Magnetic Fields May Repair Damaged Nerves

 Today's post comes from marketwatch.com (see link below) and takes us into the realms of research that may seem far removed from the human experience, especially when it comes to neuropathy. Apparently studies have shown that the myelin sheaths of peripheral nerves in mice can be repaired by using ultramagnetic fields. If you remember, the myelin sheath is the protective coating around a nerve (much like insulation around electricity wires) and in most forms of neuropathy, it is precisely the damage to this that can bring on so many neuropathic symptoms. The idea that electromagnetic fields can have a biological effect on nerves and their coatings may seem a little far fetched but that seems to be precisely what has happened in these studies. The potential benefits for neuropathy patients however, could be enormous - we'll need to wait and see.
 

Myelin Sheath of Peripheral Nerves in Mice Is Regenerated With Magnetic Fields

Oct. 10, 2012


The Jacobson Resonance Equation Calculated Extremely Low Intensity Magnetic Fields For Regeneration of Peripheral Nerves in Mice

JUPITER, Fla., Oct. 10, 2012 /

-- Dr. Jerry Jacobson, biophysicist and inventor, announced today the results of studies on the effect of extremely low intensity electromagnetic fields on the restoration of forelimb grip strength, and radial nerve ultrastructure in mice with induced motor neuropathy. After administration of neurotoxin, mice persisted to exhibit a 56% decrease in grip strength; and radial nerve electron micrographs showed axonal demyelination, inactive mitochondria and uneven dispersion of neurofilaments and microtubules. Mice were then exposed to magnetic fields, calculated on the basis of masses of molecules vital to nerve function, using the Jacobson Equation, mc2=BvLq. Magnetic fields were applied twice weekly for eight and one half weeks. Magnetic field exposure resulted in as much as 87% recovery (p=less than0.05) of grip strength that was sustained at an 82% level until the 27th week of observation. Studies were conducted at the Weill Medical College of Cornell University and then replicated at Fairleigh Dickinson University.

Principal investigator, Professor Anjali Saxena said, "The exposed groups exhibited axonal remyelination, functional condensed state of mitochondria, and evenly dispersed neurofilaments and microtubules; consistent with grip strength recovery."

Dr. Jacobson said, "Einstein predicted, shortly before his passing in 1955, that the two essential realities of nature, electromagnetic field and gravitational field - or as they might also be called - matter and space - must be unified through an algebraic theory. The equation of Jacobson Resonance accomplishes this connection, and basic science research has shown that matter and space communicate through magnetic resonance."

Prof. Saxena added, "The results are the first to demonstrate a biological effect of electromagnetic fields, in vivo, on the restoration of subcellular structures required for nerve impulse conduction and metabolism in nerves, and consequently a grip strength recovery from motor neuropathy, under controlled experimental conditions."

A role of electromagnetic fields in recovery from nerve injury, spinal cord trauma and peripheral neuropathy may be postulated on the basis of selectively modulating neurotropins and their receptors. Further dose-response studies are required to determine a therapeutic model for electromagnetic field application in the treatment of nerve dysfunctions.

References Anjali Saxena, Jerry Jacobson, William Yamanashi, Benjamin Scherlag, Brij Saxena (2003) Medical Hypotheses, 60 (6) 821-839 Elsevier Science Ltd.; Available on line at www.sciencedirect.com Albert Einstein (1956) The Meaning of Relativity, Including the Relativistic Theory of the Non-Symmetric Field; Princeton University Press, Princeton, N.J, P164-166 Jerry Jacobson (2012) Reason For Life; Positive Action With Moral Purpose; Abbott Press (A Division of Writer's Digest), p 88-122

The Resonator device is an Investigational Device limited by federal (or United States) law to investigational use; nor is therapy generally available outside of Investigational Review Board (IRB) approved clinical studies.

http://www.marketwatch.com/story/myelin-sheath-of-peripheral-nerves-in-mice-is-regenerated-with-magnetic-fields-2012-10-10

Damaged Mitochondria Lead To Nerve Pain Repair Them And The Pain Goes Away!

Today's post from the ever-informative, sciencedaily.com (see link below) delves deep into the cellular behaviour of nerve cells but comes out with a potential benefit for us all in the future. If you feel this is all beyond you on a lazy Sunday morning, don't be put off; read on, because science daily nearly always delivers text that we can all follow. In this case it concerns the energy drivers of nerve cells and they are mitochondria. If the mitochondria are damaged or inhibited in some way then neuropathy is most often the result because if the neurons are deprived of the energy they generate then they just give up the ghost and start short-circuiting in the ways we feel every day. Basically, scientists have found that if the mitochondria are damaged, they can regenerate themselves if the protein that is blocking them, is disabled and that's apparently possible...in the ever-suffering mice in the test labs. Too molecular for you? Well yes but we must take heart that scientists are learning so much more every year and this is leading to improved treatments...however long it takes.

Mobilizing mitochondria may be key to regenerating damaged neurons 
Date:June 7, 2016 Source:Rockefeller University Press

Researchers at the National Institute of Neurological Disorders and Stroke have discovered that boosting the transport of mitochondria along neuronal axons enhances the ability of mouse nerve cells to repair themselves after injury. The study, "Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits," which has been published in The Journal of Cell Biology, suggests potential new strategies to stimulate the regrowth of human neurons damaged by injury or disease.

Neurons need large amounts of energy to extend their axons long distances through the body. This energy -- in the form of adenosine triphosphate (ATP) -- is provided by mitochondria, the cell's internal power plants. During development, mitochondria are transported up and down growing axons to generate ATP wherever it is needed. In adults, however, mitochondria become less mobile as mature neurons produce a protein called syntaphilin that anchors the mitochondria in place. Zu-Hang Sheng and colleagues at the National Institute of Neurological Disorders and Stroke wondered whether this decrease in mitochondrial transport might explain why adult neurons are typically unable to regrow after injury.

Sheng and his research fellow Bing Zhou, the first author of the study, initially found that when mature mouse axons are severed, nearby mitochondria are damaged and become unable to provide sufficient ATP to support injured nerve regeneration. However, when the researchers genetically removed syntaphilin from the nerve cells, mitochondrial transport was enhanced, allowing the damaged mitochondria to be replaced by healthy mitochondria capable of producing ATP. Syntaphilin-deficient mature neurons therefore regained the ability to regrow after injury, just like young neurons, and removing syntaphilin from adult mice facilitated the regeneration of their sciatic nerves after injury.

"Our in vivo and in vitro studies suggest that activating an intrinsic growth program requires the coordinated modulation of mitochondrial transport and recovery of energy deficits. Such combined approaches may represent a valid therapeutic strategy to facilitate regeneration in the central and peripheral nervous systems after injury or disease," Sheng says.

Story Source:

The above post is reprinted from materials provided by Rockefeller University Press. Note: Materials may be edited for content and length.

Journal Reference:
Bing Zhou, Panpan Yu, Mei-Yao Lin, Tao Sun, Yanmin Chen, Zu-Hang Sheng. Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits. The Journal of Cell Biology, 2016; jcb.201605101 DOI: 10.1083/jcb.20160510

 https://www.sciencedaily.com/releases/2016/06/160607151233.htm