New Ways To Repair Nerve Pathways

Today's post from (see link below) looks at new discoveries about dendrites, which are a component of nerve cells which receive information from the brain. It explains that these dendrites are capable of rapid re-growth after injury. before it was thought that axons (part of the cell which sends information to other cells) were the only cell components capable of regeneration. Discovering that dendrites can do it even more quickly and independently of axons may lead to treatments which can promote this activity and thus repair nerve damage more effectively. Sure, all this investigation has been done via fruit flies but the science always has to be established first before it can be applied to human injury - fascinating.

New Pathway for Neuron Repair Discovered  
Jan. 9, 2014 Story Source: The above story is based on materials provided by Penn State.

— Penn State University molecular biologists have discovered a brand-new pathway for repairing nerve cells that could have implications for faster and improved healing. The researchers describe their findings in a paper titled "Dendrite injury triggers DLK-independent regeneration," which will be published in the 30 January 2014 issue of the journal Cell Reports. These findings demonstrate that dendrites, the component of nerve cells that receive information from the brain, have the capacity to regrow after an injury.

Previous studies using many models have shown that when nerve cells, or neurons, are injured they repair the damage through regrowth of axons, the component of a neuron that sends information to other cells, explained co-author Melissa Rolls, associate professor of biochemistry and molecular biology at Penn State. "For example, if you break your arm and the bone slices some axons, you may lose feeling or movement in part of your hand. Over time you get this feeling back as the axon regenerates."

Using the fruit fly (Drosophila) as a model system, the researchers took what Rolls calls a "radical approach," cutting off all of the dendrites in neuron cells. "We wanted to really push the cells to the furthest limit," she said. "By cutting off all the dendrites, the cells would no longer be able to receive information, and we expected they might die. We were amazed to find that the cells don't die. Instead, they regrow the dendrites completely and much more quickly than they regrow axons. Within a few hours they'll start regrowing dendrites, and after a couple of days they have almost their entire arbor. It's very exciting -- these cells are extremely robust."

Moreover, it appears that dendrite regeneration happens independently of axon regeneration. When Rolls and her colleagues blocked the key signaling molecules that are required for axon regeneration in all animals, they found that dendrites were unaffected and continued to regrow. "This means that, not only do these neurons have an incredible ability to generate, they have two different regeneration pathways: one for axons and one for dendrites," she said. "Because it has not even been clear that dendrites can regenerate, it's a complete open question about what might be involved in that process. The next step will be to look for markers for dendrite regrowth -- proteins that are required or genes that are turned on in the process -- so we can learn more about what's going on during dendrite repair. We don't even know in what scenarios dendrite regeneration might happen in people yet because no one has known that it exists."

The implications for human health -- although a long way down the road -- are important, Rolls said. For example, in the case of stroke, when a region of the brain suffers blood loss, dendrites on brain cells are damaged and can be repaired only if blood loss is very brief. Otherwise, it is thought those brain cells die. But if those cells are able to regenerate dendrites, and if scientists learn how dendrite regrowth happens, researchers may be able to promote this process.

"We've provided some cause for hope when it comes to neuron damage," Rolls said. "This is optimistic work we are doing. It's just great to know there is this whole other pathway for survival that no one has even looked into before."

 http://www.sciencedaily.com/releases/2014/01/140109132422.htm

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