This research suggests that NCAM plays a role in the cognitive deficits observed under conditions of chronic stress. The study contributes to our understanding of the molecular mechanisms underlying stress-related cognitive impairments and highlights the potential significance of NCAM in this context.

For more detailed report https://onlinelibrary.wiley.com/doi/abs/10.1002/hipo.20723
Downer EJ, Cowley TR, Cox F, Maher FO, Berezin V, Bock E, Lynch MA. A synthetic NCAM-derived mimetic peptide, FGL, exerts anti-inflammatory properties via IGF-1 and interferon-gamma modulation. J Neurochem. 2009 Jun;109(5):1516-25.

A synthetic NCAM-derived mimetic peptide, FGL, exerts anti-inflammatory properties via IGF-1 and interferon-gamma modulation

The study by Downer EJ et al. investigated the anti-inflammatory properties of the synthetic NCAM-derived mimetic peptide FGL. Their research found that FGL exerts its anti-inflammatory effects by modulating the activity of IGF-1 (Insulin-Like Growth Factor 1) and interferon-gamma (IFN-γ). These findings suggest that FGL may have therapeutic potential for regulating inflammation through its influence on these signaling pathways.

For more detailed report https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1471-4159.2009.06076.x
Ojo B, Rezaie P, Gabbott PL, Davies H, Colyer F, Cowley TR, Lynch M, Stewart MG. Age-related changes in the hippocampus (loss of synaptophysin and glial-synaptic interaction) are modified by systemic treatment with an NCAM-derived peptide, FGL. Brain Behav Immun. 2011 Oct 2.

Age-related changes in the hippocampus (loss of synaptophysin and glial-synaptic interaction) are modified by systemic treatment with an NCAM-derived peptide, FGL

The study by Ojo B et al. investigated age-related changes in the hippocampus, specifically the loss of synaptophysin and glial-synaptic interactions. They found that these age-related changes were modified by systemic treatment with an NCAM-derived peptide, FGL. This suggests that FGL may have a protective effect on the hippocampus against age-related synaptic and glial alterations.

For more detailed report https://www.sciencedirect.com/science/article/pii/S0889159111005319
Aonurm-helm A, Jurgenson M, Zharkovsky T, et al. Depression-like behaviour in neural cell adhesion molecule (NCAM)-deficient mice and its reversal by an NCAM-derived peptide, FGL. Eur J Neurosci. 2008;28(8):1618-28.

Depression-like behaviour in neural cell adhesion molecule (NCAM)-deficient mice and its reversal by an NCAM-derived peptide, FGL. Eur J Neurosci

The study by Aonurm-Helm et al. investigated depression-like behavior in mice deficient in the neural cell adhesion molecule (NCAM) and its reversal by an NCAM-derived peptide, FGL. The research found that NCAM-deficient mice displayed depression-like behavior, which could be reversed by treatment with the FGL peptide. This suggests a potential therapeutic role for FGL in addressing depression and highlights the importance of NCAM in mood regulation.

For more detailed report https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1460-9568.2008.06471.x
Jorgensen OS. Neural cell adhesion molecule (NCAM) and prealbumin in cerebrospinal fluid from depressed patients. ActaPsychiatrScand Suppl. 1988;345:29-37.

Neural cell adhesion molecule (NCAM) and prealbumin in cerebrospinal fluid from depressed patients

The study by Jorgensen OS investigated the levels of neural cell adhesion molecule (NCAM) and prealbumin in cerebrospinal fluid from depressed patients. This research aimed to understand potential biomarkers or factors associated with depression. The study contributes to our knowledge of the molecular and biochemical aspects of depression and may provide insights into its underlying mechanisms.

For more detailed report https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1600-0447.1988.tb08565.x
Muller D, Wang C, Skibo G, et al. PSA-NCAM is required for activity-induced synaptic plasticity. Neuron. 1996;17(3):413-22.

PSA-NCAM is required for activity-induced synaptic plasticity

The study by Müller et al. investigated the role of PSA-NCAM (Polysialylated Neural Cell Adhesion Molecule) in activity-induced synaptic plasticity. Their research demonstrated that PSA-NCAM is required for synaptic plasticity in response to neuronal activity. This study sheds light on the significance of PSA-NCAM in modulating synaptic changes in response to neural activity, which is essential for learning and memory processes.

For more detailed report https://www.cell.com/fulltext/S0896-6273(00)80174-9
Jurgenson M, Aonurm-helm A, Zharkovsky A. Partial reduction in neural cell adhesion molecule (NCAM) in heterozygous mice induces depression-related behaviour without cognitive impairment. Brain Res. 2012;1447:106-18.

Partial reduction in neural cell adhesion molecule (NCAM) in heterozygous mice induces depression-related behaviour without cognitive impairment

The study by Jurgenson et al. investigated the effects of partial reduction in neural cell adhesion molecule (NCAM) in heterozygous mice. Their research found that this reduction induced depression-related behavior without cognitive impairment. This suggests that alterations in NCAM levels can influence mood-related behaviors without affecting cognitive function. These findings contribute to our understanding of the role of NCAM in regulating emotional and behavioral processes

For more detailed report https://www.sciencedirect.com/science/article/pii/S000689931200159X
Steven R. Wainwright and Liisa A. M. Galea, “The Neural Plasticity Theory of Depression: Assessing the Roles of Adult Neurogenesis and PSA-NCAM within the Hippocampus,” Neural Plasticity, vol. 2013, Article ID 805497, 14 pages, 2013. https://doi.org/10.1155/2013/805497.

The Neural Plasticity Theory of Depression: Assessing the Roles of Adult Neurogenesis and PSA-NCAM within the Hippocampus

The paper by Steven R. Wainwright and Liisa A. M. Galea, titled “The Neural Plasticity Theory of Depression: Assessing the Roles of Adult Neurogenesis and PSA-NCAM within the Hippocampus,” explores the neural plasticity theory of depression. It assesses the roles of adult neurogenesis and PSA-NCAM (Polysialylated Neural Cell Adhesion Molecule) within the hippocampus in the context of depression. The study delves into the potential mechanisms by which these factors influence depressive behaviors and provides insights into the neurobiological basis of depression.

For more detailed report https://www.hindawi.com/journals/np/2013/805497/abs/
Downer EJ, Cowley TR, Lyons A, et al. A novel anti-inflammatory role of NCAM-derived mimetic peptide, FGL. Neurobiol Aging. 2010;31(1):118-28.

A novel anti-inflammatory role of NCAM-derived mimetic peptide, FGL

The study by Downer EJ et al. identified a novel anti-inflammatory role of the NCAM (Neural Cell Adhesion Molecule)-derived mimetic peptide FGL. This research uncovered FGL’s capacity to exert anti-inflammatory effects, expanding our understanding of the potential therapeutic applications of FGL in mitigating neuroinflammation.

For more detailed report https://www.sciencedirect.com/science/article/pii/S0197458008001012
Downer EJ, Cowley TR, Cox F, et al. A synthetic NCAM-derived mimetic peptide, FGL, exerts anti-inflammatory properties via IGF-1 and interferon-gamma modulation. J Neurochem. 2009;109(5):1516-25.

A synthetic NCAM-derived mimetic peptide, FGL, exerts anti-inflammatory properties via IGF-1 and interferon-gamma modulation

The study by Downer EJ et al. investigated the anti-inflammatory properties of the synthetic NCAM-derived mimetic peptide FGL. Their research demonstrated that FGL exerts its anti-inflammatory effects by modulating the activity of IGF-1 (Insulin-Like Growth Factor 1) and interferon-gamma (IFN-γ). These findings suggest that FGL may have therapeutic potential for regulating inflammation through its influence on these signaling pathways.

For more detailed report https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1471-4159.2009.06076.x
Downer EJ, Cowley TR, Cox F, et al. A synthetic NCAM-derived mimetic peptide, FGL, exerts anti-inflammatory properties via IGF-1 and interferon-gamma modulation. J Neurochem. 2009;109(5):1516-25.

A synthetic NCAM‐derived mimetic peptide, FGL, exerts anti‐inflammatory properties via IGF‐1 and interferon‐γ modulation

The study by Downer EJ et al. investigated the anti-inflammatory properties of the synthetic NCAM-derived mimetic peptide FGL. Their research demonstrated that FGL exerts its anti-inflammatory effects by modulating the activity of IGF-1 (Insulin-Like Growth Factor 1) and interferon-gamma (IFN-γ). These findings suggest that FGL may have therapeutic potential for regulating inflammation through its influence on these signaling pathways.

For more detailed report https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1471-4159.2009.06076.x
Gupta S, Sharma AK, Shastri V, Madhu MK, Sharma VK. Prediction of anti-inflammatory proteins/peptides: an insilico approach. J Transl Med. 2017;15(1):7. Published 2017 Jan 6. doi:10.1186/s12967-016-1103-6.

Prediction of anti-inflammatory proteins/peptides: an insilico approach

The study by Gupta et al. focused on the prediction of anti-inflammatory proteins/peptides using an in silico approach. This research aimed to identify potential anti-inflammatory molecules through computational methods, providing insights into the prediction of proteins or peptides with anti-inflammatory properties.

For more detailed report https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-016-1103-6
Touma M, Chang HC, Sasada T, Handley M, Clayton LK, Reinherz EL. The TCR C beta FG loop regulates alpha beta T cell development. J Immunol. 2006;176(11):6812-23.

The TCR C beta FG loop regulates alpha beta T cell development

The study by Touma et al. focused on the regulation of alpha beta T cell development by the TCR (T Cell Receptor) C beta FG loop. Their research explored the role of this loop in the development of alpha beta T cells, shedding light on the molecular mechanisms involved in T cell maturation and differentiation.

For more detailed report https://journals.aai.org/jimmunol/article/176/11/6812/37351

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