But findings that appeared in the publication Nature indicate that the belief may be more than a myth. The study, which used mice as models, was funded in part by the National Institutes of Health’s National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and other NIH components.

Hair color is determined by cells called melanocytes, which produce the pigment melanin. New melanocytes are made from melanocyte stem cells that live within the hair follicle at the base of the hair strand. As we age, these stem cells gradually disappear. The hair that regrows from hair follicles that have lost melanocyte stem cells has less pigment and appears gray.

A research team, led by Dr. Ya-Chieh Hsu of Harvard University, used mice to examine stress and hair graying. The mice were exposed to three types of stress involving mild, short-term pain, psychological stress, and restricted movement. All caused noticeable loss of melanocyte stem cells and hair graying.

Having established a link between stress and graying, the scientists then explored several potential causes, including the role of the stress hormone corticosterone, but altering its levels didn’t affect stress-related graying.

The researchers eventually turned to the neurotransmitter noradrenaline, which, along with corticosterone, was elevated in the stressed mice. They found that noradrenaline, also known as norepinephrine, was key to stress-induced hair graying. By injecting noradrenaline under the skin of unstressed mice, the researchers were able to cause melanocyte stem cell loss and hair graying.

Noradrenaline is produced mostly by the adrenal glands. However, mice without adrenal glands still showed stress-related graying. Noradrenaline is also the main neurotransmitter of the sympathetic nervous system, which is responsible for the “fight-or-flight” reaction in response to stress.

Discoveries from such studies could ultimately lead to new treatments for stress.

Ultimately, the team discovered that signaling from the sympathetic nervous system plays a critical role in stress-induced graying. Sympathetic nerves extend into each hair follicle and release noradrenaline in response to stress. Normally, the melanocyte stem cells in the follicle are dormant until a new hair is grown. Noradrenaline causes the stem cells to activate.

Using fluorescent labelling, the researchers observed the stem cells change to melanocytes and migrate away from their reserve in the hair follicle. With no remaining stem cells, no new pigment cells can be made, and any new hair becomes gray, then white.

“When we started to study this, I expected that stress was bad for the body — but the detrimental impact of stress that we discovered was beyond what I imagined,” Hsu says. “After just a few days, all of the melanocyte stem cells were lost. Once they’re gone, you can’t regenerate pigments anymore. The damage is permanent.”

The authors highlight the need to further study the interactions between the nervous system and stem cells in different tissues and organs. A news release from the NIH said that the knowledge gained in this work will be useful in future investigations into the impact of stress on the body and the development of new interventions.

Research has suggested that high salt intake may also be a risk factor for declining brain function with age. However, the mechanisms responsible for this link aren’t understood.

Earlier studies suggested that high levels of salt in the diet can cause immune changes in the gut that lead to reduced blood flow in the brain and impaired cognition. In previous work, a team led by Dr. Costantino Iadecola at Weill Cornell Medicine found that mice fed a high-salt diet had reduced functioning of an enzyme called eNOS, which produces nitric oxide (NO).

NO helps direct blood vessels to relax, thereby increasing blood flow. Mice with a reduction in NO from the high-salt diet had reduced blood flow to the brain. These mice had trouble performing a standard set of cognitive tasks.

But the researchers suspected that the amount of reduced blood flow seen in these experiments wasn’t enough to directly affect cognition. In their new study, they explored how changes in the brain caused by a high-salt diet—and the resulting lowered NO production—might affect thinking and memory.

The team fed mice a very high-salt diet for 12 to 36 weeks. The mice underwent tests of cognitive function, and their brains were examined for molecular changes.

The work was funded in part by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health (NIH). Results were published on October 23, 2019, in Nature.

Mice fed a high-salt diet had trouble recognizing novel objects and navigating through a maze.

The researchers found that high levels of dietary salt caused a chemical change to a protein called tau. This change—phosphorylation—can cause tau to clump together in the brain. Clumps of tau are linked with some dementias, such as Alzheimer’s disease.

As in their previous study, the team found that mice fed the high-salt diet had trouble recognizing novel objects and navigating through a maze. Mice with more phosphorylated tau in their brains had lower performance on these cognitive tasks.

When the mice were fed a high-salt diet supplemented with a compound that boosts NO production, they were protected against the accumulation of phosphorylated tau.

To confirm the link between salt intake, tau, and cognitive decline, the researchers fed the high-salt diet to mice that lacked tau. Those mice were protected from cognitive decline on the high-salt diet, even though they had reduced blood flow to the brain. Similar results were seen when tau was blocked in normal mice.

Further molecular studies showed that the effects of high salt on tau phosphorylation were mediated through NO levels, not through changes in blood flow.

“The take-home message here is that is that while there is a reduction in blood flow to the brains of mice that eat a high-salt diet, it really is tau that is causing the loss in cognitive abilities. The effect of reduced flow really is inconsequential in this setting,” Iadecola says.

The amount of salt fed to the mice was 8 to 16 times higher than that found in normal mouse chow. Most people wouldn’t approach such a high level in their diet. But the findings reveal a mechanism that might link high salt intake with reduced brain functioning. The results suggest that therapies targeting blood flow to the brain may not be enough to counter cognitive decline.

Cancer tumors have the ability to break off from their primary site and spread from their primary organ to other sites of the body via the bloodstream and lymphatic system.  The spreading of cancer, known as “metastasis,” is the leading cause of cancer-related death.  Although there are currently blood tests designed to detect cancer cells in the blood, known as circulating tumor cells, many times they cannot pick up minimal cancer cells released early on.  If these current tests return as positive, this frequently means that there is a high level of cancerous cells in the blood that have spread to other organs.

However, the diagnosis and treatment of these cancer cells in the blood may soon change.  A recent study published in Science Translation Medicine showed that researchers have devised a laser that can detect these malignant cells and zap them from outside of the body.  The current standard methods of detection have limited sensitivity for picking up minimal cells at early stages of the disease, therefore possibly missing an opportunity to eliminate them at a treatable point in the illness.   A team led by biomedical engineer Vladimir Zharov, director of nanomedicine at the University of Arkansas for Medical Sciences, has developed a method in hopes of changing that modality.

Researchers have devised a laser that can detect malignant cells and “zap” them from outside the body.

In studies with melanoma, they have coupled a laser with an ultrasound detector to create a ‘Cytophone,’ a device that identifies cells acoustically.  To break it down, a laser is first shined on the surface of a person’s skin, penetrating right into some of the near-surface blood vessels.  The passing melanoma cells will then ‘heat up’ because of their darker pigment and create a small ‘acoustic wave’ that then gets picked up by the ultrasound detector.   Melanoma cells absorb more of the energy from the laser because of their dark pigment, allowing them to heat up quickly and expand.

This method can pick up a single circulating tumor cell per liter of blood, which makes this up to approximately 1,000 times more sensitive than other available methods of detection that typically examine only about 7- 8 milliliters of a sample of blood.  Additionally, the cytophone was able to detect small clots of blood.

Researchers have tested this on 28 patients with melanoma and 19 healthy volunteers.  Researchers were able to discover that within as little as 10 seconds and as long as 1 hour, the cytophone was able to detect circulating tumor cells in 27 of the 28 patients.  It also did not return any false positives on the healthy volunteers.  Moreover, it was found that when the energy level of the laser was turned up (still to a safe intensity) that the amount of circulating tumor cells came down over the hour, without causing any side effects.

They have tested this on 28 patients with melanoma and 19 healthy volunteers.  Researchers found that within as little as 10 seconds and as long as 1 hour, the cytophone was able to detect circulating tumor cells in 27 of the 28 patients.  It also did not return any false positives on the healthy volunteers.  Moreover, it was found that when the energy level of the laser was turned up (still to a safe intensity) that the amount of circulating tumor cells came down over the hour, without causing any side effects.

Even though this has been tested recently in melanoma, and the dark pigment of melanin plays a role in its detection, Zharov and his colleagues are currently working to develop methods of “tagging” other cancer cells with small nanoparticles to be able to ‘heat up’ and be distinguished from the normal cells.

Movies aside, the future holds promise in the new hope of using lasers to fight off the evil invasions of metastasis.

The results were published in the journal Nature Communications.

“The findings underscore the complexity of color perception. Far from operating as a reflex, color perception involves a set of sophisticated brain operations that ultimately assign value and meaning to what we see,” said the study’s lead investigator, Bevil Conway, Ph.D., head of the NEI Unit on Sensation, Cognition, and Action.

The findings also suggest that social communication cues from faces factored into evolutionary selective pressures that gave rise to trichromatic color vision in our ancestors 23 million years ago.

The study grew out of a curiosity observed in Conway’s lab by graduate students Maryam Hasantash and Rosa Lafer-Sousa. They noticed that under a low-pressure sodium (LPS) lamp, which makes everything appear monochromatic, like a black and white movie with a brownish-yellow filter, everyone looked sick.

Investigating the phenomenon in a controlled setting, 20 people were each presented with 35 visual stimuli under an LPS lamp and again under white light. Visual stimuli included objects that have a characteristic color (oranges, strawberries, tomatoes), objects with arbitrary color (Legos, toy cars), and in-person actors representing a diversity of skin colors. After each item or person was presented, each study participant made a color match using a computer monitor to indicate the color of the stimulus they had just viewed.

As expected, under the white light, people matched oranges to orange, strawberries and tomatoes to reds, and faces and hands to some variation of brown or tannish pink.

Under LPS lighting, all stimuli except faces appeared brownish yellow. By contrast, every single participant matched 100 percent of the actors’ faces to greenish hues. Skin on the hand, neck and forehead, visible through cutouts in a mask, appeared brownish yellow, not green, to participants. Photographs of faces under LPS lighting were also matched to greens, but to a lesser extent. Face photographs in which the features had been scrambled were not matched with green at all.

The hypothesis was that study participants’ memory-based assumptions about color — oranges are orange, strawberries are red — would subtly influence color selection under LPS lighting, with arbitrarily colored objects such as Legos serving as the control.

“Surprisingly, we found no clear evidence of the impact of memory on the color appearance of toys, fruit or non-facial body skin. Meanwhile, significant evidence showed a paradoxical impact of memory on face color since under most circumstances, no one expects a face to be green,” Conway said.

What’s more, the perceived greenish hue of faces under LPS light deviates from what might be expected based on the spectrum of the LPS light itself, which gives a yellowish appearance. In other words, the color people were seeing could not be attributed to the light hitting the eye, but to unconscious inferences about the proper color of faces.

One theory is that in the context of in-person actors’ faces, the LPS lighting created a kind of optical illusion. The eeriness of the lamp’s glow triggered an error signal in the visual system. The theory follows that the illusion occurred because our brains are wired to try to understand what we see by factoring context into our perception. In the context of faces under LPS light, things looked so strange, the brain conjured up an explanation: the actor must be sick, according to the researchers.

“The specificity of this error signal to faces tells us that the brain has special wiring for face color,” Conway said.

Taken together, the findings suggest that human assessment of face color is an essential operation that is inherent in the human visual system. Moreover, the face-color memory effects uncovered in the study appear to be encoded by the L and M cones, the photoreceptors that make trichromatic color vision possible.

Prior work suggests that face processing and color processing are handled by largely separate brain circuits. The present study makes the surprising prediction that face processing and color processing engage some similar brain mechanisms, which provides key information about the high-level operations deep in the cerebral cortex that determine how vision works.

The study was funded by the NEI Intramural Research Program.

The experimental vaccine, known as H1ssF_3928, was developed by scientists at the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH). In the clinical trial, the scientists will examine the vaccine’s safety and tolerability as well as its ability to induce an immune response in healthy study volunteers.

According to the NIH, H1ssF_3928 is designed to teach the body to make protective immune responses against diverse influenza subtypes by focusing the immune system on a portion of the virus that varies relatively little from strain to strain. The vaccine candidate was developed as part of a broader research agenda to create a so-called “universal” influenza vaccine that can provide long-lasting protection for all age groups from multiple influenza subtypes, including some that might cause a pandemic.

“Seasonal influenza is a perpetual public health challenge, and we continually face the possibility of an influenza pandemic resulting from the emergence and spread of novel influenza viruses,” said NIAID Director Anthony S. Fauci, M.D. “This Phase 1 clinical trial is a step forward in our efforts to develop a durable and broadly protective universal influenza vaccine.”

The clinical trial is being conducted at the NIH Clinical Center in Bethesda, Maryland. It is being led by Grace Chen, M.D., of NIAID’s Vaccine Research Center (VRC) Clinical Trials Program.

The study subjects will not be exposed to any influenza virus.

The trial will gradually enroll at least 53 healthy adults aged 18 to 70 years. The first five participants will be aged 18 to 40 years and will receive a single 20-microgram (mcg) intramuscular injection of the experimental vaccine. The remaining 48 participants will receive two 60-mcg vaccinations spaced 16 weeks apart. They will be stratified by age into four groups of 12 people each: 18 to 40 years, 41 to 49 years, 50 to 59 years, and 60 to 70 years. Investigators hope to understand how participants’ immune responses to the experimental vaccine may vary based on age and the likelihood of their previous exposure to different influenza variants.

Study participants will be asked to record their temperature and any symptoms on a diary card for one week after each injection. They also will be asked to visit the clinic to provide blood samples at specific times. Investigators will test the samples in the laboratory to characterize and measure levels of anti-influenza antibodies, which are potentially indicative of immunity against influenza. Participants will return for nine to 11 follow-up visits over 12 to 15 months. They will not be exposed to any influenza virus as part of the clinical trial.

“This Phase 1 clinical trial is the culmination of years of research and development made possible by the unique collaborative setting that the VRC offers by bringing together top scientists, manufacturing expertise, and an outstanding clinical team,” said VRC Director John Mascola, M.D.

The VRC expects the clinical trial to complete enrollment by the end of 2019 and hopes to begin reporting results in early 2020. For more information about the trial, click here to visit the government’s clinical trials site and use the search identifier NCT03814720.

When new medicines are developed, they have to go and started feeling better within days, even knowing that they weren’t actual medicine, through rigorous testing processes. Scientists need to know if the new drug works, so they treat one half of the study participants with the drug and a placebo to the rest of the subjects. Placebos are basically sugar pills—there’s nothing to the “medicine” patients are taking, but they don’t know that.

There’s an interesting twist to placebos, something that is only recently being studied. Very often, patients respond to placebo treatment—even though there isn’t a pharmaceutical reason for it. This “placebo effect” doesn’t mean that new drugs aren’t effective or that people are faking illness. Instead, the interaction between brain and body is hugely complex and still not fully understood.

In a 2016 CBS News segment, Ted Kaptchuk, a professor at Harvard Medical School, explained, “Placebo effect is everything that surrounds that pill — the interaction between patient, doctor or nurse. It’s the symbols, it’s the rituals. These are powerful forces.”

When we feel like we are doing something about pain or illness, our body responds. That includes making a doctor appointment or taking a pill. And these effects can be seen on brain scans.

The interaction between brain and body is hugely complex and is still not fully understood.

Placebos seem to be most effective on medical conditions where we don’t have a lot of good treatment options. Think of chronic pain or irritable bowel syndrome. “Any symptom the brain can modulate itself” is where the placebo effect can be seen, says Kaptchuk. Illnesses such as cancer aren’t open to the effect because it doesn’t involve the brain, but cancer-related depression qualifies.

The Program in Placebo Studies and Therapeutic Encounter (PiPS) is run through Harvard University and Beth Israel Deaconess Medical Center in Boston. This is where current research on placebos is centered. There’s a molecule, called COMT, that seems to be involved, though the scientists don’t fully understand yet what its role is.

Writer Robert Anthony Siegel worked with PiPS deputy director John Kelley to see how he’d react to a placebo. His goal for the non-drug pill? “Getting rid of my chronic writer’s block and the panic attacks and insomnia that have always come along with it,” Siegel writes in Smithsonian.

Siegel and Kelley worked together to design a pill and dosage instructions, then had a lab create them.  For the first two weeks, Siegel actually felt like his anxiety increased. But then something shifted—he was writing and not erasing. The treatment was “working.”

The good news for those suffering who haven’t been able to find treatment, is that placebos may be a new avenue to pursue. BMJ, a medical journal, recently published results from several Kaptchuk trials. “Placebo treatments in randomized controlled trials produce significant improvement in many subjective symptoms,” Kaptchuk wrote in the journal.

Your general practitioner might not be comfortable prescribing a placebo quite yet, but the body of evidence continues to grow. It might be time to start a conversation about how a capsule each day can improve your quality of life – even if it is made of starch or sugar.

Sepsis is one of the leading causes of death in intensive care units and, with an estimated price tag of $20 billion in 2011, the most expensive condition that hospitals treat.

Researchers at the Medical University of South Carolina (MUSC) found that sepsis outcomes in a preclinical model significantly improved when a nanocarrier, a type of molecule, was delivered to a microRNA (miRNA), specifically miR-126, which is known to protect against sepsis.

“The exciting part is that we can use nanoparticles as a delivery system to carry microRNAs. It’s feasible–we can do this,” said Hongkuan Fan, Ph.D., senior author of the article and an assistant professor in the Department of Pathology and Laboratory Medicine at MUSC who studies vascular dysfunction in sepsis.

Sepsis is an overreaction of the body’s immune system to an infection. Chemicals called cytokines flood the bloodstream in an attempt to fight the infection but also cause blood vessels to become leaky. White blood cells escape from the vessels, causing inflammation and damage to surrounding tissue, ultimately leading to multi-organ failure and death.

“Something is working, and that is exciting in a condition as severe and complicated as sepsis.”

The MUSC researchers showed that a proprietary nanocarrier (DEAC-pGlcNAc; Marine Polymer Technologies [Burlington, MA]) deliver miR-126 effectively in a mouse model of sepsis, protecting it against damage. The researchers were also able to verify that the nanoparticle successfully delivered miR-126 into the cell’s nucleus by tagging it with a fluorescent dye. (Click here to read more from thirdAGE about sepsis research.)

“We could actually see them together through the microscope,” says Joy N. Jones Buie, Ph.D., MSCR, a postdoctoral fellow at MUSC and the first author on the article. “That showed that the micro-RNA was actually getting into the cell and associating with the cell’s nucleus.”

The mIR-126/nanocarrier complex more than doubled the proportion of mice alive at seven days vs. untreated mice in a preclinical model of sepsis (almost 67 percent vs. 25 percent). The nanoparticle, which has antibacterial properties, improved survival even when not complexed with miR-126, though not to a significant degree.

“Based on this and our previous studies, we know that targeted delivery of miR-126 has some therapeutic effect in a preclinical model of sepsis,” says Fan. “Something is working, and that is exciting in a condition as severe and complicated as sepsis. We think that miR-126 has a promising future and will continue to explore it as well as the use of nanocarriers and other vehicles for its delivery.”

The findings were reported in the journal Inflammation.

“Coffee consumption does seem to have some correlation to a decreased risk of developing Alzheimer’s disease and Parkinson’s disease,” said Dr. Donald Weaver, co-director of the Krembil Brain Institute, in Toronto. “But we wanted to investigate why that is — which compounds are involved and how they may impact age-related cognitive decline.”

A compound found in coffee inhibits proteins associated with Alzheimer’s and Parkinson’s.

Weaver enlisted Dr. Ross Mancini, a research fellow in medicinal chemistry, and Yanfei Wang, a biologist, to help. The team chose to investigate three different types of coffee – light roast, dark roast, and decaffeinated dark roast. Mancini then identified a group of compounds known as phenylindanes, which emerge as a result of the roasting.

“The caffeinated and de-caffeinated dark roast both had identical potencies in our initial experimental tests,” said Mancini. “So we observed early on that [the] protective effect could not be due to caffeine.” Phenylindanes are the only compound investigated in the study that inhibit beta amyloid and tau from clumping. These two protein fragments are common in both Alzheimer’s and Parkinson’s. “So phenylindanes are a dual-inhibitor,” Weaver said. “Very interesting. We were not expecting that.”

Because roasting leads to higher quantities of phenylindanes, dark roasted coffee appears to be more protective than light roasted coffee.

“It’s the first time anybody’s investigated how phenylindanes interact with the proteins that are responsible for Alzheimer’s and Parkinson’s,” Mancini said. “The next step would be to investigate how beneficial these compounds are, and whether they have the ability to enter the bloodstream or cross the blood-brain barrier.” Much more research is needed, he said.

But, he admits, there is much more research needed before the team’s discovery can, or would be, recognized as a treatment.

“What this study does is [try]to demonstrate that there are indeed components within coffee that are beneficial to warding off cognitive decline. It’s interesting, but are we suggesting that coffee is a cure? Absolutely not.”

Reducing blood pressure is usually a good thing, but doctors have been concerned about intensive blood pressure lowering during hypertension therapy and the accompanying elevations of the molecule creatinine. Until the most recent research they worried that the creatinine elevations might be an indicator of kidney disease.

Signs of kidney disease may have been misleading for some patients.

Now, though, a study published in the Annals of Internal Medicine says that the elevations are more likely to reflect a benign reduction in kidney blood flow that occurs naturally during the intensive blood pressure lowering treatment.

The findings represent a major advancement in the understanding of whether kidney tissue damage accompanies the diagnosis of chronic kidney disease (CKD) during hypertension therapy.

The study was conducted by researchers from the University of California San Diego and the University of California San Diego.

The most recent discovery was made in a study funded by the National Institutes of Health and published in Science Translation Medicine. The scientists used mice to show how the gene may play an essential role in the nervous system’s reaction to injury and inflammation, making PIEZO2 a target for developing precise treatments for relieving pain caused by cuts, burns, and other skin injuries.

“For years scientists have been trying to solve the mystery of how gentle touch becomes painful. These results suggest PIEZO2 is the gene for tactile allodynia. We hope that these results will help researchers develop better treatments for managing this form of pain,” said Alexander T. Chesler, Ph.D., a Stadtman Investigator at the National Center for Complementary and Integrative Health (NCCIH) and a senior author of one of the studies.

The PIEZO2 gene encodes what scientists call a mechanosensitive protein; that, in turn, produces electrical nerve signals in response to changes in cell shape, such as when skin cells and neurons of the hand are pressed against a table. Since its discovery in mice by a team led by Ardem Patapoutian, Ph.D., Scripps Research, La Jolla, CA, the lead author of the second paper, scientists have proposed that PIEZO2 plays an important role in touch and pain in humans.

In 2016, Chesler’s team worked with the group of Carsten G. Bönnemann, M.D., senior investigator at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), to show that two patients who had mutations in PIEZO2 that eliminated its activity lacked proprioception, or a sixth sense of how our bodies are positioned in space. They were also unable to feel vibrations and were less sensitive to certain forms of gentle touch.

In this new study, . Chesler and Bönnemann worked with pain expert Catherine Bushnell, Ph.D., at NCCIH, to examine four patients at the NIH’s Clinical Center, They found that PIEZO2 controls tactile allodynia after a skin injury. To test for allodynia the researchers had participants sit at a table facing a barrier that blocked their view of their arms. The researchers then dabbed two creams onto a participant’s arm. One was a placebo, which had no effect, and the other contained capsaicin, the ingredient that makes chili peppers hot and causes inflammation, as seen with sunburns.

The researchers found stark differences between how the capsaicin affected control participants and ones with mutations in PIEZO2. Swiping a cotton swab around the capsaicin patch consistently caused control participants to feel pain, which allowed each one to correctly identify where the inflammation was even though they could not see their arms. In contrast, the participants with the PIEZO2 mutation felt no difference between the areas where capsaicin and placebo had been applied.

“What’s remarkable about the PIEZO2-deficient participants is the ‘clarity’ of their conditions. With their help we’re getting fundamental new insights about how the loss of PIEZO2 affects them specifically and learning what PIEZO2 is normally used for, which could be of immense medical importance to all other people,” said Bönnemann. “This type of PIEZO2-dependent pain makes it very hard to apply bandages to burns and wounds that are important for healing. Most pain treatments numb large areas of the body. Our results suggest that if we could shut down PIEZO2 in the area of a wound, we would hopefully relieve the pain and speed recovery.”

Further experiments in mice by Chesler and Dr. Patapoutian confirmed the results observed in patients. Deleting PIEZO2 eliminated gentle touch sensations in mice as well as those felt during inflammation and injury.

Although neither study shows exactly how inflammation causes pain, their results suggest that inflammation does not alter the ability of PIEZO2 to detect gentle touches. For instance,  Chesler’s group showed in control mice that inflammation had no major effect on how the PIEZO2-containing neurons fired in response to gentle brushing. Instead, their results support the Gate Theory, which states that inflammation causes gentle touches to feel painful because neurons in the brain or spinal cord reinterpret signals from the rest of the body.

“It appears that inflammation doesn’t change the ability of neurons in the skin to sense gentle touch but instead reroutes the information that’s sent throughout the rest of the nervous system,” said  Patapoutian. “We hope these results help pain researchers better understand the mechanisms behind tactile allodynia.”