2

The first chart is being hyped by the right-wing media outlets like Fox News and the Drudge Report to prove that too many Americans are on disability.

Notice they compare the U.S. to Greece and Tunisia, which have smaller populations than Ohio.

The second, more accurate chart shows the number of Americans who receive disability benefits compared to the total number of Americans with disabilities and the total number of Americans who are on disability. 

White matter is one of the two components of the central nervous system and consists mostly of glial cells and myelinated axons that transmit signals from one region of the cerebrum to another and between the cerebrum and lower brain centers. White matter tissue of the freshly cut brain appears pinkish white to the naked eye because myelin is composed largely of lipid tissue veined with capillaries. Its white color is due to its usual preservation in formaldehyde.

White matter is composed of bundles of myelinated nerve cell processes (or axons), which connect various grey matter areas (the locations of nerve cell bodies) of the brain to each other, and carry nerve impulses between neurons. Myelin acts as an insulator, increasing the speed of transmission of all nerve signals.

Image: White matter structure of human brain (taken by MRI).

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Fungal protein found to cross blood-brain barrier

In a remarkable series of experiments on a fungus that causes cryptococcal meningitis, a deadly infection of the membranes that cover the spinal cord and brain, investigators at UC Davis have isolated a protein that appears to be responsible for the fungus’ ability to cross from the bloodstream into the brain.

image

The discovery — published online June 3 in mBio, the open-access, peer-reviewed journal of the American Society for Microbiology — has important implications for developing a more effective treatment for Cryptococcus neoformans, the cause of the condition, and other brain infections, as well as for brain cancers that are difficult to treat with conventional medications. 

“This study fills a significant gap in our understanding of how C. neoformans crosses the blood-brain barrier and causes meningitis,” said Angie Gelli, associate professor of pharmacology at UC Davis and principal investigator of the study. “It is our hope that our findings will lead to improved treatment for this fungal disease as well as other diseases of the central nervous system.”

Normally the brain is protected from bacterial, viral and fungal pathogens in the bloodstream by a tightly packed layer of endothelial cells lining capillaries within the central nervous system — the so-called blood-brain barrier. Relatively few organisms — and drugs that could fight brain infections or cancers — can breach this protective barrier.

The fungus studied in this research causes cryptococcal meningoencephalitis, a usually fatal brain infection that annually affects some 1 million people worldwide, most often those with an impaired immune system. People typically first develop an infection in the lungs after inhalation of the fungal spores of C. neoformans in soil or pigeon droppings. The pathogen then spreads to the brain and other organs.

Unique protein identified

In an effort to discover how C. neoformans breaches the blood-brain barrier, the investigators isolated candidate proteins from the cryptococcal cell surface. One was a previously uncharacterized metalloprotease that they named Mpr1. (A protease is an enzyme — a specialized protein — that promotes a chemical reaction; a metalloprotease contains a metal ion — in this case zinc — that is essential for its activity.) The M36 class of metalloproteases to which Mpr1 belongs is unique to fungi and does not occur in mammalian cells.

The investigators next artificially generated a strain of C. neoformans that lacked Mpr1 on the cell surface. Unlike the normal wild-type C. neoformans, the strain without Mpr1 could not cross an artificial model of the human blood-brain barrier.

They next took a strain of common baking yeast — Saccharomyces cerevisiae — that does not cross the blood-brain barrier and does not normally express Mpr1, and modified it to express Mpr1 on its cell surface. This strain then gained the ability to cross the blood-brain barrier model.

Investigators then infected mice with either the C. neoformans that lacked Mpr1 or the wild-type strain by injecting the organisms into their bloodstream. Comparing the brain pathology of mice 48 hours later, they found numerous cryptococci-filled cysts throughout the brain tissue of mice infected with the wild-type strain; these lesions were undetectable in those infected with the strain lacking Mpr1. In another experiment, after 37 days of being infected by the inhalation route, 85 percent of the mice exposed to the wild-type C. neoformans had died, while all of those given the fungus without Mpr1 were alive.

“Our studies are the first clear demonstration of a specific role for a fungal protease in invading the central nervous system,” said Gelli. “The details of exactly how it crosses is an important new area under investigation.”

New targeted therapies possible

According to Gelli, their discovery has significant therapeutic potential via two important mechanisms. Either Mpr1 — or an aspect of the mechanism by which it crosses the blood-brain barrier — could be a target of new drugs for treating meningitis caused by C. neoformans. In a person who develops cryptococcal lung infection, such a treatment would ideally make the fungus less likely to enter the brain and lead to a rapidly fatal meningitis.

Secondly, Mpr1 could be developed as part of a drug-delivery vehicle for brain infections and cancers. An antibiotic or cancer-fighting drug that is unable to cross the blood-brain barrier on its own could be attached to a nanoparticle containing Mpr1, allowing it to hitch a ride and deliver its goods to where it is needed.

“The biggest obstacle to treating many brain cancers and infections is getting good drugs through the blood-brain barrier,” said Gelli. “If we could design an effective delivery system into the brain, the impact would be enormous for treating some of these terrible diseases.”

Gelli’s group is currently pursuing such a nanoparticle drug-delivery system using Mpr1. They are also further investigating the exact molecular mechanism by which Mpr1 breaches the blood-brain barrier.

6

Just a Signal Boost for some Really Good Slenderseries

1. TheAbbeyDiaries
2. CaughtNotSleeping
3. TheUndecidedFive
4. tea13time
5. tulpaeffect
6. CoyoteIsAwesome
7. AfraidAtHome
8. DownMyCellarDoor — sadly, I’ve found out the videos were deleted for this one. so sorry friends—
9. proxyjack spicer
10. TJAProjects
11. Keratin Garden

·.·. ANNOUNCEMENT COMPLETE.·.·

Effects of Chronic Stress Can be Traced to Your Genes

New research shows that chronic stress changes gene activity in immune cells before they reach the bloodstream. With these changes, the cells are primed to fight an infection or trauma that doesn’t actually exist, leading to an overabundance of the inflammation that is linked to many health problems.

This is not just any stress, but repeated stress that triggers the sympathetic nervous system, commonly known as the fight-or-flight response, and stimulates the production of new blood cells. While this response is important for survival, prolonged activation over an extended period of time can have negative effects on health.

A study in animals showed that this type of chronic stress changes the activation, or expression, of genes in immune cells before they are released from the bone marrow. Genes that lead to inflammation are expressed at higher-than-normal levels, while the activation of genes that might suppress inflammation is diminished.

Ohio State University scientists made this discovery in a study of mice. Their colleagues from other institutions, testing blood samples from humans living in poor socioeconomic conditions, found that similarly primed immune cells were present in these chronically stressed people as well.

“The cells share many of the same characteristics in terms of their response to stress,” said John Sheridan, professor of oral biology in the College of Dentistry and associate director of Ohio State’s Institute for Behavioral Medicine Research (IBMR), and co-lead author of the study. “There is a stress-induced alteration in the bone marrow in both our mouse model and in chronically stressed humans that selects for a cell that’s going to be pro-inflammatory.

“So what this suggests is that if you’re working for a really bad boss over a long period of time, that experience may play out at the level of gene expression in your immune system.”

The findings suggest that drugs acting on the central nervous system to treat mood disorders might be supplemented with medications targeting other parts of the body to protect health in the context of chronic social stress.

Steven Cole, a professor of medicine and a member of the Cousins Center for Psychoneuroimmunology at UCLA, is a co-corresponding author of the study. The research is published in a recent issue of the journal Proceedings of the National Academy of Sciences.

The mind-body connection is well established, and research has confirmed that stress is associated with health problems. But the inner workings of that association – exactly how stress can harm health – are still under investigation.

Sheridan and colleagues have been studying the same mouse model for a decade to reveal how chronic stress – and specifically stress associated with social defeat – changes the brain and body in ways that affect behavior and health.

The mice are repeatedly subjected to stress that might resemble a person’s response to persistent life stressors. In this model, male mice living together are given time to establish a hierarchy, and then an aggressive male is added to the group for two hours at a time. This elicits a “fight or flight” response in the resident mice as they are repeatedly defeated by the intruder.

“These mice are chronically in that state, so our research question is, ‘What happens when you stimulate the sympathetic nervous system over and over and over, or continuously?’ We see deleterious consequences to that,” Sheridan said.

Under normal conditions, the bone marrow in animals and humans is making and releasing billions of red blood cells every day, as well as a variety of white blood cells that constitute the immune system. Sheridan and colleagues already knew from previous work that stress skews this process so that the white blood cells produced in the bone marrow are more inflammatory than normal upon their release – as if they are ready to defend the body against an external threat.

A typical immune response to a pathogen or other foreign body requires some inflammation, which is generated with the help of immune cells. But when inflammation is excessive and has no protective or healing role, the condition can lead to an increased risk for cardiovascular diseases, diabetes and obesity, as well as other disorders.

In this work, the researchers compared cells circulating in the blood of mice that had experienced repeated social defeat to cells from control mice that were not stressed. The stressed mice had an average fourfold increase in the frequency of immune cells in their blood and spleen compared to the normal mice.

Genome-wide analysis of these cells that had traveled to the spleen in the stressed mice showed that almost 3,000 genes were expressed at different levels – both higher and lower – compared to the genes in the control mice. Many of the 1,142 up-regulated genes in the immune cells of stressed mice gave the cells the power to become inflammatory rapidly and efficiently.

“There is no traditional viral or bacterial challenge – we’re generating the challenge via a psychological response,” said study first author Nicole Powell, a research scientist in oral biology at Ohio State. “This study provides a nice mechanism for how psychology impacts biology. Other studies have indicated that these cells are more inflammatory; our work shows that these cells are primed at the level of the gene, and it’s directly due to the sympathetic nervous system.”

The researchers confirmed that the sympathetic nervous system was activated by showing that a beta blocker reduced symptoms associated with chronic stress. The beta receptors that were turned off by this intervention are major participants in the sympathetic nervous system response.

Meanwhile, UCLA’s Cole performs specialized statistical analyses of genome function to determine how people’s perception of their surroundings affects their biology. He and colleagues analyzed blood samples both from Sheridan’s mice and from healthy young adult humans whose socioeconomic status had been previously characterized as either high or low.

The human analysis identified differing levels of expression of 387 genes between the low- and high-socioeconomic status adults – and as in the mice, the up-regulated genes were pro-inflammatory in nature. The researchers also noted that almost a third of the genes with altered expression levels in immune cells from chronically stressed humans were the same genes differentially expressed in mice that had experienced repeated social defeat – a much higher similarity than would occur by chance.

This same pro-inflammatory immune-cell profile has been seen in research on parents of children with cancer.

“What we see in this study is a convergence of animal and human data showing similar genomic responses to adversity,” Cole said. “The molecular information from animal research integrates nicely with the human findings in showing a significant up-regulation of pro-inflammatory genes as a consequence of stress – and not just experimental stress, but authentic environmental stressors humans experience in everyday life.”

How the Human Brain Works

The brain is the master organ of the body. The brain takes in all information relating to the body’s internal and external environments, and it produces the appropriate responses.

In humans, the nervous system is divided into the central nervous system (CNS), which consists of the brain and spinal cord, and the peripheral nervous system (PNS), which contains all the nerves that run everywhere in the body.

The spinal cord, which is attached to the brain, runs down the center of your body, so equate that with the CNS. All the nerves that branch off the spinal cord, including the cranial nerves and spinal nerves, and reach to the periphery of your body make up the PNS.

The structures of the brain

Inside the skull, the meninges cover the cerebrum (the large, gray, bumpy part of the brain). The meninges are strong membranes that cover the brain and spinal cord. Cerebrovascular fluid flows between the membranes. An infection here is called meningitis for inflammation of the meninges.

The cerebrum is the largest part of the brain and is the part responsible for consciousness. The cerebrum is divided into left and right halves, which are called cerebral hemispheres. Each cerebral hemisphere has four lobes named for the bones of the skull that cover them: frontal, parietal, temporal, and occipital.

Specific areas of the lobes are responsible for certain functions, such as concentration, understanding speech, recognizing objects, memory, and so on.

At the center of the brain are the thalamus and hypothalamus, which form the structure called the diencephalon. The hypothalamus generates many neurosecretions, which are carried to the pituitary gland at the base of the hypothalamus. The hypothalamus controls homeostasis by regulating hunger, thirst, sleep, body temperature, water balance, and blood pressure.

The pituitary gland is called the master gland because, along with the hypothalamus, it helps to maintain homeostasis by secreting many important hormones.

At the base of the brain are the cerebellum and the brain stem. The cerebellum coordinates muscle functions such as maintaining normal muscle tone and maintaining posture. The brain stem is formed by three structures: the midbrain, the pons, and the medulla oblongata. The spinal cord is a continuation of the brain stem that runs down through the vertebrae of the spine.

How reflex arcs work

Reflex arcs are connections between sensory neurons, the spinal cord, and motor neurons. They are good examples of how the nervous system protects you by making you get out of danger almost before you realize you are in danger.

Here’s an example: You are cooking dinner, and you accidentally grab the lid of a pot without using a hot pad. You just want to check on the vegetables. Your nervous system has other ideas:

1) When you grab that hot lid, the endings of the sensory nerves in your skin detect the heat and send an impulse up through the axon of a sensory neuron to the nerve cell body of the sensory neuron.

2) The impulse continues through sensory neurons until it reaches an interneuron in the spinal cord.

The interneuron determines the appropriate response — which, in this case, would be stimulating the muscles to pull your hand away.

3) The excitatory impulse is transferred to the cell body of a motor neuron and travels down the axon of the motor neuron until it reaches muscle tissue.

The muscle responds by contracting to pull your hand away from the hot lid.

With all these words describing what happens, it makes it seem like this process takes quite a while. But think about when you’ve touched something hot by mistake. You pulled your hand away immediately thanks to a quick-reacting reflex arc. Without the reflex arc protecting you, you might just unknowingly hold that hot lid in your hand until real damage is done!

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Robotic advances promise artificial legs that emulate healthy limbs

Recent advances in robotics technology make it possible to create prosthetics that can duplicate the natural movement of human legs. This capability promises to dramatically improve the mobility of lower-limb amputees, allowing them to negotiate stairs and slopes and uneven ground, significantly reducing their risk of falling as well as reducing stress on the rest of their bodies.

That is the view of Michael Goldfarb, the H. Fort Flowers Professor of Mechanical Engineering, and his colleagues at Vanderbilt University’s Center for Intelligent Mechatronics expressed in a perspective’s article in the Nov. 6 issue of the journal Science Translational Medicine.

For the last decade, Goldfarb’s team has been doing pioneering research in lower-limb prosthetics. It developed the first robotic prosthesis with both powered knee and ankle joints. And the design became the first artificial leg controlled by thought when researchers at the Rehabilitation Institute of Chicago created a neural interface for it.

In the article, Goldfarb and graduate students Brian Lawson and Amanda Shultz describe the technological advances that have made robotic prostheses viable. These include lithium-ion batteries that can store more electricity, powerful brushless electric motors with rare-Earth magnets, miniaturized sensors built into semiconductor chips, particularly accelerometers and gyroscopes, and low-power computer chips.

The size and weight of these components is small enough so that they can be combined into a package comparable to that of a biological leg and they can duplicate all of its basic functions. The electric motors play the role of muscles. The batteries store enough power so the robot legs can operate for a full day on a single charge. The sensors serve the function of the nerves in the peripheral nervous system, providing vital information such as the angle between the thigh and lower leg and the force being exerted on the bottom of the foot, etc. The microprocessor provides the coordination function normally provided by the central nervous system. And, in the most advanced systems, a neural interface enhances integration with the brain.

Unlike passive artificial legs, robotic legs have the capability of moving independently and out of sync with its user’s movements. So the development of a system that integrates the movement of the prosthesis with the movement of the user is “substantially more important with a robotic leg,” according to the authors.

Not only must this control system coordinate the actions of the prosthesis within an activity, such as walking, but it must also recognize a user’s intent to change from one activity to another, such as moving from walking to stair climbing.

Identifying the user’s intent requires some connection with the central nervous system. Currently, there are several different approaches to establishing this connection that vary greatly in invasiveness. The least invasive method uses physical sensors that divine the user’s intent from his or her body language. Another method – the electromyography interface – uses electrodes implanted into the user’s leg muscles. The most invasive techniques involve implanting electrodes directly into a patient’s peripheral nerves or directly into his or her brain. The jury is still out on which of these approaches will prove to be best. “Approaches that entail a greater degree of invasiveness must obviously justify the invasiveness with substantial functional advantage,” the article states.

There are a number of potential advantages of bionic legs, the authors point out.

Studies have shown that users equipped with the lower-limb prostheses with powered knee and heel joints naturally walk faster with decreased hip effort while expending less energy than when they are using passive prostheses.

In addition, amputees using conventional artificial legs experience falls that lead to hospitalization at a higher rate than elderly living in institutions. The rate is actually highest among younger amputees, presumably because they are less likely to limit their activities and terrain. There are several reasons why a robotic prosthesis should decrease the rate of falls: Users don’t have to compensate for deficiencies in its movement like they do for passive legs because it moves like a natural leg. Both walking and standing, it can compensate better for uneven ground. Active responses can be programmed into the robotic leg that helps users recover from stumbles.

Before individuals in the U.S. can begin realizing these benefits, however, the new devices must be approved by the U.S. Food and Drug Administration (FDA).

Single-joint devices are currently considered to be Class I medical devices, so they are subject to the least amount of regulatory control. Currently, transfemoral prostheses are generally constructed by combining two, single-joint prostheses. As a result, they have also been considered Class I devices.

In robotic legs the knee and ankle joints are electronically linked. According to the FDA that makes them multi-joint devices, which are considered Class II medical devices. This means that they must meet a number of additional regulatory requirements, including the development of performance standards, post-market surveillance, establishing patient registries and special labeling requirements.

Another translational issue that must be resolved before robotic prostheses can become viable products is the need to provide additional training for the clinicians who prescribe prostheses. Because the new devices are substantially more complex than standard prostheses, the clinicians will need additional training in robotics, the authors point out.

In addition to the robotics leg, Goldfarb’s Center for Intelligent Mechatronics has developed an advanced exoskeleton that allows paraplegics to stand up and walk, which led Popular Mechanics magazine to name him as one of the 10 innovators who changed the world in 2013, and a robotic hand with a dexterity that approaches that of the human hand.

LOOOK 👋😃 we got full length mirrors for our fitness room!
Of course to celebrate I took a FULL BODY #selfie 😊.

(Yeah, I don’t wear street clothes that often..😕…comfy clothes and workout clothes are my cup of tea 😏)

I’m gonna finish my volume leg sesh today - actually…start it over - cause I’m a #beast.

#cbl #cns #progress #girlswithabs #girlswhoflex #flex

Major advance in understanding risky but effective Multiple Sclerosis treatment

A new study by Multiple Sclerosis researchers at three leading Canadian centres addresses why bone marrow transplantation (BMT) has positive results in patients with particularly aggressive forms of MS.  The transplantation treatment, which is performed as part of a clinical trial and carries potentially serious risks, virtually stops all new relapsing activity as observed upon clinical examination and brain MRI scans.  The study reveals how the immune system changes as a result of the transplantation.  Specifically, a sub-set of T cells in the immune system known as Th17 cells, have a substantially diminished function following the treatment. The finding to be published in the upcoming issue of Annals of Neurology and currently in the early online version, provides important insight into how and why BMT treatment works as well as how relapses may develop in MS.

“Our study examined why patients essentially stop having relapses and new brain lesions after the bone marrow transplant treatment, which involves ablative chemotherapy followed by stem cell transplantation using the patient’s own cells,” said Prof. Amit Bar-Or, the principle investigator of the study, who is a neurologist and MS researcher at The Montreal Neurological Institute and Hospital -The Neuro, McGill University, and Director of The Neuro’s Experimental Therapeutics Program. “We discovered differences between the immune responses of these patients before and after treatment, which point to a particular type of immune response as the potential perpetrator of relapses in MS.”

“Although the immune system that re-emerges in these patients from their stem cells is generally intact, we identified a selectively diminished capacity of their Th17 immune responses following therapy - which could explain the lack of new MS disease activity. In untreated patients, these Th17 cells may be particularly important in breaching the blood-brain-barrier, which normally protects the central nervous system. This interaction of Th17 cells with the blood-brain barrier can facilitate subsequent invasion of other immune cells such as Th1 cells, which are thought to also contribute to brain cell injury.

Twenty-four patients participated in the overall clinical trial as part of the ‘Canadian MS BMT’ clinical trial, coordinated by Drs. Mark Freedman and Harry Atkins at the Ottawa General Hospital. The new discovery, made in a subset of patients participating in the clinical trial, was based on immunological studies carried out jointly in laboratories at The Neuro and the Université de Montréal. Results of this study not only show the clinical benefits of BMT treatment, but also open a unique window into the immunological mechanisms underlying relapses in MS. Th17 cells could be the immune cells associated with the initiation of new relapsing disease activity in this group of patients with aggressive MS. This finding deepens our understanding of MS and could guide the development of personalized medicine with a more favourable risk/benefit profile.

Among the patients treated in the Canadian MS BMT clinical trial, was Dr. Alexander Normandin, a family doctor, who was a third- year McGill medical student getting ready for his surgery exams when he first learned he had MS, “I was so engrossed in my studies that I didn’t pay attention to the first sign but within a few days of waking up with a numb temple, my face felt frozen. I learned that I had a very aggressive form of MS and would probably be in a wheelchair within a year. It was a brutal blow. I became patient #19 – of only 24 for this experimental treatment. My immune system was knocked out and then rebooted with my stem cells. Today, my MS has stabilized. I now have this disease under control and I take it one day at a time.”

Extrasynaptic NMDA Receptor Involvement in Central Nervous System Disorders

NMDA receptor (NMDAR)-induced excitotoxicity is thought to contribute to the cell death associated with certain neurodegenerative diseases, stroke, epilepsy, and traumatic brain injury. Targeting NMDARs therapeutically is complicated by the fact that cell signaling downstream of their activation can promote cell survival and plasticity as well as excitotoxicity. However, research over the past decade has suggested that overactivation of NMDARs located outside of the synapse plays a major role in NMDAR toxicity, whereas physiological activation of those inside the synapse can contribute to cell survival, raising the possibility of therapeutic intervention based on NMDAR subcellular localization. Here, we review the evidence both supporting and refuting this localization hypothesis of NMDAR function and discuss the role of NMDAR localization in disorders of the nervous system. Preventing excessive extrasynaptic NMDAR activation may provide therapeutic benefit, particularly in Alzheimer disease and Huntington disease.

Full Article

I don’t want to date someone just to say I’m with them. When I’m dating someone, I want that shit to last. It may not be forever, but I want it to be a long one. I don’t care about titles and showing you off to the world, I just want you and I to be happy, and together.

Hope for Spinal Cord Injuries

Laura Wong has coaxed damaged nerve cells to grow and send messages to the brain again

“An ailment not to be treated,” read the prescription for a spinal cord injury on an Egyptian papyrus in 1,700 B.C. Not much has changed in the intervening millennia. Despite decades of research, modern medicine has made little headway in its quest to reverse damage to the central nervous system.

That is not to say, however, that there isn’t a glimmer of hope. Laura Wong, an M.D./Ph.D. student in Professor Eric Frank’s molecular physiology lab at the Sackler School, has been able to coax damaged nerve cells known as sensory neurons to regenerate, growing as much as 10 times longer than previously documented. What’s more, the new neurons make organized connections with their counterparts inside the spinal cord and brain stem, ensuring information from the outside world paints an accurate picture inside the brain.

“All the regeneration in the world isn’t going to make any difference if they don’t reconnect. You’re still not going to get any function,” says Wong, who has worked since 2010 in Frank’s lab, which is trying to develop therapies for spinal cord injuries.

Her findings, which she presented at the annual meeting of the Society for Neuroscience in 2011 and 2012, shed light on the complex processes behind nerve cell growth and regeneration. If those results can be replicated in patients, it could prevent certain types of nerve damage and improve quality of life for some.

Going the Distance

Unlike tissues such as skin and bone, the cells of the central nervous system in an adult are notoriously resistant to healing. Not only does the supply of natural growth stimulants decline as we age, but the body also produces chemicals that discourage nerve cells from regenerating. Worse, the scar tissue that starts to form immediately after a spinal cord injury also contains compounds that hinder nerve cell growth.

Researchers in Frank’s lab have been seeking ways to either stimulate growth or block the mechanisms that inhibit nerve cell growth—or both—since 2005. Wong’s predecessor in the lab, Pamela Harvey, a 2009 graduate of the Sackler School, tested a synthetic version of a nerve cell growth factor, called artemin, on crushed sensory neurons that relay information from the hands, arms and shoulders to the brain.

The damage mimics a common injury called Erb’s palsy, which can occur when a baby’s shoulder gets caught behind the mother’s pelvis during labor and delivery, creating undue strain on nerves in the newborn’s neck. Riders thrown head first off a motorcycle or snowmobile can suffer similar injuries.

“Anytime the shoulder goes one way and the head and neck go the other, that’s when you see these injuries,” Wong says.

In earlier experiments, Harvey and Frank found that treating with artemin did indeed stimulate the sensory nerve fibers to regenerate and grow back into the spinal cord over the course of about six weeks. In her follow-up experiments, Wong showed that artemin could induce those nerve fibers to grow the 3- to 4-centimeter distance from there up to the brainstem, where the brain and the spinal cord meet. That’s a little more than an inch—or roughly 10 times longer than any other researchers have been able to demonstrate with artemin or any other growth factor.

“A lot of other researchers just haven’t seen this length,” notes Wong, who saw the artemin-induced growth occur over a period of three to six months.

That’s important, because while axons only have to grow across microscopic distances in a developing embryo, they would have to bridge much wider gaps—depending on the site of the injury—to heal a neural injury in an adult, Wong says. Nerves that extend from the spine to the foot or toe can reach lengths of about 60 centimeters, she adds.

But Wong’s artemin-treated nerve fibers achieved more than unprecedented growth. They also reestablished connections with correct regions in the brain stem, just as Harvey had seen the nerve cells do in the spinal cord. That is, the axons essentially plugged themselves back in just as they were prior to the injury, and, like an old-fashioned telephone switchboard, they sent the right messages to the right parts of the brain.

That’s crucial because should the sensory nerves that relay pain signals become crossed, for example, it could result in a patient feeling phantom pain or the sensation of pain from something that shouldn’t cause discomfort at all.

“With some other growth-promoting compounds you get regeneration, but you see those axons growing kind of willy-nilly,” says Wong. “You can see where it would be just as detrimental to have things wired incorrectly as it would be to have things not wired at all.”

Just a Start

Artemin isn’t a panacea for spinal cord injuries, Wong and Frank stress. To work its cellular magic, the compound must be administered within a day or two, and the sooner the better. Also, artemin promotes growth only in sensory neurons—and so far, only in rats—which means such growth wouldn’t improve motor function for someone who had been paralyzed by a spinal cord injury, for example.

But if the findings, which Wong presented at the Society for Neuroscience meetings in 2011 and 2012, prove applicable to humans, restoring sensation alone could still improve quality of life, even for those living with paralysis. Giving these people the ability to sense heat, cold and pain could help them avoid other accidental injuries, says Frank.

Wong hopes her work with sensory neurons will help unlock the secrets to promoting regeneration of other, more obstinate types of neurons in the brainstem and spinal cord. While she demonstrated that the sensory nerves plugged themselves back into the spinal cord precisely where they should have, it’s not clear how they did that.

Frank speculates that chemical cues guided the cells back into place. Should researchers be able to identify those cues, they potentially could use that knowledge to spark regeneration of other classes of neurons, such as motor neurons.

“There is hope—not proof—that even in humans these guidance molecules will persist into adulthood,” says Frank. “That means if we are able to get neurons to regenerate in patients, we might be able to make them go back to the right place. These experiments suggest we have some reason to believe it may work.”

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