Desert Farming Experiment Yields First Results
A project to “green” desert areas with an innovative mix of technologies—producing food, biofuel, clean water, energy, and salt—reached a milestone this week in the Gulf state of Qatar. A pilot plant built by the Sahara Forest Project (SFP) produced 75 kilograms of vegetables per square meter in three crops annually, comparable to commercial farms in Europe, while consuming only sunlight and seawater. The heart of the SFP concept is a specially designed greenhouse. At one end, salt water is trickled over a gridlike curtain so that the prevailing wind blows the resulting cool, moist air over the plants inside. This cooling effect allowed the Qatar facility to grow three crops per year, even in the scorching summer. At the other end of the greenhouse is a network of pipes with cold seawater running through them. Some of the moisture in the air condenses on the pipes and is collected, providing a source of fresh water.
One of the surprising side effects of such a seawater greenhouse, seen during early experiments, is that cool moist air leaking out of it encourages other plants to grow spontaneously outside. The Qatar plant took advantage of that effect to grow crops around the greenhouse, including barley and salad rocket (arugula), as well as useful desert plants. The pilot plant accentuated this exterior cooling with more “evaporative hedges” that reduced air temperatures by up to 10°C. “It was surprising how little encouragement the external crops needed,” says SFP chief Joakim Hauge.
The third key element of the SFP facility is a concentrated solar power plant. This uses mirrors in the shape of a parabolic trough to heat a fluid flowing through a pipe at its focus. The heated fluid then boils water, and the steam drives a turbine to generate power. Hence, the plant has electricity to run its control systems and pumps and can use any excess to desalinate water for irrigating the plants.
The Qatar plant has also experimented with other possibilities such as culturing heat-tolerant algae, growing salt-tolerant grasses for fodder or biofuel, and evaporating the concentrated saline the plant emits to produce salt.
The Qatar plant—which is supported by Qatari fertilizer companies Yara International and Qafco—is just 1 hectare in extent with 600 square meters of growing area in the greenhouse. The fact that this small greenhouse produced such good yields, Hauge says, suggests that a commercial plant—with possibly four crops a year—could do even better. SFP researchers estimate that a facility with 60 hectares of growing area under greenhouses could provide all the cucumbers, tomatoes, peppers, and egglants now imported into Qatar. The results “reveal the potential for enabling restorative growth and value creation in arid land,” Hauge says. “I personally think that it is very important that people promote and invest in these ideas. Protected agriculture (I call it “indoor food production”) is an important option for the desert areas, particularly in the Middle East,” says Richard Tutwiler, director of the Desert Development Center at the American University in Cairo. “The big question is economic feasibility. How much did it cost to produce 75 kg of cucumbers per square meter?”
SFP is now engaged in studies aimed at building a 20-hectare test facility near Aqaba in Jordan. “This will be a considerable scaling up from the 1 hectare in Qatar,” Hauge says, and big enough to demonstrate commercial operation.
Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.
How Exercise Beefs Up the Brain
New research explains how abstract benefits of exercise—from reversing depression to fighting cognitive decline—might arise from a group of key molecules.
While our muscles pump iron, our cells pump out something else: molecules that help maintain a healthy brain. But scientists have struggled to account for the well-known mental benefits of exercise, from counteracting depression and aging to fighting Alzheimer’s and Parkinson’s disease. Now, a research team may have finally found a molecular link between a workout and a healthy brain.
Much exercise research focuses on the parts of our body that do the heavy lifting. Muscle cells ramp up production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin, gets lopped off and released into the bloodstream, where it drives the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the villains.)
While studying the effects of FNDC5 in muscles, cellular biologist Bruce Spiegelman of Harvard Medical School in Boston happened upon some startling results: Mice that did not produce a so-called co-activator of FNDC5 production, known as PGC-1α, were hyperactive and had tiny holes in certain parts of their brains. Other studies showed that FNDC5 and PGC-1α are present in the brain, not just the muscles, and that both might play a role in the development of neurons.
Spiegelman and his colleagues suspected that FNDC5 (and the irisin created from it) was responsible for exercise-induced benefits to the brain—in particular, increased levels of a crucial protein called brain-derived neurotrophic factor (BDNF), which is essential for maintaining healthy neurons and creating new ones. These functions are crucial to staving off neurological diseases, including Alzheimer’s and Parkinson’s. And the link between exercise and BDNF is widely accepted. “The phenomenon has been established over the course of, easily, the last decade,” says neuroscientist Barbara Hempstead of Weill Cornell Medical College in New York City, who was not involved in the new work. “It’s just, we didn’t understand the mechanism.”
To sort out that mechanism, Spiegelman and his colleagues performed a series of experiments in living mice and cultured mouse brain cells. First, they put mice on a 30-day endurance training regimen. They didn’t have to coerce their subjects, because running is part of a mouse’s natural foraging behavior. “It’s harder to get them to lift weights,” Spiegelman notes. The mice with access to a running wheel ran the equivalent of a 5K every night.
Aside from physical differences between wheel-trained mice and sedentary ones—“they just look a little bit more like a couch potato,” says co-author Christiane Wrann, also of Harvard Medical School, of the latter’s plumper figures—the groups also showed neurological differences. The runners had more FNDC5 in their hippocampus, an area of the brain responsible for learning and memory.
Using mouse brain cells developing in a dish, the group next showed that increasing the levels of the co-activator PGC-1α boosts FNDC5 production, which in turn drives BDNF genes to produce more of the vital neuron-forming BDNF protein. They report these results online today in Cell Metabolism. Spiegelman says it was surprising to find that the molecular process in neurons mirrors what happens in muscles as we exercise. “What was weird is the same pathway is induced in the brain,” he says, “and as you know, with exercise, the brain does not move.”
So how is the brain getting the signal to make BDNF? Some have theorized that neural activity during exercise (as we coordinate our body movements, for example) accounts for changes in the brain. But it’s also possible that factors outside the brain, like those proteins secreted from muscle cells, are the driving force. To test whether irisin created elsewhere in the body can still drive BDNF production in the brain, the group injected a virus into the mouse’s bloodstream that causes the liver to produce and secrete elevated levels of irisin. They saw the same effect as in exercise: increased BDNF levels in the hippocampus. This suggests that irisin could be capable of passing the blood-brain barrier, or that it regulates some other (unknown) molecule that crosses into the brain, Spiegelman says.
Hempstead calls the findings “very exciting,” and believes this research finally begins to explain how exercise relates to BDNF and other so-called neurotrophins that keep the brain healthy. “I think it answers the question that most of us have posed in our own heads for many years.”
The effect of liver-produced irisin on the brain is a “pretty cool and somewhat surprising finding,” says Pontus Boström, a diabetes researcher at the Karolinska Institute in Sweden. But Boström, who was among the first scientists to identify irisin in muscle tissue, says the work doesn’t answer a fundamental question: How much of exercise’s BDNF-promoting effects come from irisin reaching the brain from muscle cells via the bloodstream, and how much are from irisin created in the brain?
Though the authors point out that other important regulator proteins likely play a role in driving BDNF and other brain-nourishing factors, they are focusing on the benefits of irisin and hope to develop an injectable form of FNDC5 as a potential treatment for neurological diseases and to improve brain health with aging.
Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.
New research suggests diet soda may do more harm than good
Diet soda drinkers have the same health issues as those who drink regular soda, according to a new report published Wednesday.
Purdue University researchers reviewed a dozen studies published in past five years that examined the relationship between consuming diet soda and health outcomes for the report, published as an opinion piece in the journal Trends in Endocrinology & Metabolism. They say they were “shocked” by the results.
“Honestly, I thought that diet soda would be marginally better compared to regular soda in terms of health,” said Susan Swithers, the report’s author and a behavioral neuroscientist and professor of psychological sciences. “But in reality it has a counterintuitive effect.”
Artificial sweeteners in diet soda fulfill a person’s craving for a sweet taste, without the calories. But that’s the problem, according to researchers. Think of it like crying wolf.
Fake sugar teases your body by pretending to give it real food. But when your body doesn’t get the things it expects to get, it becomes confused on how to respond.
“You’ve messed up the whole system, so when you consume real sugar, your body doesn’t know if it should try to process it because it’s been tricked by the fake sugar so many times,” says Swithers.
On a physiological level, this means when diet soda drinkers consume real sugar, the body doesn’t release the hormone that regulates blood sugar and blood pressure.
Diet soda drinkers also tend to pack on more pounds than those who don’t drink it, the report says.
“The taste of sweet does cause the release of insulin, which lowers blood sugar , and if carbohydrates are not consumed, it causes a drop in blood sugar, which triggers hunger and cravings for sugar,” says CNN diet and fitness expert Dr. Melina Jampolis.
The artificial sweeteners also dampen the “reward center” in your brain, which may lead you to indulge in more calorie-rich, sweet-tasting food, according to the report.
The American Beverage Association says the report was “an opinion piece, not a scientific study.
“Low-calorie sweeteners are some of the most studied and reviewed ingredients in the food supply today,” the association said in a statement. “They are safe and an effective tool in weight loss and weight management, according to decades of scientific research and regulatory agencies around the globe.”
Diet soda’s negative effects are not just linked to weight gain, however, the report says.
It found that diet soda drinkers who maintained a healthy weight range still had a significantly increased risk of the top three killers in the United States: diabetes, heart disease and stroke.
“We’ve gotten to a place where it is normal to drink diet soda because people have the false impression that it is healthier than indulging in a regular soda,” says Swithers. “But research is now very clear that we need to also be mindful of how much fake sugar they are consuming.”
There are five FDA-approved artificial sweeteners: acesulfame potassium (Sunett, Sweet One), aspartame (Equal, NutraSweet), neotame, saccharin (SugarTwin, Sweet’N Low), and sucralose (Splenda).
“Saccharin was one of the first commercially-available artificially sweeteners, and it’s actually a derivative of tar,” says Swithers.
Even natural sweeteners like Stevia, which has no calories and is 250 times sweeter than regular sugar, are still processed extracts of a natural plant and may have increased health risks.
“Just because something is natural does not always mean that it is safer,” says Jampolis.
There more studies and research that need to be done. But in the meantime, experts say: Limit consumption.
“No one is saying cut it out completely,” says Swithers. “But diet soda should be a treat or indulgence just like your favorite candy, not an everyday
NASA funds development of 3D printer to make food in space, starting with a pizza
Delicious Uncle Sam’s Meal Cubes are laser-sintered from granulated mealworms; part of this healthy breakfast.
NASA is funding research into 3D printed food which would provide astronauts with meals during long space flights. The futuristic food printers would use cartridges of powder and oils which would have a shelf life of 30 years.
While the idea may seem like something out of a Sci-Fi movie, the process of printing food has already been proven possible. The brains behind the innovation, Anjan Contractor, previously printed chocolate in a bid to prove his concept.
Contractor and his company, Systems & Materials Research Corporation, will now use NASA’s $125,000 grant to attempt to print a pizza. The grant was applied for on March 28, 2013. The pizza printer is still in the conceptual stage, and will begin to be built in two weeks.
The printer will first print a layer of dough, which will be cooked while being printed. Tomato powder will then be mixed with water and oil to print a tomato sauce. The topping for the pizza will be a “protein layer” which could come from any source – animals, milk, or plants.
The concept is to use basic “building blocks” of food in replaceable powder cartridges. Each block will be combined to create a range of foods which can be created by the printer. The cartridges will have a shelf life of 30 years – more than long enough to enable long-distance space travel.
Contractor and his team hope the 3D printer will be used not only by NASA, but also by regular Earthlings. His vision would mean the end of food waste, due to the powder’s long shelf life.
“I think, and many economists think, that current food systems can’t supply 12 billion people sufficiently, ” he said, as quoted by Quartz.
“So we eventually have to change our perception of what we see as food.” There are some conveniences which would come along with the printer. For example, recipes could be traded with others through software. Each recipe would have a set of instructions which tells the printer which cartridge of powder to mix with which liquids, and at what rate and how it should be sprayed.
Another perk includes personalized nutrition.
“If you’re male, female, someone is sick—they all have different dietary needs. If you can program your needs into a 3D printer, it can print exactly the nutrients that person requires,” Contractor said.
Contractor plans on keeping the software portion of his 3D printer entirely open-source, so that anyone can look at its code. He believes this will allow people to find creative uses for the hardware.
United Nations encourages more world-wide consumption of insects as important food source
Insects are high in protein and minerals, need far less feed per kilo of mass than cattle do and produce far less greenhouse gas per kilo than pigs.
A United Nations food agency is pushing a new kind of diet for a hungry world.
It ranks high in nutritional value and gets good grades for protecting the environment: edible insects.
The Rome-based Food and Agriculture Organization hailed the likes of grasshoppers, ants and other members of the insect world as an underutilised food for people, livestock and pets. A new report says two billion people worldwide already supplement their diets with insects. Insects are high in protein and minerals, need far less feed per kilo of mass than cattle do and produce far less greenhouse gas per kilo than pigs. While most edible insects are gathered in forests, the UN says mechanisation can boost insect-farming production. Currently most insect farming serves niche markets.
Cholesterol-lowering statin drugs may partially block the health benefits of exercise
An important new study suggests that statins, the cholesterol-lowering medications that are the most prescribed drugs in the world, may block some of the fitness benefits of exercise, one of the surest ways to improve health. No one is saying that people with high cholesterol or a family history of heart disease should avoid statins, which studies show can be lifesaving. But the discovery could create something of dilemma for doctors and patients, since the people who should benefit the most from exercise — those who are sedentary, overweight, at risk of heart disease or middle-aged — are also the people most likely to be put on statins, possibly undoing some of the good of their workouts.
For the new study, which was published online in The Journal of the American College of Cardiology, researchers from the University of Missouri and other institutions gathered a group of overweight, sedentary men and women, all of whom had multiple symptoms of metabolic problems, including wide waistlines, high blood pressure or excess abdominal fat.
Most had slightly but not dangerously elevated cholesterol levels. None had exercised regularly in the past year. All underwent muscle biopsies and treadmill testing to determine their aerobic fitness — which was generally quite low — and agreed to continue with their normal diet. Then they all began a supervised 12-week exercise program, during which they visited the university lab five times a week and walked or jogged on a treadmill for 45 minutes at a moderately vigorous pace (about 65 to 70 percent of their individual aerobic maximum).
Half of the group also began taking a daily 40-milligram dose of simvastatin, a particular type of statin sold under the brand name Zocor. At the end of 12 weeks, the participants fitness and muscles were retested.
Statins, as most of us know, are medications designed to reduce the body’s cholesterol levels, particularly levels of low-density lipoprotein, or “bad” cholesterol. The drugs routinely are prescribed for those with high cholesterol and other risk factors for heart disease, and some physicians believe that they should be used prophylactically by virtually everyone over 50.
Exercise also typically is recommended as a means of fighting heart disease and prolonging life span.
And both statins and sweating indisputably are effective. In past studies, researchers have shown that statins reduce the risk of a heart attack in people at high risk by 10 to 20 percent for every 1-millimole-per-liter reduction in blood cholesterol levels (millimoles measure the actual number of cholesterol molecules in the bloodstream), equivalent to about a 40-point drop in LDL levels. Meanwhile, improving aerobic fitness by even a small percentage through exercise likewise has been found to lessen someone’s likelihood of dying prematurely by as much as 50 percent.
So, theoretically, it would seem that combining statins and exercise should provide the greatest possible health benefit. But until the current study, no experiment scrupulously had explored the interactions of statin drugs and workouts in people. And the results, as it turns out, are worrisome.
The unmedicated volunteers improved their aerobic fitness significantly after three months of exercise, by more than 10 percent on average. But the volunteers taking the statins gained barely 1 percent on average in their fitness, and some possessed less aerobic capacity at the end of the study than at its start.
Why there should be such a discrepancy between the two groups’ fitness levels wasn’t clear on the surface. But when the researchers looked microscopically at biopsied muscle tissue, they found notable differences in the levels of an enzyme related to the health of mitochondria, the tiny energy-producing parts of a cell. Mitochondria generally increase in number and potency when someone exercises.
But in the volunteers taking statins, enzyme levels related to mitochondrial health fell by about 4.5 percent over the course of the experiment. The same levels increased by 13 percent in the group not taking the drug. In effect, the volunteers taking statins “were not getting the same bang from their exercise buck” as the other exercisers, says John P. Thyfault, a professor of nutrition and exercise physiology at the University of Missouri and senior author of the study.
This finding joins a small but accumulating body of other studies indicating that statins can negatively affect exercise response. Lab rodents given statins, for instance, can’t run as far as unmedicated animals, while in humans, marathon runners on statins develop more markers of muscle damage after a race than runners not using the drugs.
None of which suggests, Dr. Thyfault says, that statins are not worthwhile. For people who have a family history of high cholesterol or heart disease or who themselves have high cholesterol, he says, “there’s no doubt that statins save lives.”
But for other people, the risk-benefit calculation involving statins may be trickier in light of this and other new science.
“Low aerobic fitness is one of the best predictors” of premature death, Dr. Thyfault says. And if statins prevent people from raising their fitness through exercise, then “that is a concern.”
A possible remedy, he continues, could be for people to get in shape and raise their aerobic fitness before starting the drug, but that’s an issue to discuss with your doctor. “There’s still a great deal we don’t understand” about how statins and exercise mix, he says.
Thanks to Dr. Aarati Didwania for bringing this to the attention of the It’s Interesting community.
Irish farmer has revived a potato not seen since the Great Famine
by Catherine Zuckerman
National Geographic News
“It struck down the growing plants like frost in summer. It spread faster than the cholera amongst men.”
That description of Ireland’s historic potato blight—from English writer E.C. Large’s book The Advance of the Fungi—may sound extreme, but it’s not. The devastating disease nearly wiped out many Irish potato varieties, igniting the country’s Great Famine in the mid-19th century.
But now, one of those blighted potatoes is making a comeback. Meet the Lumper.
As its name implies, this potato is not especially beautiful. It’s large, knobby, and, well, lumpy, with pale brown skin and yellow flesh. Still, it was widely grown in Ireland before the famine because it did well in poor soil and could feed a lot of mouths.
According to University College Dublin’s Cormac O’Grada, an expert on the history of famines, the blight (Phytophtora infestans) destroyed about one-third of Ireland’s potato crop in 1845 and almost all of it in 1846. Because so many people were poor and relied on potatoes for sustenance, the blight had catastrophic consequences, including food riots and mass death from starvation.
Spuds are faring much better today thanks to modern farming techniques and technology, although potato blight is still an ongoing concern for Irish farmers.
The Lumper was a thing of the mashed, roasted, and baked potato past until about five years ago, when farmer Michael McKillop—a grower and packer for Northern Ireland’s Glens of Antrim potato suppliers—became interested in the antique tuber. He got his hands on some heirloom seeds and cultivated them.
Why revive this particular potato? “I chose the Lumper because of its history and its unusual look and feel,” he said. “The history books said the taste wasn’t particularly nice, so I was fascinated to find out what it was really like myself.”
So how does it taste? Descriptions range from “good” and “pleasing” to “not bad” and “soapy.” The Daily Spud blog calls the Lumper’s texture “waxy,” rather than floury like other potatoes—not necessarily a compliment.
Dermot Carey, the head grower at Ireland’s Lissadell/Langford Potato Collection, which contains more than 200 varieties, has tasted his fair share of different potatoes. He’s not a huge fan of the Lumper: “It’s edible, but it wouldn’t be my favorite.”
The debate over the Lumper’s flavor appeal may never be settled, but one thing is clearly established: The Irish love their spuds. The Irish Potato Federation lists several popular varieties on its website, including the widely grown, red-skinned Rooster, the traditional, floury Golden Wonder, and the newly developed, highly blight-resistant Orla.
Chef and native Dubliner Cathal Armstrong, who owns several Washington, D.C.-area restaurants, has mixed feelings about the return of the Lumper: “I think it’s both exciting and a little frightening, to bring back this species of potato that is related to so much devastation. But I would still love to get my hands on some and see how they taste. I guess it would be similar to bumping into the ghost of a long-lost relative in a dark alley.”
Too bad it’s not available in the U.S. But in Ireland, McKillop’s Lumpers—which he grew to be a bit smaller than those of the 1800s—can be purchased at the retail chain Marks & Spencer through the end of March. As for the future, McKillop has plans to plant ten new acres of Lumpers—enough to yield 150 metric tons for 2014.
Whether or not the public will embrace the somewhat homely spud remains to be seen. For now, said gardener Carey, “it’s pure nostalgia.”
It’s a new product getting lots of attention. Welcome to the somewhat uncomfortable world of selling Sex Cereal. The brainchild of a Toronto businessman, Sex Cereal is quickly rising to fame after making an appearance on CBC’s Dragon’s Den just before Valentine’s Day.
Peter Ehrlich came up with the concept while walking through a vegan food fair. The lightbulb went off and the idea of a cereal with different recipes for men and women was born. “Sexual health is so important,” Ehrlich said from his office in Toronto. “I wanted to create something sexy and fun in the health food industry because nothing is. Everything is very serious.”
Ehrlich used nutritionists to formulate two separate recipes that are supposed to improve the sexual health of men and women in different ways. The person behind the image and packaging of Sex Cereal is St. Catharines designer Maximilian Kaiser – the son of Inniskillin winery co-founder Karl Kaiser – who has been designing labels for wine bottles and packaging for other industries for 20 years. The packaging Kaiser came up with has a blonde pin-up girl on the cereal for women and a fit guy on the cereal for men.
“Initially we had some pin-up girl positions that were a little more racy, but we dialed it back a bit because of the legitimacy of the product,” Kaiser said. “We didn’t want it to look like a gag gift. It’s about trying to get the attention without being like a novelty.”
That continues to be one of the big challenges of selling the cereal – even though it’s available in hundreds of nutrition and grocery stores across Canada. “We’ve put a lot of effort into making people realize it’s a whole food and high-quality stuff,” said Kaiser. Ehrlich said after launching the cereal last June, it wasn’t until the beginning of this year that distributors and stores finally started agreeing to carry it. But interest is picking up – especially since the Dragon’s Den appearance. It’s now available in 700 stores across Canada including a handful in St. Catharines.
Tina Lee, the owner of Well! Well! Well! Nutrition Centre said she didn’t mind carrying it after the popularity of another natural cereal with a unique name. “When a company came out with Holy Crap we thought ‘you’ve gotta be kidding.’ But it sold like crazy,” Lee said about the B.C.-produced cereal. “After that, Sex Cereal came out and it was the same idea.”
As for Sex Cereal, it’s produced and packaged at a factory in St. Catharines. But the people who run that factory said they don’t want to be known as the company that makes the product. They asked that their name and location not be published.
“We have come across that a couple of times,” Kaiser said. “But I think people see the big picture. This is an honest product and people are being honest about sexuality a lot more now, too.”
At about $12 a bag, Sex Cereal isn’t cheap, but Ehrlich said there’s a reason for that. “The ingredients are quite rare,” he said. “I wasn’t creating a cereal for the sake of shock value. I know scientifically it had to be the real thing, but the real thing is expensive.”
Rolled oats, wheat germ, water, chia seeds, black sesame seeds, pumpkin seeds, blueberries (sweetened with apple juice), cacao nibs, goji berries, bee pollen, maca powder, camu camu, coconut sugar
Rolled oats, oat bran, sunflower seeds, water, flax seeds, chia seeds, soy protein, cranberries (sweetened with apple juice), goji berries, cacao nibs, almonds, ginger ground, maca powder, coconut sugar
Flip of a single molecular switch makes an old brain young
The flip of a single molecular switch helps create the mature neuronal connections that allow the brain to bridge the gap between adolescent impressionability and adult stability. Now Yale School of Medicine researchers have reversed the process, recreating a youthful brain that facilitated both learning and healing in the adult mouse.
Scientists have long known that the young and old brains are very different. Adolescent brains are more malleable or plastic, which allows them to learn languages more quickly than adults and speeds recovery from brain injuries. The comparative rigidity of the adult brain results in part from the function of a single gene that slows the rapid change in synaptic connections between neurons.
By monitoring the synapses in living mice over weeks and months, Yale researchers have identified the key genetic switch for brain maturation a study released March 6 in the journal Neuron. The Nogo Receptor 1 gene is required to suppress high levels of plasticity in the adolescent brain and create the relatively quiescent levels of plasticity in adulthood. In mice without this gene, juvenile levels of brain plasticity persist throughout adulthood. When researchers blocked the function of this gene in old mice, they reset the old brain to adolescent levels of plasticity.
“These are the molecules the brain needs for the transition from adolescence to adulthood,” said Dr. Stephen Strittmatter. Vincent Coates Professor of Neurology, Professor of Neurobiology and senior author of the paper. “It suggests we can turn back the clock in the adult brain and recover from trauma the way kids recover.”
Rehabilitation after brain injuries like strokes requires that patients re-learn tasks such as moving a hand. Researchers found that adult mice lacking Nogo Receptor recovered from injury as quickly as adolescent mice and mastered new, complex motor tasks more quickly than adults with the receptor.
“This raises the potential that manipulating Nogo Receptor in humans might accelerate and magnify rehabilitation after brain injuries like strokes,” said Feras Akbik, Yale doctoral student who is first author of the study.
Researchers also showed that Nogo Receptor slows loss of memories. Mice without Nogo receptor lost stressful memories more quickly, suggesting that manipulating the receptor could help treat post-traumatic stress disorder.
“We know a lot about the early development of the brain,” Strittmatter said, “But we know amazingly little about what happens in the brain during late adolescence.”
Other Yale authors are: Sarah M. Bhagat, Pujan R. Patel and William B.J. Cafferty
The study was funded by the National Institutes of Health. Strittmatter is scientific founder of Axerion Therapeutics, which is investigating applications of Nogo research to repair spinal cord damage.