Overall Health Benefits of Dihexa

Treats Alzheimer’s disease. Combats Parkinson’s disease. Improves learning and memory retention. Improves stroke recovery. Accelerates recovery from spinal cord injury and nerve damage. Protects against hearing loss.

How Dihexa treats Alzheimer’s Disease?

There is increasing evidence that Dihexa may help treat not only the symptoms of AD but the root cause of the disease itself. Studies show that Dihexa exerts its beneficial effects on AD through various important mechanisms: Dihexa activates the c-Met receptor which in turn stimulates mitogenesis (cell division), motogenesis (promotion of cellular motility), morphogenesis (structural development), neurogenesis (growth and development of nervous tissue), production of stem cells, and protection of a wide range of cells against injury. Dihexa induces the development of dendritic spines in neurons of the brain. Activation of HGF by Dihexa augments synaptic connectivity, protects neurons from underlying death inducers, and promotes renewal of lost neurons. Dihexa may actually prevent and improve symptoms of AD by decreasing the production of amyloid beta peptide, which are abnormal protein structures that cause the disease. In aged rat models, Dihexa administration improves synaptogenic activity. In rats with reduced blood flow to the brain, administration of Angiotensin IV such as Dihexa suppresses inflammation.

What is the latest treatment for Parkinson disease?

People with Parkinson’s disease (PD), a neurodegenerative disorder that destroys dopamine-producing nerve cells in the brain, can also benefit from Dihexa supplementation. Studies show that this powerful nootropic can help combat PD through various mechanisms: Dihexa can help treat PD symptoms by augmenting synaptic connectivity via the formation of new functional synapses. Activation of the HGF/c-Met system by Dihexa stimulates protection and restoration of neurons in the brain. In patients with PD, HGF promoted the survival and migration of immature neurons in the brain. In a PD lesion model, Dihexa administration improved behavioral deficits. Gene transfer of human hepatocyte growth factor in a rodent model of PD prevented neuronal death, suggesting that Dihexa activation of HGF can be a potential novel therapy for PD. Dihexa along with Angiotensin IV can prevent the progression of PD by increasing the production of dopamine.

How dihexa improve memory retention?

According to studies, this powerful nootropic also has memory-enhancing properties that can benefit people with memory problems associated with aging and neurodegenerative disorders: Dihexa shows promise in treating memory and motor dysfunctions by enhancing synaptic connectivity through the formation of new functional synapses. In rats, oral Dihexa administration at a dose of 2 mg/kg per day improved memory retention and performance in the Morris water maze test. Administration of Angiotensin IV-related peptides such as Dihexa in rats reversed scopolamine-induced deficits in Morris water maze performance. Dihexa and Angiotensin IV-related peptides are involved in spatial memory processing, and that activation of their binding sites can help combat spatial memory disruption. In rats with Alzheimer’s-like mental impairment, Dihexa supplementation improved memory retention by building new brain cell connections. In rats, HGF activation by Dihexa prevented learning and memory dysfunction after sustained cerebral ischemia (decreased blood flow to the brain) by protecting against injury to brain neurons. Dihexa administration in rats improved performance in a series of tests related to learning and memory. Dihexa exerts its cognitive-enhancing effects by increasing the production of acetylcholine and/or dopamine. In a mouse model of cognitive impairment, oral administration with Dihexa restored spatial learning and cognitive functions in the Morris water maze test. In animal models of cognitive deficit, Dihexa improved performance on spatial working memory and passive avoidance tasks.

How Dihexa Improve Stroke Recovery?

There’s also a great deal of evidence supporting the ability of Dihexa to accelerate recovery from stroke: In a mouse model of stroke, activation of HGF induced long-term neuroprotection and stroke recovery. Pharmacological doses of Angiotensin IV-related peptides such as Dihexa are protective against acute cerebral ischemia. Dihexa can help prevent stroke by increasing blood flow to the brain. In rats with stroke caused by cerebral artery occlusion, Dihexa administration prevented programmed cell death of brain cells.

How Dihexa take for damaged spinal nerves to heal?

Numerous studies also found that Dihexa has the ability to treat the most debilitating nervous system injuries – spinal cord injury and nerve damage: By activating HGF, Dihexa may retard the progression of spinal cord injury caused by amyotrophic lateral sclerosis (ALS). Patients with ALS especially those in the advanced disease stage have disruption of the neuronal HGF-c-Met system, suggesting that Dihexa may play a part in preventing cellular degeneration and programmed cell death of spinal motor neurons. In an animal model of spinal cord injury, Dihexa administration accelerated functional recovery. In a rat with damage to the sciatic nerve (the largest nerve in the body located in the spinal cord), Dihexa (2-4 mg/kg body weight) administration via hydrogel and injection promoted limb function recovery.

Dihexa helps in hearing loss?

Evidence found that Dihexa can help protect against hearing loss caused by toxins: In the larval zebrafish, the administration of Dihexa at a concentration of 1 μM provided optimal protection against hearing loss caused by the toxic medications neomycin and gentamicin.

Dihexa Peptide: Benefits, Uses & Side Effects

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

Potential Benefits of Dihexa

Treats Alzheimer’s disease [1-8]
Combats Parkinson’s disease [9-14]
Improves learning and memory retention [15-25]
Improves stroke recovery [26-29]
Accelerates recovery from spinal cord injury and nerve damage [30-34]
Protects against hearing loss [35]

What is Dihexa?

Dihexa, also known as N-hexanoic-Tyr-Ile-(6) aminohexanoic amideor PNB-0408, is a relatively new drug for the treatment of Alzheimer’s disease (AD) and cognitive impairment. Unlike other drugs for AD, this potent nootropic does not only impede the progression of the disease but it actually repairs the damage in the synapse (junction) between neurons. Because of its regenerative properties, most medical professionals prescribe Dihexa for the treatment of a wide array of medical conditions that affect cognitive function.

How Dihexa Works?

By binding to hepatocyte growth factor (also known as HGF, c-Met or tyrosine-protein kinase Met), Dihexa increases HGF’s activity while lowering harmful chemical reactions in the body. This in turn doubles the capacity of the available growth factors to promote signaling cascades necessary for cell development and regeneration.

Chemical Structure of Dihexa

Research on Dihexa

Treats Alzheimer’s Disease

There is increasing evidence that Dihexa may help treat not only the symptoms of AD but the root cause of the disease itself. Studies show that Dihexa exerts its beneficial effects on AD through various important mechanisms:

Dihexa activates the c-Met receptor which in turn stimulates mitogenesis (cell division), motogenesis (promotion of cellular motility), morphogenesis (structural development), neurogenesis (growth and development of nervous tissue), production of stem cells, and protection of a wide range of cells against injury. [1-2]
Dihexa induces the development of dendritic spines in neurons of the brain. [3]
Activation of HGF by Dihexa augments synaptic connectivity, protects neurons from underlying death inducers, and promotes renewal of lost neurons. [4]
Dihexa may actually prevent and improve symptoms of AD by decreasing the production of amyloid beta peptide, which are abnormal protein structures that cause the disease. [5]
In aged rat models, Dihexa administration improves synaptogenic activity. [6-7]
In rats with reduced blood flow to the brain, administration of Angiotensin IV such as Dihexa suppresses inflammation. [8]

Combats Parkinson’s Disease

People with Parkinson’s disease (PD), a neurodegenerative disorder that destroys dopamine-producing nerve cells in the brain, can also benefit from Dihexa supplementation. Studies show that this powerful nootropic can help combat PD through various mechanisms:

Dihexa can help treat PD symptoms by augmenting synaptic connectivity via the formation of new functional synapses. [9]
Activation of the HGF/c-Met system by Dihexa stimulates protection and restoration of neurons in the brain. [10]
In patients with PD, HGF promoted the survival and migration of immature neurons in the brain. [11]
In a PD lesion model, Dihexa administration improved behavioral deficits. [12]
Gene transfer of human hepatocyte growth factor in a rodent model of PD prevented neuronal death, suggesting that Dihexa activation of HGF can be a potential novel therapy for PD. [13]
Dihexa along with Angiotensin IV can prevent the progression of PD by increasing the production of dopamine. [14]

Improves Learning and Memory Retention

According to studies, this powerful nootropic also has memory-enhancing properties that can benefit people with memory problems associated with aging and neurodegenerative disorders:

Dihexa shows promise in treating memory and motor dysfunctions by enhancing synaptic connectivity through the formation of new functional synapses. [15]
In rats, oral Dihexa administration at a dose of 2 mg/kg per day improved memory retention and performance in the Morris water maze test. [16]
Administration of Angiotensin IV-related peptides such as Dihexa in rats reversed scopolamine-induced deficits in Morris water maze performance. [17]
Dihexa and Angiotensin IV-related peptides are involved in spatial memory processing, and that activation of their binding sites can help combat spatial memory disruption. [18-19]
In rats with Alzheimer’s-like mental impairment, Dihexa supplementation improved memory retention by building new brain cell connections. [20]
In rats, HGF activation by Dihexa prevented learning and memory dysfunction after sustained cerebral ischemia (decreased blood flow to the brain) by protecting against injury to brain neurons. [21]
Dihexa administration in rats improved performance in a series of tests related to learning and memory. [22]
Dihexa exerts its cognitive-enhancing effects by increasing the production of acetylcholine and/or dopamine. [23]
In a mouse model of cognitive impairment, oral administration with Dihexa restored spatial learning and cognitive functions in the Morris water maze test. [24]
In animal models of cognitive deficit, Dihexa improved performance on spatial working memory and passive avoidance tasks. [25]

Improves Stroke Recovery

There’s also a great deal of evidence supporting the ability of Dihexa to accelerate recovery from stroke:

In a mouse model of stroke, activation of HGF induced long-term neuroprotection and stroke recovery. [26]
Pharmacological doses of Angiotensin IV-related peptides such as Dihexa are protective against acute cerebral ischemia. [27]
Dihexa can help prevent stroke by increasing blood flow to the brain. [28]
In rats with stroke caused by cerebral artery occlusion, Dihexa administration prevented programmed cell death of brain cells. [29]

Accelerates Recovery from Spinal Cord Injury and Nerve Damage

Numerous studies also found that Dihexa has the ability to treat the most debilitating nervous system injuries – spinal cord injury and nerve damage:

By activating HGF, Dihexa may retard progression of spinal cord injury caused by amyotrophic lateral sclerosis (ALS). [30]
Patients with ALS especially those in advanced disease stage have disruption of the neuronal HGF-c-Met system, suggesting that Dihexa may play a part in preventing cellular degeneration and programmed cell death of spinal motor neurons. [31-32]
In an animal model of spinal cord injury, Dihexa administration accelerated functional recovery. [33]
In a rat with damage to the sciatic nerve (largest nerve in the body located in the spinal cord), Dihexa (2-4 mg/kg body weight) administration via hydrogel and injection promoted limb function recovery. [34]

Protects against Hearing Loss

Evidence found that Dihexa can help protect against hearing loss caused by toxins:

In the larval zebrafish, the administration of Dihexa at a concentration of 1 μM provided optimal protection against hearing loss caused by the toxic medications neomycin and gentamicin. [35]

Associated Side Effects of Dihexa

Dihexa 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 Dihexa. However, the issue wasn’t’ confirmed to be caused by the treatment and could have been a coincidence and not related to the use of Dihexa. Despite this, it was listed as a side effect associated with Dihexa even these associated side effects are very uncommon.

Side effects associated with Dihexa may include the following:

Anxiety
Change of taste
Insomnia
Irritability
Mood swings
Nausea

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Reference

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A New Target for the Treatment of Alzheimer’s Disease

The 2015 study by Wright and Harding explores the brain hepatocyte growth factor (HGF)/c-Met receptor system as a potential target for Alzheimer’s disease treatment. This research delves into the role of the HGF/c-Met system in neural growth, repair, and neurogenesis. It suggests that modulating this system could offer new therapeutic strategies for Alzheimer’s, a condition currently lacking effective treatments. This study contributes to the growing field of Alzheimer’s research, particularly in identifying novel therapeutic targets.

For more details https://content.iospress.com/articles/journal-of-alzheimers-disease/jad142814
Alene T. McCoy; Caroline C. Benoist; John W. Wright; Leen H. Kawas; JyoteBule-Ghogare; Mingyan Zhu; Suzanne M. Appleyard; Gary A. Wayman; Joseph W. Harding (January 2013). “Evaluation of metabolically stabilized angiotensin IV analogs as pro-cognitive/anti-dementia agents”. The Journal of Pharmacology and Experimental Therapeutics. 344 (1): 141–154. doi: 10.1124/jpet.112.199497. PMC 3533412. PMID 23055539.

Evaluation of metabolically stabilized angiotensin IV analogs as pro-cognitive/anti-dementia agents

The 2013 study by McCoy et al. evaluated the effectiveness of metabolically stabilized angiotensin IV analogs as potential therapeutic agents for cognitive enhancement and dementia treatment. This research focused on understanding the role of angiotensin IV in brain functions related to memory and learning, and its potential in addressing cognitive impairments associated with diseases like Alzheimer’s. The study contributes to the field of neuropharmacology by exploring new avenues for treating cognitive disorders.

For more details https://jpet.aspetjournals.org/content/344/1/141.short
Benoist CC, Kawas LH, Zhu M, et al. The procognitive and synaptogenic effects of angiotensin IV-derived peptides are dependent on activation of the hepatocyte growth factor/c-met system. J PharmacolExpTher. 2014;351(2):390–402. doi:10.1124/jpet.114.218735

The procognitive and synaptogenic effects of angiotensin IV-derived peptides are dependent on activation of the hepatocyte growth factor/c-met system

The 2014 study by Benoist et al. investigated the role of angiotensin IV-derived peptides in cognitive enhancement, focusing on their procognitive and synaptogenic effects. This research emphasized the importance of the hepatocyte growth factor/c-met system in mediating these effects. The findings contribute to understanding the molecular mechanisms involved in memory and learning, potentially offering new therapeutic targets for cognitive disorders.

For more details https://jpet.aspetjournals.org/content/351/2/390.short
Nagahara and Tuszynski (2011) Potential therapeutic uses of BDNF in neurological and psychiatric disorders. Nat Rev Drug Discov 10:209-19

Potential therapeutic uses of BDNF in neurological and psychiatric disorders

The 2011 study by Nagahara and Tuszynski reviewed the potential therapeutic applications of Brain-Derived Neurotrophic Factor (BDNF) in treating neurological and psychiatric disorders. This research highlighted the significance of BDNF in brain function, including its role in neuroprotection, synaptic plasticity, and cognitive enhancement. The study also discussed the challenges in delivering BDNF as a therapeutic agent and proposed strategies for overcoming these challenges. The findings underscore the potential of BDNF in developing new treatments for various brain disorders.

For more details https://www.nature.com/articles/nrd3366
Calissano P, Matrone C, Amadoro G. Nerve growth factor as a paradigm of neurotrophins related to Alzheimer’s disease. DevNeurobiol. 2010;70(5):372-83.

Nerve growth factor as a paradigm of neurotrophins related to Alzheimer’s disease

The 2010 study by Calissano, Matrone, and Amadoro focused on the role of nerve growth factor (NGF) as a neurotrophin related to Alzheimer’s disease. This research discussed NGF’s biological functions, particularly in the context of neurodegenerative diseases. The study highlighted NGF’s potential as a therapeutic agent for Alzheimer’s disease, emphasizing its significance in neuronal survival, maintenance, and regeneration.

For more details https://onlinelibrary.wiley.com/doi/abs/10.1002/dneu.20759
McCoy AT, Benoist CC, Wright JW, et al. Evaluation of metabolically stabilized angiotensin IV analogs as procognitive/antidementia agents. J PharmacolExpTher. 2013;344(1):141–154. doi:10.1124/jpet.112.199497

Evaluation of metabolically stabilized angiotensin IV analogs as procognitive/antidementia agents

The 2013 study by McCoy et al. evaluated metabolically stabilized angiotensin IV analogs for their potential as procognitive and antidementia agents. This research explored the efficacy of these analogs in enhancing cognitive functions and their possible applications in treating dementia-related disorders. The study contributes to the understanding of angiotensin IV’s role in cognitive processes and its therapeutic potential in neurodegenerative diseases.

For more details https://jpet.aspetjournals.org/content/344/1/141.short
Wright JW, Kawas LH, Harding JW. The development of small molecule angiotensin IV analogs to treat Alzheimer’s and Parkinson’s diseases. ProgNeurobiol. 2015;125:26-46.

The development of small molecule angiotensin IV analogs to treat Alzheimer’s and Parkinson’s diseases

The 2015 study by Wright, Kawas, and Harding discussed the development of small molecule angiotensin IV analogs for treating Alzheimer’s and Parkinson’s diseases. This research focused on the potential of these analogs in neurodegenerative disease therapy, exploring their role in neuroprotection, cognitive enhancement, and modulation of brain function. The study contributes significantly to the ongoing search for effective treatments for these challenging neurological conditions.

For more details https://www.sciencedirect.com/science/article/pii/S0301008214001245
Wang QG, Xue X, Yang Y, Gong PY, Jiang T, Zhang YD. Angiotensin IV suppresses inflammation in the brains of rats with chronic cerebral hypoperfusion. J Renin Angiotensin Aldosterone Syst. 2018;19(3):1470320318799587. doi:10.1177/1470320318799587

Angiotensin IV suppresses inflammation in the brains of rats with chronic cerebral hypoperfusion

The 2018 study by Wang et al. investigated the effects of angiotensin IV on inflammation in rat brains with chronic cerebral hypoperfusion. This research explored the anti-inflammatory properties of angiotensin IV, particularly in the context of brain conditions characterized by reduced blood flow. The study’s findings contribute to understanding the potential therapeutic uses of angiotensin IV in neurological conditions with inflammatory components.

For more details https://journals.sagepub.com/doi/abs/10.1177/1470320318799587
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Prevention of onset of Parkinson’s disease by in vivo gene transfer of human hepatocyte growth factor in rodent model

The 2006 study by Koike et al. investigated the use of gene therapy for preventing Parkinson’s disease. Specifically, it focused on the in vivo transfer of human hepatocyte growth factor in a rodent model. The study aimed to explore the potential of this approach in preventing the onset of Parkinson’s disease, offering insights into new therapeutic strategies. This research is significant in the field of neurodegenerative disease treatment, particularly in the use of gene therapy for Parkinson’s disease.

For more details https://www.nature.com/articles/3302810
Salehi Z, Rajaei F. Expression of hepatocyte growth factor in the serum and cerebrospinal fluid of patients with Parkinson’s disease. J ClinNeurosci. 2010;17(12):1553-6.

Expression of hepatocyte growth factor in the serum and cerebrospinal fluid of patients with Parkinson’s disease

The 2010 study by Salehi and Rajaei explored the expression of hepatocyte growth factor (HGF) in the serum and cerebrospinal fluid of patients with Parkinson’s disease. This research aimed to understand the potential relationship between HGF levels and Parkinson’s disease, contributing to the broader understanding of the disease’s pathophysiology and potential biomarkers.

For more details https://www.sciencedirect.com/science/article/pii/S0967586810003942
Friedman LG, Price K, Lane RF, et al. Meeting report on the Alzheimer’s Drug Discovery Foundation 14th International Conference on Alzheimer’s Drug Discovery. Alzheimers Res Ther. 2014;6(2):22. Published 2014 Apr 28. doi:10.1186/alzrt252.

Meeting report on the Alzheimer’s drug discovery foundation 14th international conference on Alzheimer’s drug discovery

The meeting report on the Alzheimer’s Drug Discovery Foundation 14th International Conference on Alzheimer’s Drug Discovery, published in 2014 in “Alzheimer’s Research & Therapy,” provides insights into the latest developments in Alzheimer’s research and drug discovery. The conference highlighted various innovative therapeutic strategies and findings from recent research aimed at tackling Alzheimer’s disease. This report is a valuable resource for understanding the current state and future directions in Alzheimer’s disease research and treatment.

For more details https://link.springer.com/article/10.1186/alzrt252
Koike H, Ishida A, Shimamura M, et al. Prevention of onset of Parkinson’s disease by in vivo gene transfer of human hepatocyte growth factor in rodent model: a model of gene therapy for Parkinson’s disease. Gene Ther. 2006;13(23):1639-44

Prevention of onset of Parkinson’s disease by in vivo gene transfer of human hepatocyte growth factor in rodent model

The 2006 study by Koike et al. investigated the potential of gene therapy in preventing the onset of Parkinson’s disease. The research utilized in vivo gene transfer of human hepatocyte growth factor in a rodent model to explore its efficacy in precluding Parkinson’s disease development. This innovative approach contributes to the understanding of gene therapy as a potential intervention for Parkinson’s disease.

For more details https://www.nature.com/articles/3302810
Gard PR. Cognitive-enhancing effects of angiotensin IV. BMC Neurosci. 2008;9Suppl 2:S15.

Cognitive-enhancing effects of angiotensin IV

The 2008 study by Gard PR in BMC Neuroscience reviewed the cognitive-enhancing effects of angiotensin IV. The research focused on the role of angiotensin IV in memory and cognitive functions, discussing its potential as a therapeutic agent for cognitive impairments. The study highlights the importance of angiotensin IV in neurobiological research, particularly in understanding and treating cognitive disorders.

For more details https://bmcneurosci.biomedcentral.com/articles/10.1186/1471-2202-9-S2-S15
Benoist CC, Wright JW, Zhu M, Appleyard SM, Wayman GA, Harding JW. Facilitation of hippocampal synaptogenesis and spatial memory by C-terminal truncated Nle1-angiotensin IV analogs. J PharmacolExpTher. 2011;339(1):35-44.

Facilitation of hippocampal synaptogenesis and spatial memory by C-terminal truncated Nle1-angiotensin IV analogs

The 2011 study by Benoist et al. in the Journal of Pharmacology and Experimental Therapeutics explored the effects of C-terminal truncated Nle1-angiotensin IV analogs on hippocampal synaptogenesis and spatial memory. The research investigated how these analogs facilitate cognitive functions, particularly focusing on their impact in the hippocampus, a brain region crucial for memory formation. This study contributes to understanding potential treatments for cognitive impairments related to memory.

For more details https://jpet.aspetjournals.org/content/339/1/35.short
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A role for the angiotensin AT4 receptor subtype in overcoming scopolamine-induced spatial memory deficits

The 2001 study by Pederson, Krishnan, Harding, and Wright investigated the role of the angiotensin AT4 receptor subtype in counteracting memory deficits caused by scopolamine, a substance known to impair spatial memory. The research aimed to understand how the AT4 receptor could be targeted to improve cognitive functions, especially in conditions where memory is adversely affected. This study contributes to the field of memory research and pharmacological interventions for memory impairments.

For more details https://www.sciencedirect.com/science/article/pii/S0167011501003123
Albiston AL, Fernando RN, Yeatman HR, et al. Gene knockout of insulin-regulated aminopeptidase: loss of the specific binding site for angiotensin IV and age-related deficit in spatial memory. Neurobiol Learn Mem. 2010;93(1):19-30

Gene knockout of insulin-regulated aminopeptidase: loss of the specific binding site for angiotensin IV and age-related deficit in spatial memory

The 2010 study by Albiston et al. in “Neurobiology of Learning and Memory” investigated the effects of knocking out the gene for insulin-regulated aminopeptidase. This gene knockout resulted in the loss of the specific binding site for angiotensin IV. The study found an age-related deficit in spatial memory, highlighting the significance of this binding site in memory functions. This research provides insight into the molecular mechanisms underlying memory and cognitive aging.

For more details https://www.sciencedirect.com/science/article/pii/S1074742709001488
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Hepatocyte growth factor improved learning and memory dysfunction of microsphere‐embolized rats

The 2004 study by Date et al. in the Journal of Neuroscience Research explored the effects of hepatocyte growth factor (HGF) on learning and memory dysfunction in rats subjected to microsphere embolization. The study aimed to understand the therapeutic potential of HGF in addressing cognitive impairments associated with brain ischemia. This research contributes to the knowledge of neuroprotective strategies and cognitive rehabilitation following cerebral injuries.

For more details https://onlinelibrary.wiley.com/doi/abs/10.1002/jnr.20263
Braszko JJ, Kupryszewski G, Witczuk B, Wiśniewski K. Angiotensin II-(3-8)-hexapeptide affects motor activity, performance of passive avoidance and a conditioned avoidance response in rats. Neuroscience. 1988;27(3):777-83

Angiotensin II-(3-8)-hexapeptide affects motor activity, performance of passive avoidance and a conditioned avoidance response in rats

The 1988 study by Braszko et al. examined the effects of Angiotensin II-(3-8)-hexapeptide on motor activity and memory performance in rats. The research focused on how this peptide influences passive avoidance behavior and conditioned avoidance responses, providing insights into the neuromodulatory role of angiotensin fragments. This study contributes to the understanding of the complex interactions between neuropeptides and brain function.

For more details https://www.sciencedirect.com/science/article/pii/0306452288901820
Gard PR. Cognitive-enhancing effects of angiotensin IV. BMC Neurosci. 2008;9Suppl 2:S15.

Cognitive-enhancing effects of angiotensin IV

The 2008 study by Gard in BMC Neuroscience reviewed the cognitive-enhancing effects of angiotensin IV. This research focused on understanding how angiotensin IV could potentially improve cognitive functions, offering insights into its therapeutic applications for cognitive impairments. The study contributes to the field of neuropharmacology and the exploration of new treatments for cognitive disorders.

For more details https://bmcneurosci.biomedcentral.com/articles/10.1186/1471-2202-9-S2-S15
Sun, X., Deng, Y., Fu, X., Wang, S., Duan, R., & Zhang, Y. (2021). AngIV-Analog Dihexa Rescues Cognitive Impairment and Recovers Memory in the APP/PS1 Mouse via the PI3K/AKT Signaling Pathway. Brain sciences, 11(11), 1487. https://doi.org/10.3390/brainsci11111487

AngIV-Analog Dihexa Rescues Cognitive Impairment and Recovers Memory in the APP/PS1 Mouse via the PI3K/AKT Signaling Pathway.

The 2021 study by Sun et al. focused on the effects of the Angiotensin IV analog Dihexa in treating cognitive impairment and restoring memory in APP/PS1 mice, a model for Alzheimer’s disease. The research demonstrated that Dihexa could enhance cognitive functions and recover memory, likely through the activation of the PI3K/AKT signaling pathway. This study provides insights into potential therapeutic approaches for Alzheimer’s disease using AngIV analogs.

For more details https://doi.org/10.3390/brainsci11111487
Ho, J. K., & Nation, D. A. (2018). Cognitive benefits of angiotensin IV and angiotensin-(1-7): A systematic review of experimental studies. Neuroscience and biobehavioral reviews, 92, 209–225. https://doi.org/10.1016/j.neubiorev.2018.05.005.

Cognitive benefits of angiotensin IV and angiotensin-(1-7): A systematic review of experimental studies

The 2018 systematic review by Ho and Nation examined the cognitive benefits of angiotensin IV and angiotensin-(1-7) based on experimental studies. The review synthesized evidence from various studies to assess the potential of these peptides in enhancing cognitive functions. The findings contribute to the understanding of the role of angiotensin peptides in cognitive processes and their potential therapeutic applications in cognitive disorders.

For more details https://doi.org/10.1016/j.neubiorev.2018.05.005
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Acute hepatocyte growth factor treatment induces long-term neuroprotection and stroke recovery via mechanisms involving neural precursor cell proliferation and differentiation

The 2011 study by Doeppner et al. investigated the long-term neuroprotective and recovery effects of acute hepatocyte growth factor (HGF) treatment in stroke models. The study revealed that HGF treatment leads to neuroprotection and enhances stroke recovery by mechanisms that involve the proliferation and differentiation of neural precursor cells. These findings contribute to understanding potential therapeutic approaches for stroke recovery.

For more details https://journals.sagepub.com/doi/abs/10.1038/jcbfm.2010.211
Faure S, Chapot R, Tallet D, Javellaud J, Achard JM, Oudart N. Cerebroprotective effect of angiotensin IV in experimental ischemic stroke in the rat mediated by AT(4) receptors. J PhysiolPharmacol. 2006;57(3):329-42.

Cerebroprotective effect of angiotensin IV in experimental ischemic stroke in the rat mediated by AT(4) receptors

The 2006 study by Faure et al. explored the cerebroprotective effects of angiotensin IV in ischemic stroke in rats, mediated by AT(4) receptors. This research aimed to understand how angiotensin IV could be utilized for stroke therapy, focusing on its interaction with AT(4) receptors. The findings provide insights into potential therapeutic approaches for ischemic stroke using angiotensin IV.

For more details https://www.jpp.krakow.pl/journal/archive/09_06/articles/02_article.html
Kramár EA, Harding JW, Wright JW. Angiotensin II- and IV-induced changes in cerebral blood flow. Roles of AT1, AT2, and AT4 receptor subtypes. RegulPept. 1997;68(2):131-8.

Angiotensin II- and IV-induced changes in cerebral blood flow

The 1997 study by Kramár, Harding, and Wright investigated the effects of Angiotensin II and IV on cerebral blood flow, examining the roles of AT1, AT2, and AT4 receptor subtypes. This research provided insights into how these angiotensin receptors influence cerebral blood flow, which is crucial in understanding cerebrovascular regulation and potential therapeutic targets for cerebral disorders.

For more details https://www.sciencedirect.com/science/article/pii/S0167011596021167
Shang J, Deguchi K, Yamashita T, et al. Antiapoptotic and antiautophagic effects of glial cell line-derived neurotrophic factor and hepatocyte growth factor after transient middle cerebral artery occlusion in rats. J Neurosci Res. 2010;88(10):2197-206

Antiapoptotic and antiautophagic effects of glial cell line-derived neurotrophic factor and hepatocyte growth factor after transient middle cerebral artery occlusion in rats

The 2010 study by Shang et al. in the Journal of Neuroscience Research explored the effects of glial cell line-derived neurotrophic factor (GDNF) and hepatocyte growth factor (HGF) following transient middle cerebral artery occlusion in rats. The study focused on the antiapoptotic and antiautophagic effects of these growth factors, providing insights into potential therapeutic strategies for stroke and related cerebral injuries.

For more details https://onlinelibrary.wiley.com/doi/abs/10.1002/jnr.22373
Kadoyama K, Funakoshi H, Ohya W, Nakamura T. Hepatocyte growth factor (HGF) attenuates gliosis and motoneuronal degeneration in the brainstem motor nuclei of a transgenic mouse model of ALS. Neurosci Res. 2007;59(4):446-56.

Hepatocyte growth factor (HGF) attenuates gliosis and motoneuronal degeneration in the brainstem motor nuclei of a transgenic mouse model of ALS

The 2007 study by Kadoyama et al. investigated the effects of hepatocyte growth factor (HGF) on gliosis and motor neuron degeneration in the brainstem motor nuclei of a transgenic mouse model of Amyotrophic Lateral Sclerosis (ALS). The research aimed to explore the potential therapeutic benefits of HGF in ALS, focusing on its neuroprotective properties. This study contributes to the understanding of ALS pathology and potential treatment strategies.

For more details https://www.sciencedirect.com/science/article/pii/S0168010207017646
Kato S, Funakoshi H, Nakamura T, et al. Expression of hepatocyte growth factor and c-Met in the anterior horn cells of the spinal cord in the patients with amyotrophic lateral sclerosis (ALS): immunohistochemical studies on sporadic ALS and familial ALS with superoxide dismutase 1 gene mutation. ActaNeuropathol. 2003;106(2):112-20.

Expression of hepatocyte growth factor and c-Met in the anterior horn cells of the spinal cord in the patients with amyotrophic lateral sclerosis (ALS)

The 2003 study by Kato et al. examined the expression of hepatocyte growth factor (HGF) and its receptor c-Met in the anterior horn cells of the spinal cord in patients with Amyotrophic Lateral Sclerosis (ALS). This study included cases of sporadic ALS as well as familial ALS with superoxide dismutase 1 gene mutation. The research provided insights into the molecular pathology of ALS and potential targets for therapy.

For more details https://link.springer.com/article/10.1007/s00401-003-0708-z
Ebens A, Brose K, Leonardo ED, et al. Hepatocyte growth factor/scatter factor is an axonal chemoattractant and a neurotrophic factor for spinal motor neurons. Neuron. 1996;17(6):1157-72.

Hepatocyte growth factor/scatter factor is an axonal chemoattractant and a neurotrophic factor for spinal motor neurons

The 1996 study by Ebens et al. in the journal Neuron investigated the roles of hepatocyte growth factor/scatter factor (HGF/SF) in spinal cord development. The research found that HGF/SF acts as an axonal chemoattractant and a neurotrophic factor for spinal motor neurons. This study provides significant insights into the molecular mechanisms guiding the development of motor neuron pathways and their potential therapeutic implications.

For more details https://www.cell.com/fulltext/S0896-6273(00)80247-0
Kitamura K, Fujiyoshi K, Yamane J, et al. Human hepatocyte growth factor promotes functional recovery in primates after spinal cord injury. PLoS ONE. 2011;6(11):e27706.

Human hepatocyte growth factor promotes functional recovery in primates after spinal cord injury

The 2011 study by Kitamura et al. explored the effects of human hepatocyte growth factor (HGF) on recovery after spinal cord injury in primates. The research demonstrated that HGF promoted significant functional recovery, highlighting its potential as a therapeutic agent for spinal cord injuries. This study is important in understanding treatments that can aid in neuroregeneration and recovery post-injury.

For more details https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0027706
Weiss, J. B., Phillips, C. J., Malin, E. W., Gorantla, V. S., Harding, J. W., & Salgar, S. K. (2021). Stem cell, Granulocyte-Colony Stimulating Factor and/or Dihexa to promote limb function recovery in a rat sciatic nerve damage-repair model: Experimental animal studies. Annals of medicine and surgery (2012), 71, 102917. https://doi.org/10.1016/j.amsu.2021.102917.

Granulocyte-Colony Stimulating Factor and/or Dihexa to promote limb function recovery in a rat sciatic nerve damage-repair model: Experimental animal studies

The 2021 study by Weiss et al. investigated the efficacy of stem cells, Granulocyte-Colony Stimulating Factor (G-CSF), and Dihexa in promoting limb function recovery in a rat model of sciatic nerve damage and repair. This experimental animal study aimed to understand the potential therapeutic effects of these treatments on nerve regeneration and functional recovery. The findings contribute to the development of new strategies for treating nerve injuries.

For more details https://doi.org/10.1016/j.amsu.2021.102917
Uribe, P. M., Kawas, L. H., Harding, J. W., & Coffin, A. B. (2015). Hepatocyte growth factor mimetic protects lateral line hair cells from aminoglycoside exposure. Frontiers in cellular neuroscience, 9, 3. https://doi.org/10.3389/fncel.2015.00003.

Hepatocyte growth factor mimetic protects lateral line hair cells from aminoglycoside exposure

The 2015 study by Uribe et al. investigated the protective effects of a hepatocyte growth factor mimetic on lateral line hair cells in response to aminoglycoside exposure. This study focused on understanding how this mimetic can safeguard sensory cells from the damaging effects of aminoglycosides, which are known for their ototoxic properties. The research contributes to potential protective strategies against aminoglycoside-induced hair cell damage.

For more details https://www.frontiersin.org/articles/10.3389/fncel.2015.00003/full

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