Posts tagged nerve fibers
Articles and news from the latest research reports.
Why Wet Feels Wet: Understanding the Illusion of Wetness
Human sensitivity to wetness plays a role in many aspects of daily life. Whether feeling humidity, sweat or a damp towel, we often encounter stimuli that feel wet. Though it seems simple, feeling that something is wet is quite a feat because our skin does not have receptors that sense wetness. The concept of wetness, in fact, may be more of a “perceptual illusion” that our brain evokes based on our prior experiences with stimuli that we have learned are wet.
So how would a person know if he has sat on a wet seat or walked through a puddle? Researchers at Loughborough University and Oxylane Research proposed that wetness perception is intertwined with our ability to sense cold temperature and tactile sensations such as pressure and texture. They also observed the role of A-nerve fibers—sensory nerves that carry temperature and tactile information from the skin to the brain—and the effect of reduced nerve activity on wetness perception. Lastly, they hypothesized that because hairy skin is more sensitive to thermal stimuli, it would be more perceptive to wetness than glabrous skin (e.g., palms of the hands, soles of the feet), which is more sensitive to tactile stimuli.
Davide Filingeri et al. exposed 13 healthy male college students to warm, neutral and cold wet stimuli. They tested sites on the subjects’ forearms (hairy skin) and fingertips (glabrous skin). The researchers also performed the wet stimulus test with and without a nerve block. The nerve block was achieved by using an inflatable compression (blood pressure) cuff to attain enough pressure to dampen A-nerve sensitivity.
They found that wet perception increased as temperature decreased, meaning subjects were much more likely to sense cold wet stimuli than warm or neutral wet stimuli. The research team also found that the subjects were less sensitive to wetness when the A-nerve activity was blocked and that hairy skin is more sensitive to wetness than glabrous skin. These results contribute to the understanding of how humans interpret wetness and present a new model for how the brain processes this sensation.
“Based on a concept of perceptual learning and Bayesian perceptual inference, we developed the first neurophysiological model of cutaneous wetness sensitivity centered on the multisensory integration of cold-sensitive and mechanosensitive skin afferents,” the research team wrote. “Our results provide evidence for the existence of a specific information processing model that underpins the neural representation of a typical wet stimulus.”
The article “Why wet feels wet? A neurophysiological model of human cutaneous wetness sensitivity” is published in the Journal of Neurophysiology.
Nerve impulses can collide and continue unaffected
According to the traditional theory of nerves, two nerve impulses sent from opposite ends of a nerve annihilate when they collide. New research from the Niels Bohr Institute now shows that two colliding nerve impulses simply pass through each other and continue unaffected. This supports the theory that nerves function as sound pulses. The results are published in the scientific journal Physical Review X.
Nerve signals control the communication between the billions of cells in an organism and enable them to work together in neural networks. But how do nerve signals work?
Old model
In 1952, Hodgkin and Huxley introduced a model in which nerve signals were described as an electric current along the nerve produced by the flow of ions. The mechanism is produced by layers of electrically charged particles (ions of sodium and potassium) on either side of the nerve membrane that change places when stimulated. This change in charge creates an electric current.
This model has enjoyed general acceptance. For more than 60 years, all medical and biology textbooks have said that nerves function is due to an electric current along the nerve pathway. However, this model cannot explain a number of phenomena that are known about nerve function.
New model
Researchers at the Niels Bohr Institute at the University of Copenhagen have now conducted experiments that raise doubts about this well-established model of electrical impulses along the nerve pathway.
“According to the theory of this ion mechanism, the electrical signal leaves an inactive region in its wake, and the nerve can only support new signals after a short recovery period of inactivity. Therefore, two electrical impulses sent from opposite ends of the nerve should be stopped after colliding and running into these inactive regions,” explains Thomas Heimburg, Professor and head of the Membrane Biophysics Group at the Niels Bohr Institute at the University of Copenhagen.
Thomas Heimburg and his research group conducted experiment in the laboratory using nerves from earthworms and lobsters. The nerves were removed and used in an experiment which allowed the researchers to stimulate the nerve fibres with electrodes on both ends. Then they measured the signals en route.
“Our study showed that the signals passed through each other completely unhindered and unaltered. That’s how sound waves work. A sound wave doesn’t stop when it meets another sound wave. Both waves continue on unimpeded. The nerve impulse can therefore be explained by the fact that the pulse is a mechanical wave in the form of a sound pulse, a soliton, that moves along the nerve membrane,” explains Thomas Heimburg.
The theory is confirmed
When the sound pulse moves through the nerve pathway, the membrane changes locally from a liquid to a more solid form. The membrane is compressed slightly, and this change leads to an electrical pulse as a consequence of the piezoelectric effect.
“The electrical signal is thus not based on an electric current but is caused by a mechanical force,” points out Thomas Heimburg.
Thomas Heimburg, along with Professor Andrew Jackson, first proposed the theory that nerves function by sound pulses in 2005. Their research has since provided support for this theory, and the new experiments offer additional confirmation for the theory that nerve signals are sound pulses.
(Figure 1: Axons grow and turn in response to guidance cues (arrows), which regulate endocytosis and exocytosis at the tips of growing axons. Credit: © 2014 T. Tojima et al.)
Steering the filaments of the developing brain
During brain development, nerve fibers grow and extend to form brain circuits. This growth is guided by molecular cues (Fig. 1), but exactly how these cues guide axon extension has been unclear. Takuro Tojima and colleagues from the RIKEN Brain Science Institute have now uncovered the signaling pathways responsible for turning growing nerve fibers, or axons, toward or away from guidance cues.
The researchers previously showed that axon-repelling cues act by inducing the removal of cell membrane—a process called endocytosis—from the side of the axon closest to the repulsive cue. The enzyme PIPKIγ90 is known to be involved in endocytosis in axons during certain types of synaptic activity, so the researchers investigated whether PIPKIγ90 also played a role in endocytosis during axon turning. By examining the developing brains of chicken embryos expressing an inactive form of PIPKIγ90, the researchers found that cues normally inducing endocytosis were no longer effective in repelling axon growth.
Cues that normally attract axons do so by driving membrane addition—exocytosis—on the side of the axon closest to the cue and also by suppressing endocytosis. Tojima’s team found that axons continued to be attracted to such cues even in the absence of PIPKIγ90, suggesting that PIPKIγ90 signaling is not involved in axon attraction.
The activity of PIPKIγ90 is known to be regulated by an enzyme called CDK5, a subunit of which binds to the protein kinase CaMKII. The researchers found that by inhibiting CDK5 or CaMKII, and thereby blocking the regulation of PIPKIγ90 that is needed to suppress endocytosis, endocytosis could occur in response to attractive cues.
They also found, however, that blocking CDK5 or CaMKII did not have any effect on endocytosis if the neurons expressed a mutant version of PIPKIγ90 that was unaffected by CDK5 and CaMKII signaling. As inhibitors of CDK5 or CaMKII did not alter endocytosis in response to repulsive cues, the team’s findings indicate that different signaling pathways are responsible for turning axons toward or away from guidance cues.
Additionally, Tojima and his colleagues showed that they could induce the attraction of axons toward drugs that inhibit endocytosis, suggesting that being able to control the direction of axon growth has potential therapeutic applications. “We hope our findings will aid in the development of future therapeutic strategies for rewiring neuronal networks after spinal cord injury and neurodegenerative diseases,” explains Tojima.
With the right rehabilitation, paralyzed rats learn to grip again
After a large stroke, motor skills barely improve, even with rehabilitation. An experiment conducted on rats demonstrates that a course of therapy combining the stimulation of nerve fiber growth with drugs and motor training can be successful. The key, however, is the correct sequence: Paralyzed animals only make an almost complete recovery if the training is delayed until after the growth promoting drugs have been administered, as researchers from the University of Zurich, ETH Zurich and the University of Heidelberg reveal.
Only if the timing, dosage and kind of rehabilitation are right can motor functions make an almost full recovery after a large stroke. Rats that were paralyzed down one side by a stroke almost managed to regain their motor functions fully if they were given the ideal combination of rehabilitative training and substances that boosted the growth of nerve fibers. Anatomical studies confirmed the importance of the right rehabilitation schedule: Depending on the therapeutic design, different patterns of new nerve fibers that sprouted into the cervical spinal cord from the healthy part of the brain and thus aid functional recovery to varying degrees were apparent. The study conducted by an interdisciplinary team headed by Professor Martin Schwab from the Brain Research Institute at the University of Zurich and ETH Zurich’s Neuroscience Center is another milestone in research on the repair of brain and spinal cord injuries.
“This new rehabilitative approach at least triggered an astonishing recovery of the motor skills in rats, which may become important for the treatment of stroke patients in the future,” says first author Anna-Sophia Wahl. At present, patients have to deal with often severe motor-function, language and vision problems, and their quality of life is often heavily affected.
Allow nerves to grow first, then train
On the one hand, the treatment of rats after a stroke involves specific immune therapy, where so-called Nogo proteins are blocked with antibodies. These proteins in the tissue around the nerve fibers inhibit nerve-fiber growth. If they are blocked, nerve fibers begin to sprout in the injured sections of the brain and spinal cord and relay nerve impulses again. On the other hand, the stroke animals, whose front legs were paralyzed, underwent physical training – namely, gripping food pellets. All the rats received antibody treatment first to boost nerve-fiber growth and – either at the same time or only afterwards – motor training. The results are surprising: The animals that began their training later regained a remarkable 85 percent of their original motor skills. For the rats that were trained straight after the stroke in parallel with the growth-enhancing antibodies, however, it was a different story: At 15 percent, their physical performance in the grip test remained very low.
On the one hand, the treatment of rats after a stroke involves specific immune therapy, where so-called Nogo proteins are blocked with antibodies. These proteins in the tissue around the nerve fibers inhibit nerve-fiber growth. If they are blocked, nerve fibers begin to sprout in the injured sections of the brain and spinal cord and relay nerve impulses again. On the other hand, the stroke animals, whose front legs were paralyzed, underwent physical training – namely, gripping food pellets. All the rats received antibody treatment first to boost nerve-fiber growth and – either at the same time or only afterwards – motor training. The results are surprising: The animals that began their training later regained a remarkable 85 percent of their original motor skills. For the rats that were trained straight after the stroke in parallel with the growth-enhancing antibodies, however, it was a different story: At 15 percent, their physical performance in the grip test remained very low.
Meticulous design very promising
The researchers consider timing a crucial factor for the success of the rehabilitation: An early application of growth stimulators – such as antibodies against the protein Nogo-A – triggers an increased sprouting and growth of nerve fibers. The subsequent training is essential to sift out and stabilize the key neural circuits for the recovery of the motor functions. For instance, an automatic, computer-based analysis of the anatomical data from the imaging revealed that new fibers in the spinal cord sprouted in another pattern depending on the course of treatment. By reversibly deactivating the new nerve fibers that grow, the neurobiologists were ultimately able to demonstrate for the first time that a group of these fibers is essential for the recovery of the motor function observed: Nerve fibers that grew into the spinal cord from the intact front half of the brain – changing sides – can reconnect the spinal cord circuits of the rats’ paralyzed limbs to the brain, enabling the animals to grip again.
“Our study reveals how important a meticulous therapeutic design is for the most successful rehabilitation possible,” sums up study head Martin Schwab. “The brain has enormous potential for the reorganization and reestablishment of its functions. With the right therapies at the right time, this can be increased in a targeted fashion.
Literature:
Wahl, A.S., Omlor, W., Rubio, J.C., Chen, J.L., Zheng, H., Schröter, A., Gullo, M., Weinmann, O., Kobayashi, K., Helmchen, F., Ommer, B., Schwab, M.E. Asynchronous therapy restores motor control by rewiring of the rat corticospinal tract after stroke. Science, June 13, 2014.
Previously Unstudied Gene Is Essential for Normal Nerve Development
Our ability to detect heat, touch, tickling and other sensations depends on our sensory nerves. Now, for the first time, researchers at Albert Einstein College of Medicine of Yeshiva University have identified a gene that orchestrates the crucially important branching of nerve fibers that occurs during development. The findings were published online today in the journal Cell.
The research focuses on dendrites, the string-like extensions of sensory nerves that penetrate tissues of the skin, eyes and other sensory organs. “The formation of dendritic branches—‘arbors’ as we call them—is vital for allowing sensory nerves to collect information and sample the environment appropriately,” said Hannes Buelow, Ph.D., senior author of the Cell paper and associate professor of genetics at Einstein. “These arbors vary greatly in shape and complexity, reflecting the different types of sensory input they receive. The loss of dendritic complexity has been linked to a range of neurological problems including Alzheimer’s disease, schizophrenia and autism spectrum disorders.” Dr. Buelow is also associate professor in the Dominick P. Purpura Department of Neuroscience.
The Human Genome Project, completed in 2003, revealed that humans possess some 20,500 genes and determined the DNA sequence of each. But for many of those genes, their function in the body has remained unknown. The newly identified gene falls into this “previously unknown function” category. In fact, the gene belongs to an entire class of genes that had no known function in any organism.
One way to learn what genes do is to study a model organism like the roundworm, which possesses a similar number of genes as people but only 956 cells, of which 302 are nerve cells (neurons). By knocking out or mutating roundworm genes and observing the effects, researchers can obtain insight into how genes influence the animal’s structure or physiology.
The Einstein scientists were looking for genes that organize the structure of the developing nervous system. They focused on a pair of roundworm sensory neurons, known as PVD neurons, which together produce the largest web of dendrites of any neurons in the roundworm—a sensory web that covers almost the entire skin surface of the worm and detects pain and extreme temperatures.
Suspecting that a gene acts in the skin to “instruct” nearby dendrites to branch, the researchers set out to identify the one responsible. To find it, they induced random mutations in the worms, singled out those worms displaying defects in PVD dendrite branching, and then identified the gene mutations that caused the defective branching.
This lengthy procedure, known as a genetic screen, was carried out by Yehuda Salzberg, Ph.D., the study’s lead author and a postdoctoral fellow in Dr. Buelow’s lab. The screen revealed that four mutations in the same gene caused defective branching of PVD dendrites. The researchers showed that this gene’s expression in the skin produces an extracellular protein that triggers normal branching of PVD dendrites during development. The dendritic branches of PVD neurons had previously been described as resembling menorahs, so the Einstein scientists named this gene mnr-1 and dubbed its protein menorin, or MNR-1.
The mnr-1 gene’s newly identified function in orchestrating dendrite branching is presumably not limited to roundworms. Versions of this gene are present in multicellular animals from the simplest to the most complex, including humans. Genes conserved in this way, through millions of years of evolution, tend to be genes that are absolutely necessary for maintaining life.
Further study revealed that menorin synthesized in the skin was necessary but not sufficient to prompt PVD dendrite branching. The menorin protein appears to form a complex with SAX-7/L1CAM, a well-known cell-adhesion protein found in the skin and elsewhere in the roundworm. The researchers found evidence that dendrite branching ensues when this two-protein complex is sensed by DMA-1, a receptor molecule found on growing sensory dendrites.
"A fair amount was already known about factors within sensory neurons that regulate dendrite branching," said Dr. Buelow. "But until now, we knew next to nothing about external cues that pattern the sensory dendrites crucial to the functioning of any of our five senses. Hopefully, our success in finding two skin-derived cues that orchestrate dendrite branching will help in identifying cues involved in other sensory organs and possibly in the brain. Finding such cues could conceivably lead to therapies for replacing dendrite arbors depleted by injury or disease."
Phase 1 ALS trial is first to test antisense treatment of neurodegenerative disease
The initial clinical trial of a novel approach to treating amyotrophic lateral sclerosis (ALS) – blocking production of a mutant protein that causes an inherited form of the progressive neurodegenerative disease – may be a first step towards a new era in the treatment of such disorders. Investigators from Massachusetts General Hospital (MGH) and Washington University School of Medicine report that infusion of an antisense oligonucleotide against SOD1, the first gene to be associated with familial ALS, had no serious adverse effects and the drug was successfully distributed thoughout the central nervous system.
"This therapy directly targets the cause of this form of ALS – a mutation in SOD1, which was originally discovered here at the MGH by my mentor Robert Brown," says Merit Cudkowicz, MD, chief of Neurology at MGH and senior author of the report in Lancet Neurology, which has been released online. “It’s very exciting that we have reached a stage when we can start clinical trials against this type of ALS.”
ALS causes the death of motor neurons in the brain and spinal cord, stopping transmission of neural signals to nerve fibers and leading to weakness, paralysis and usually death from respiratory failure. Only 10 percent of ALS cases are inherited, and mutations in SOD1 – which produce an aberrant, toxic form of the protein – account for about 20 percent of familial cases. Although that first SOD1 mutation was identified 20 years ago by the team lead by Brown – who is now professor and chief of Neurology at the University of Massachusetts Medical School – a technology that directly addresses such mutations became available only recently.
The current study, the first author of which is Timothy Miller, MD, PhD, of Washington University, used what are called antisense oligonucleotides – small, single-stranded DNA or RNA molecules that prevent production of a protein by binding to its messenger RNA. While antisense medications have been tested against several types of disease, this was the first trial in a neurological disorder, making the assurance of safety – a primary goal of a phase 1 study – particular important. Studies in animal models led by Miller and others found that the experimental antisense drug used in this trial reduced expression of mutated and nonmutated SOD1 and slowed the progression of ALS.
Conducted at the MGH, Washington University, Johns Hopkins University and the Methodist Neurological Institute in Houston, the trial enrolled a total of 21 patients with SOD1 familial ALS. Four sequential groups of participants received spinal infusions over an 11-hour period of the antisense drug or a placebo, with the active drug being administered at one of four dosage levels. Since participants in one group were free to join a subsequent group more than 60 days later, seven received two infusions and two received a total of three.
Some of the participants reported the type of adverse effects typically associated with spinal infusions – headache and back pain – with no difference between the active drug and placebo groups. Participants who receive subsequent infusions reported fewer adverse effects. Cerebrospinal fluid samples taken immediately after infusion revealed the presence of the antisense oligonucleotidein all participants receiving the drug at levels close to what was predicted based on animal studies. Analysis of spinal cord samples from one participant who had later died from ALS found drug levels highest at the site of the infusion and lowest at the furthest point and suggested that prior estimates of how long the drug would persist in the spinal cord were accurate.
Cudkowicz notes that the next step will be a larger study to address long-term safety and take a first look at the effectiveness of antisense treatment against ALS “This is a very important step forward for neurodegenerative disorders in general,” she explains. “There are other ALS gene mutations that antisense technology may be useful against. There also is an ongoing study of a different oligonucleotide against spinal muscular atrophy, and ongoing preclinical studies in Huntington’s disease, myotonic dystrophy and other neurological disorders are in development.
"The first person with ALS that I cared for had SOD1 ALS," she adds, "and I promised her a commitment to finding a treatment for this form of the disease. It’s so gratifying to finally be at the stage of knowledge where we can start testing this treatment in patients with SOD1 ALS. We also hope that this treatment may apply to the broader population of patient with sporadic ALS." Cudkowicz is the Julieanne Dorn Professor of Neurology at Harvard Medical School.
(Source: massgeneral.org)
Researchers discover primary role of the olivocochlear efferent system
New research from the Massachusetts Eye and Ear, Harvard Medical School and Harvard Program in Speech and Hearing Bioscience and Technology may have discovered a key piece in the puzzle of how hearing works by identifying the role of the olivocochlear efferent system in protecting ears from hearing loss. The findings could eventually lead to screening tests to determine who is most susceptible to hearing loss. Their paper is published today in the Journal of Neuroscience.
Until recently, it was common knowledge that exposure to a noisy environment (concert, iPod, mechanical tools, firearm, etc.), could lead to permanent or temporary hearing loss. Most audiologists would assess the damage caused by this type of exposure by measuring hearing thresholds, the lowest level at which one starts to detect/sense a sound at a particular frequency (pitch). Drs. Sharon Kujawa and Charles Liberman, both researchers at Mass. Eye and Ear, showed in 2009 that noise exposures leading to a temporary hearing loss in mice (when hearing thresholds return to what they were before exposure) in fact can be associated with cochlear neuropathy, a situation in which, despite having a normal threshold, a portion of auditory nerve fibers is missing).
The inner ear, the organ that converts sounds into messages that will be conveyed to and decoded by the brain, receives in turn fibers from the central nervous system. Those fibers are known as the olivocochlear efferent system. Up to now, the involvement of this efferent system in the protection from acoustic injury – although clearly demonstrated – has been a matter of debate because all the previous experiments were probing its protective effects following noise exposures very unlikely to be found in nature.
Stephane Maison, Ph.D., investigator at the Eaton-Peabody Laboratory at Mass. Eye and Ear and lead author, explains. “Humans are currently exposed to the type of noise used in those experiments but it’s hard to conceive that some vertebrates, thousands of years ago, were submitted to stimuli similar to those delivered by speakers. So many researchers believed that the protective effects of the efferent system were an epiphenomenon – not its true function.”
Instead of using loud noise exposures evoking a change in hearing threshold, we used a moderate noise exposure at a level similar to those found in restaurants, conferences, malls, and also in nature (some frogs emit vocalizations at similar or higher levels) and instead of looking at thresholds, we looked for signs of cochlear neuropathy, Dr. Maison continued.
The researchers demonstrated that such moderate exposure lead to cochlear neuropathy (loss of auditory nerve fibers), which causes difficulty to hear in noisy environments.
"This is tremendously important because all of us are submitted to such acoustic environments and it takes a lot of auditory nerve fiber loss before it gets to be detected by simply measuring thresholds as it’s done when preforming an audiogram," Dr. Maison said. "The second important discovery is that, in mice where the efferent system has been surgically removed, cochlear neuropathy is tremendously exacerbated. That second piece proves that the efferent system does play a very important role in protecting the ear from cochlear neuropathy and we may have found its main function."
The researchers say they are excited about this discovery because the strength of the efferent system can be recorded non-invasively in humans and a non-invasive assay to record the efferent system strength has already been developed and shows that one is able to predict vulnerability to acoustic injury (Maison and Liberman, Predicting vulnerability to acoustic injury with a noninvasive assay of olivocochlear reflex strength, Journal of Neuroscience, 20:4701-4707, 2000).
"One could envision applying this assay or a modified version of it to human populations to screen for individuals most at risk in noise environments," Dr. Maison concluded.
(Source: eurekalert.org)
Researchers Link Gulf War Illness to Physical Changes in Brain Fibers that Process Pain
Researchers at Georgetown University Medical Center (GUMC) have found what they say is evidence that veterans who suffer from “Gulf War Illness” have physical changes in their brains not seen in unaffected individuals. Brain scans of 31 veterans with the illness, compared to 20 control subjects, revealed anomalies in the bundles of nerve fibers that connect brain areas involved in the processing and perception of pain and fatigue.
The discovery, published online March 20 in PLOS ONE, could provide insight into the mysterious medical symptoms reported by more than one-fourth of the 697,000 veterans deployed to the 1990-1991 Persian Gulf War, the researchers say. These symptoms, termed Gulf War Illness, range from mild to debilitating and can include widespread pain, fatigue, and headache, as well as cognitive and gastrointestinal dysfunctions.
Although these veterans were exposed to nerve agents, pesticides and herbicides, among other toxic chemicals, no one has definitively linked any single exposure or underlying mechanism to Gulf War Illness according to the scientists.
This is the first study to show veterans, compared to unaffected subjects, have significant axonal damage. Bundles of axons, which form the brain white matter, are akin to telephone wires that carry nerve impulses between different parts of the gray matter in the brain. The researchers found that damage to the right inferior fronto-occipital fasciculus was significantly correlated with the severity of pain, fatigue, and tenderness.
“This tract of axons links cortical gray matter regions involved in fatigue, pain, emotional and reward processing. This bundle also supports activity in the ventral attention network, which searches for unexpected signals in the surrounding environment that may be inappropriately interpreted as causing pain or being dangerous. Altered function in this tract may explain the increased vigilance and distractibility observed in veterans.” says lead author Rakib Rayhan, MS, a researcher in the lab of the study’s senior investigator, James Baraniuk, MD, a professor of medicine at GUMC.
In this Department of Defense-funded study, the research team used a form of functional magnetic resonance imaging (fMRI) called diffusion tensor imaging. This imaging method examines patterns of water diffusion in the brain to look for changes in the integrity of white matter, which is not seen on regular MRI scans. “This provides a completely new perspective on Gulf War Illness,” says Baraniuk. “While we can’t exactly tell how this tract is affected at the molecular level — the scans tell us these axons are not working in a normal fashion.”
Although preliminary, “the changes appear distinct from multiple sclerosis, major depression, Alzheimer’s disease and other neurodegenerative diseases,” says Rayhan. “These novel findings are really exciting because they provide validation for many veterans who have long said that no one believes them.”
The results must be replicated, say its authors, but for the first time a potential biomarker for Gulf War Illness may be on the horizon as well as a possible target for therapy aimed at regenerating these neurons.
“Pain and fatigue are perceptions, just like other sensory input, and Gulf War Illness could be due to extensive damage to the structures that facilitate them,” says Rayhan. “Some of the veterans we studied feel pain when doing something as simple as putting on a shirt. Now we have something to tell them about why their lives have been so greatly affected.”
(Source: explore.georgetown.edu)
Finding challenges accepted view of MS: Unexpectedly, damaged nerve fibers survive
Multiple sclerosis, a brain disease that affects over 400,000 Americans, causes movement difficulties and many neurologic symptoms. MS has two key elements: The nerves that direct muscular movement lose their electrical insulation (the myelin sheath) and cannot transmit signals as effectively. And many of the long nerve fibers, called axons, degenerate.
Many scientists believe that axons are doomed once they lose the insulation, but a new study by graduate student Chelsey Smith and former undergraduate Elizabeth Cooksey in the Journal of Neuroscience shows axons can survive for long periods in rats even after losing myelin.
"This was the first study to demonstrate long-term axon survival after myelin deterioration," says senior author Ian Duncan, a professor in the School of Veterinary Medicine at the University of Wisconsin-Madison.
The mutant rats in the experiment have substantial myelin at first, but by eight weeks the essential myelin insulation is lost. “It was surprising,” says Duncan, an expert in MS pathology. “Nine months is a relatively long period in a rat’s lifetime, and there wasn’t a loss of axons, so the assumption that axons must automatically die without myelin seems incorrect.”
Researcher uncovers potential cause, biomarker for autism and proposes study to investigate theory
A New York-based physician-researcher from Touro College of Osteopathic Medicine, best known for his research into fertility and twinning, has uncovered a potential connection between autism and a specific growth protein that could eventually be used as a way to predict an infant’s propensity to later develop the disease. The protein, called insulin-like growth factor (IGF), is especially involved in the normal growth and development of babies’ brain cells. Based on findings of prior published studies, Touro researcher Gary Steinman, MD, PhD, proposes that depressed levels of this protein in the blood of newborns could potentially serve as a biomarker for the later development of autism. However, this connection, described below in greater detail, has never been directly studied. Steinman presents his exciting theory in the journal Medical Hypotheses.
IGF stimulates special cells in the brain to provide an essential insulating material, called myelin, around the developing nerves that is needed to efficiently transmit important messages about everything the brain controls — from physical functions such as movement to mental functions such as sensory perception, thinking and emotions. In the developing fetal and pediatric brain, myelin is also important for nerve fibers in one area of the brain to form proper pathways to other regions, allowing the body to hone functions over time. Insufficient IGF results in insufficient insulating material, as has been seen in brain biopsies of autistic individuals, and may impede proper pathway development. Steinman is proposing that this potential relationship between neonatal IGF levels and autism be directly studied.
"Autism is on the rise, especially in the last two decades — either because of environmental factors, expanded diagnostic criteria, or both. Yet almost nothing is currently known about the predisposing molecular and histological changes that differentiate a newborn destined to be neurologically normal from an autistic one," said Steinman.
Because no effective treatment or prevention for autism exists, research examining Steinman’s idea is critical, as it may hold the key to understanding the cause of this often devastating illness. In his article, Steinman proposes a study to investigate this hypothesis, and if this study supports his theory that identification of reduced IGF at birth is later followed by the appearance of autistic characteristics, then the subsequent development of a simple biomarker blood test is equally critical.