ok THIS was interresting...
studies are still being done...AND in fact several places are recruiting participants
(if anyone is interrested)in the US at this very moment:
This is just one : Nutritional Supplementation With Agmatine Sulfate to Treat Small Fiber NeuropathyThis study is currently recruiting participants.
Verified February 2012 by JFK Medical Center
First Received on January 31, 2012. Last Updated on February 2, 2012 History of Changes
Sponsor: Dr Charles Porbeni
Information provided by (Responsible Party): Dr Charles Porbeni, JFK Medical Center
ClinicalTrials.gov Identifier: NCT01524666
Purpose
This is a nonblinded Case-only study that evaluates the treatment effects of Agmatine Sulfate on small fiber peripheral neuropathy. Patients will be started on Agmatine sulfate (a metabolite of Arginine) and monitored for two months. Improvement will be noted on their response to the Neuropathic Pain Questionnaire. Additionally the investigators will note improvement by performing autonomic function testing at the beginning and end of the study.
Condition
Peripheral Neuropathy
Study Type: Observational
Study Design: Observational Model: Case-Only
Time Perspective: Prospective
Official Title: Nutritional Supplementation With Agmatine Sulfate to Treat Small Fiber Neuropathy
Genetics Home Reference related topics: Charcot-Marie-Tooth disease hereditary neuropathy with liability to pressure palsies
MedlinePlus related topics: Dietary Fiber Dietary Supplements Peripheral Nerve Disorders
U.S. FDA Resources
Further study details as provided by JFK Medical Center:
Primary Outcome Measures:
•Neuropathic Pain Questionnaire [ Time Frame: After 2 months ] [ Designated as safety issue: No ]
Secondary Outcome Measures:
•QSART & ANSAR testing [ Time Frame: After 2 months ] [ Designated as safety issue: No ]
Biospecimen Retention: Samples Without DNA
Skin Biopsy
Estimated Enrollment: 15
Study Start Date: February 2012
Estimated Study Completion Date: July 2012
Estimated Primary Completion Date: May 2012 (Final data collection date for primary outcome measure)
Eligibility
Ages Eligible for Study: 18 Years to 75 Years
Genders Eligible for Study: Both
Accepts Healthy Volunteers: No
Sampling Method: Non-Probability Sample
Study Population
Clinic patients at JFK Med CTR
Criteria
Inclusion Criteria:
•Men and Women Ages 18-75 with symptoms of small Fiber Neuropathy and have been diagnosed via autonomic function testing and or skin biopsy
Exclusion Criteria:
•Women who are pregnant or breast feeding, patients with history of substance abuse, and patients with myelopathy
Contacts and Locations
Please refer to this study by its ClinicalTrials.gov identifier: NCT01524666
Locations
United States, New Jersey
JFK Medical Center Recruiting
Edison, New Jersey, United States, 07712
Contact: Karna D Sherwood, M.D. 732-321-7010
[email protected]
Sponsors and Collaborators
Dr Charles Porbeni
Investigators
Study Director: Michael Rosenber, M.D. JFK Medical Center
Publications:
Keynan O, Mirovsky Y, Dekel S, Gilad VH, Gilad GM. Safety and Efficacy of Dietary Agmatine Sulfate in Lumbar Disc-associated Radiculopathy. An Open-label, Dose-escalating Study Followed by a Randomized, Double-blind, Placebo-controlled Trial. Pain Med. 2010 Mar;11(3):356-68.
Responsible Party: Dr Charles Porbeni, Research Coordinator, JFK Medical Center
ClinicalTrials.gov Identifier: NCT01524666 History of Changes
Other Study ID Numbers: AgS-001
Study First Received: January 31, 2012
Last Updated: February 2, 2012
Health Authority: United States: Institutional Review Board
Additional relevant MeSH terms:
Peripheral Nervous System Diseases
Demyelinating Diseases
Polyneuropathies
Nerve Compression Syndromes
Neurologic Manifestations
Neurotoxicity Syndromes
Neuromuscular Diseases
Nervous System Diseases
Signs and Symptoms
Poisoning
Substance-Related Disorders
ClinicalTrials.gov processed this record on March 07, 2012
also there is some stuff comming out...from: Department of Psychiatry and Human Behavior
The University of Mississippi Medical CenterDr. Soundar Regunathan serves as a Basic Science Mentor for the CPN. Dr. Regunathan completed his graduate training in Neurochemistry of amino acid transmitter systems in 1985 at the University of Madras. After completing two year post-doctoral program at McGill University in Montreal, he spent several years in the Division of Neurobiology at Cornell University Medical College in New York, working on novel receptors and neurotransmitter systems. He is a tenure-track Professor of the Division of Neurobiology and Behavior Research (since 2002). His research has been funded by R01 grant from NINDS.
Dr. Regunathan's laboratory's research interests have been the molecular and functional characterization of neurotransmitters and their receptors with particular focus in neuropsychiatric disorders.
Recently, during attempts to identify endogenous ligand for imidazoline receptors, agmatine (decarboxylated arginine) was discovered in brain and other tissues. Since then, several studies have shown that agmatine exhibits various biological effects in mammalian brain and other tissues. Dr. Regunathan's laboratory currently focuses on the neurobiological role of this novel amine and its alterations during diseases. We have shown the expression of arginine decarboxylase (ADC), the biosynthetic enzyme, and agmatinase, the degradative enzyme in brain and we are in the process of molecular cloning of ADC.
We have also shown that agmatine has potent anti-inflammatory properties and plays a protective role in drugs of abuse.
The current research programs in Dr. Regunathan's laboratory can be divided into following four distinct but inter related projects.
1. The localization and regulation of agmatine biosynthesis in brain: In this project, the objectives are to clone the biosynthetic enzyme, arginine decarboxylase (ADC), to investigate the regulation of ADC in glia as the source of neuronal agmatine and to determine the distribution of agmatine and ADC in brain. The aims of this project are to establish that mammalian ADC is a novel enzyme by molecular cloning, to express ADC in mammalian cells by transient and stable transfection and to determine the tissue/cell specific expression pattern by RNA analysis. Further studies are planned to establish that agmatine is primarily synthesized by ADC in glia and stored in neurons by measuring the activity of ADC in cultured neurons and glial cells, immunocytochemical localization of agmatine and ADC, measuring the activity of ADC in adult rat brain glial cells and synaptosomes, and immunohistochemical localization of ADC and agmatine in rat brain.
2.
Anti-inflammatory effects of agmatine: Dr. Regunathan's earlier studies indicated that agmatine is a potent anti-proliferative agent in vascular smooth muscle cells and in brain astrocytes. More recently Dr. Regunathan has observed that agmatine is also effective in blocking the production of pro-inflammatory molecules such as nitric oxide synthase-2 (NOS-2) and tumor necrosis factor (TNF) in glia and macrophages. Although these are distinct actions, one common feature is the signal transduction pathways mediating these responses. Conceivably these agents could interfere with a common signal that mediate proliferation (ERK pathway) or inflammation (38P MAPK pathway).
Dr. Regunathan's lab is currently working to identify the signal transduction molecules that are involved in the anti-proliferative/anti-inflammatory actions of agmatine.
3.
Neuroprotective effects of agmatine: Agmatine protects neurons against injury in vivo and in vitro. The mechanism of this neuroprotection is not known. Our hypothesis is that agmatine acts at multiple sites to protect neurons/cells against ischemic/excitotoxic injury. One mechanism could be the blockade of ligand gated cation channels including N-methyl-D-aspartate (NMDA) channels. Agmatine could also prevent delayed neuronal degeneration by inhibiting inflammatory responses and as an anti-apoptotic agent.
Studies are also in progress that will reveal the mechanisms of actions of agmatine in neuroprotection.
4.
Agmatine and opioid system: Since our discovery of agmatine in brain, several studies have shown that agmatine interacts with opioid system to reduce morphine tolerance and withdrawal syndrome and potentiates morphine analgesia.
Dr. Regunathan's lab is currently investigating the molecular mechanism of these actions of agmatine as well as the effect of chronic morphine exposure on agmatine biosynthesis in specific brain regions.
Selected Publications
Li, G., Regunathan, S., Barrow, C.J., Eshraghi, J. Cooper, R. and Reis, D.J.: Agmatine: An endogenous clonidine-displacing substance in brain. Science, 263: 966-969, 1994.
Regunathan, S., Youngson, C., Raasch, W., Wang, H. and Reis, D.J.: Imidazoline receptors and agmatine in blood vessels: A novel system inhibiting vascular smooth muscle proliferation. J. Pharmacol. & Exp. Ther., 276: 1272-1282 ,1996.
Galea, E., Regunathan, S., Eliopoulos, V., Feinstein, D.L. and Reis, D.J.: Inhibition of mammalian nitric oxide synthase by agmatine, an endogenous decarboxylated arginine. Biochem. J., 316: 247-249, 1996.
Sastre, M., Regunathan, S., Galea, E. and Reis, D.J.: Agmatinase activity in rat brain: A metabolic pathway for the degradation of agmatine. J. Neurochem., 67: 1761-1765, 1996.
Gonzelez, C., Regunathan, S., Reis, D.J. and Estrada, C.: Agmatine is an endogenous modulator of noradrenergic neurotransmission in the rat tail artery. Br. J. Pharmacol., 119: 677-684, 1996.
Sastre, M., Regunathan, S. and Reis, D.J.: Uptake of agmatine into rat brain synaptosomes: possible role of cation channels. J. Neurochem., 69: 2421-2426, 1997.
Otake, K., Ruggiero, D.A., Regunathan, S., Wang, H., Milner, T.A. and Reis, D.J.: Regional: localization of agmatine in the rat brain: an immunocytochemical study. Brain Res., 787: 1-14, 1998.
Sastre, M., Galea, E., Feinstein, D., Reis, D.J. and Regunathan, S.: Metabolism of agmatine in macrophages: modulation by LPS and inhibitory cytokines. Biochem. J., 330: 1405-1409, 1998.
Regunathan, S. and Reis, D. J.: Characterization of arginine decarboxylase in rat brain and liver: Distinction from ornithine decarboxylase. J. Neurochem., 74: 2201-2208, 2000.
Fairbanks, C.A., Schreiber, K.L., Brewer, K.L., Yu, C.H., Stone, L.S., Kitto, K.F., Nguyen, O.H., Grocholski, B.M., Shoeman, D.W., Kehl, L.J., Regunathan, S., Reis, D.J., Yezieski, R.P. and Wilcox, G.L.: Agmatine reverses pain induced by inflammation, neuropathy and spinal cord injury. Proc. Natl. Acad. Sci., 97: 10584-10589, 2000.
Gorbatyuk, O.S., Milner, T.A., Wang, G., Reis, D.J. and Regunathan, S.: Localization of agmatine in vasopressin and oxytocin neurons of the rat hypothalamic paraventricular and supraoptic nuclei. Exp. Neurology., 171: 235-245, 2001.
Wang, G., Gorbatyuk, O.S., Dayanithi, G., Wang, J., Ouyang, W., Milner, T.A., Regunathan, S. and Reis, D.J.: Evidence for endogenous agmatine in hypothalamo-neurohypophysial tract and its specific modulation on Ca++ channels and neuropeptide release. Brain Res., 932:25-36, 2002.
Arcioglu-Kartal, F. and Regunathan, S.: Effect of chronic morphine treatment of the biosynthesis of agmatine in rat brain and other tissues. Life Sciences, 71: 1695-1701, 2002.
Zhu, M.-Y., Piletz, J.E., Harlaris, A. and Regunathan, S.: Effect of agmatine against cell death induced by NMDA and glutamate in neurons and PC12 cells. Cellular & Molecular Neurobiology, (in press).
I love following studies and am not too keen on taking stuff that has not been researched and validated, on the market for some time...not that I expect miricals but I do want what I pay for to work/not eff me up lol
for me ~ i would pass on this for now, yall may wanna check it out more as well

I could only find wishey washey info with no back bone...