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Dihexa

Dihexa, also known as N-hexanoic-Tyr-Ile-(6) aminohexanoic amide or 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 supplement 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. Dihexa is available in the form of oral supplements and injection.

Overall Health Benefits of Dihexa

  • Treats Alzheimer’s Disease [1-8]
  • Combats Parkinson’s Disease [9-14]
  • Improves Learning and Memory Retention [15-23]
  • Improves Stroke Recovery [24-27]
  • Accelerates Recovery from Spinal Cord Injury [28-31]

How does Dihexa Work?

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.

Proven Health Benefits of Dihexa

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 promotes the survival and migration of immature neurons in the brain. [11]
  • In a PD lesion model, Dihexa administration improves behavioral deficits. [12]
  • Gene transfer of human hepatocyte growth factor in a rodent model of PD prevents 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 improves memory retention and performance in the Morris water maze test. [16]
  • Administration of Angiotensin IV-related peptides such as Dihexa in rats reverses 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 improves memory retention by building new brain cell connections. [20]
  • In rats, HGF activation by Dihexa prevents 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 improves 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]

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 induces long-term neuroprotection and stroke recovery. [24]
  • Pharmacological doses of Angiotensin IV-related peptides such as Dihexa are protective against acute cerebral ischemia. [25]
  • Dihexa can help prevent stroke by increasing blood flow to the brain. [26]
  • In rats with stroke caused by cerebral artery occlusion, Dihexa administration prevents programmed cell death of brain cells. [27]

Accelerates Recovery from Spinal Cord Injury

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

  • By activating HGF, Dihexa may retard progression of spinal cord injury caused by amyotrophic lateral sclerosis (ALS). [28]
  • 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. [29-30]
  • In an animal model of spinal cord injury, Dihexa administration accelerates functional recovery. [31]

References:

  1. Wright JW, Harding JW. The Brain Hepatocyte Growth Factor/c-Met Receptor System: A New Target for the Treatment of Alzheimer’s Disease. J Alzheimers Dis. 2015;45(4):985-1000.
  2. Alene T. McCoy; Caroline C. Benoist; John W. Wright; Leen H. Kawas; Jyote Bule-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.
  3. 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 Pharmacol Exp Ther. 2014;351(2):390–402. doi:10.1124/jpet.114.218735.
  4. Nagahara and Tuszynski (2011) Potential therapeutic uses of BDNF in neurological and psychiatric disorders. Nat Rev Drug Discov 10:209-19.
  5. Calissano P, Matrone C, Amadoro G. Nerve growth factor as a paradigm of neurotrophins related to Alzheimer’s disease. Dev Neurobiol. 2010;70(5):372-83.
  6. McCoy AT, Benoist CC, Wright JW, et al. Evaluation of metabolically stabilized angiotensin IV analogs as procognitive/antidementia agents. J Pharmacol Exp Ther. 2013;344(1):141–154. doi:10.1124/jpet.112.199497
  7. Wright JW, Kawas LH, Harding JW. The development of small molecule angiotensin IV analogs to treat Alzheimer’s and Parkinson’s diseases. Prog Neurobiol. 2015;125:26-46.
  8. 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
  9. Wright JW, Kawas LH, Harding JW. The development of small molecule angiotensin IV analogs to treat Alzheimer’s and Parkinson’s diseases. Prog Neurobiol. 2015;125:26-46.
  10. 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.
  11. Salehi Z, Rajaei F. Expression of hepatocyte growth factor in the serum and cerebrospinal fluid of patients with Parkinson’s disease. J Clin Neurosci. 2010;17(12):1553-6.
  12. 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.
  13. 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.
  14. Gard PR. Cognitive-enhancing effects of angiotensin IV. BMC Neurosci. 2008;9 Suppl 2:S15.
  15. Wright JW, Kawas LH, Harding JW. The development of small molecule angiotensin IV analogs to treat Alzheimer’s and Parkinson’s diseases. Prog Neurobiol. 2015;125:26-46.
  16. 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 Pharmacol Exp Ther. 2014;351(2):390–402. doi:10.1124/jpet.114.218735.
  17. 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 Pharmacol Exp Ther. 2011;339(1):35-44.
  18. Pederson ES, Krishnan R, Harding JW, Wright JW. A role for the angiotensin AT4 receptor subtype in overcoming scopolamine-induced spatial memory deficits. Regul Pept. 2001;102(2-3):147-56.
  19. 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.
  20. Available from https://www.sciencedaily.com/releases/2012/10/121011090653.htm.
  21. Date I, Takagi N, Takagi K, et al. Hepatocyte growth factor improved learning and memory dysfunction of microsphere-embolized rats. J Neurosci Res. 2004;78(3):442-53.
  22. 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.
  23. Gard PR. Cognitive-enhancing effects of angiotensin IV. BMC Neurosci. 2008;9 Suppl 2:S15.
  24. Doeppner TR, Kaltwasser B, Elali A, Zechariah A, Hermann DM, Bähr M. Acute hepatocyte growth factor treatment induces long-term neuroprotection and stroke recovery via mechanisms involving neural precursor cell proliferation and differentiation. J Cereb Blood Flow Metab. 2011;31(5):1251-62.
  25. 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 Physiol Pharmacol. 2006;57(3):329-42.
  26. Kramár EA, Harding JW, Wright JW. Angiotensin II- and IV-induced changes in cerebral blood flow. Roles of AT1, AT2, and AT4 receptor subtypes. Regul Pept. 1997;68(2):131-8.
  27. 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.
  28. 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.
  29. 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. Acta Neuropathol. 2003;106(2):112-20.
  30. 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.
  31. 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.
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