New clues to how the brain and body communicate to regulate weight
Maintaining a healthy body weight may be difficult for many people, but it’s reassuring to know that our brains and bodies are wired to work together to do just that—in essence, to achieve a phenomenon known as energy balance, a tight matching between the number of calories consumed versus those expended. This careful balance results from a complex interchange of neurobiological crosstalk within regions of the brain’s hypothalamus, and when this “conversation” goes awry, obesity or anorexia can result.
Given the seriousness of these conditions, it’s unfortunate that little is known about the details of this complex interchange. Now research led by investigators at Beth Israel Deaconess Medical Center (BIDMC) provides new insights that help bring order to this complexity. Described in the October 26 issue of the journal Cell, the findings demonstrate how the GABA neurotransmitter selectively drives energy expenditure, and importantly, also help explain the neurocircuitry underlying the fat-burning properties of brown fat.
"Our group has built up a research program with the overall goal of unraveling the ‘wiring diagram’ by which the brain controls appetite and the burning of calories," says senior author Bradford Lowell, MD, PhD, a Professor of Medicine in BIDMC’s Division of Endocrinology and Harvard Medical School. "To advance our understanding to this level, we need to know the function of specific subsets of neurons, and in addition, the upstream neurons providing input to, and the downstream neurons receiving output from, these functionally defined neurons. Until recently, such knowledge in the hypothalamus has been largely unobtainable."
Filed under weight obesity brain body GABA neurotransmitters neuroscience science
Omega-3 Intake Heightens Working Memory in Healthy Young Adults
While Omega-3 essential fatty acids—found in foods like wild fish and grass-fed livestock—are necessary for human body functioning, their effects on the working memory of healthy young adults have not been studied until now.
In the first study of its kind, researchers at the University of Pittsburgh have determined that healthy young adults ages 18-25 can improve their working memory even further by increasing their Omega-3 fatty acid intake. Their findings have been published online in PLOS One.
“Before seeing this data, I would have said it was impossible to move young healthy individuals above their cognitive best,” said Bita Moghaddam, project investigator and professor of neuroscience. “We found that members of this population can enhance their working memory performance even further, despite their already being at the top of their cognitive game.”
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(Image credit: Matt Allworth/Courtesy Flickr)
Filed under brain performance memory working memory omega-3 cognitive abilities neuroscience psychology science
Robots in the Home: Will Older Adults Roll Out the Welcome Mat?
Robots have the potential to help older adults with daily activities that can become more challenging with age. But are people willing to use and accept the new technology? A study by the Georgia Institute of Technology indicates the answer is yes, unless the tasks involve personal care or social activities.
After showing adults (ages 65 to 93 years) a video of a robot’s capabilities, researchers interviewed them about their willingness for assistance with 48 common household tasks. Participants generally preferred robotic help over human help for chores such as cleaning the kitchen, doing laundry and taking out the trash. But when it came to help getting dressed, eating and bathing, the adults tended to say they would prefer human assistance over robot assistance. They also preferred human help for social activities, such as calling family and friends or entertaining guests.
Georgia Tech’s Cory-Ann Smarr will present the results this week at the Human Factors Ergonomics Society Annual Meeting in Boston.
“There are many misconceptions about older adults having negative attitudes toward robots,” said Smarr, a School of Psychology graduate teaching assistant. “The people we interviewed were very enthusiastic and optimistic about robots in their daily lives. They were also very particular in their preferences, something that can assist researchers as they determine what to design and introduce in the home.”
Filed under attitude robot assistance robotics robots technology aging science
Robots get around by mimicking primates
By mimicking how primates visualise an unfamiliar environment - a process called mental rotation - researchers are building a new kind of guidance system for robots.
Many species of animals perform mental rotation - a poorly understood aspect of spatial reasoning that is nonetheless an integral part of high-level cognition.
"If I tell you to turn left, you will probably ask whose left, mine or yours?" says Ronald Arkin of Georgia Institute of Technology in Atlanta, who is leading the effort to incorporate this technique into software for controlling robots. "You have to transform your frame of reference," he says.
The team is now testing their software in a lab setting. The researchers first supply the robot with a destination - a simplified image of how objects in their environment will look from a given perspective. The robot then uses depth information from an on-board Kinect motion sensor to establish how objects look in its surroundings.
Once it has built a picture of where it is, the robot “mentally” rotates the orientation of objects to match its destination, and then plots a path. As it trundles along, it continues to take images of its surroundings and compare them to its destination, just to make sure it is on the right track. In tests, a small four-wheeled robot used this method to find its way 6 metres across a lab floor to the right spot.
It’s a humble beginning, but Arkin says it’s the first time a robot has demonstrated the ability to receive visual instructions and act on them without a map. The work will be presented in December at the ROBIO conference in Guangzhou, China. “When the world isn’t as you expect it to be, this will help you,” he says, adding that the system could also be adapted to use speech recognition software to understand voice commands and use them to build a picture of the destination being described.
Filed under ROBIO conference mental rotation primates robotics robots neuroscience visual instructions science
Genetics researchers at the University of Adelaide have solved a 40-year mystery for a family beset by a rare intellectual disability - and they’ve discovered something new about the causes of intellectual disability in the process.
While many intellectual disabilities are caused directly by a genetic mutation in the so-called “protein coding” part of our genes, the researchers found that in their case the answer laid outside the gene and in the regulation of proteins.
Protein regulation involves the switching on or off of a protein by specific genes. As a consequence in this case, either too much or too little of this protein can trigger the disability.
The team has studied a large (anonymous) Australian family of 100 people, who for generations have not known the source of their genetically inherited condition.
The disability - which results in a lower IQ, behavioural problems such as aggression, and memory loss, and is linked with developmental delays, epilepsy, schizophrenia and other problems - affects only the male family members and can be passed on by the female family members to their children.
Genetic samples taken from the family and laboratory testing involving mice have confirmed that the protein produced by the HCFC1 (host cell factor C1) gene is the cause of this disability.
"The causes of intellectual disability generally are highly variable and the genetic causes in particular are numerous. The vast majority of intellectual disabilities are due to genetic mutations in proteins, so it was rather unexpected that we found this particular disability to be due to a regulatory mutation," says the leader of the study, Professor Jozef Gecz from the University of Adelaide’s School of Paediatrics and Reproductive Health.
"We’ve been researching this specific disability for 10 years and it’s taken us the last three years to convince ourselves that the protein regulation is the key," he says.
"For the family, this means we now have a genetic test that will determine whether or not a female member of the family is a carrier, which brings various benefits for the family.
"From a scientific point of view, this widens our viewpoint on the causes of these disabilities and tells us where we should also look for answers for those families and individuals without answers.
"This is just the tip of the iceberg in understanding the impact of altered gene regulation on intellectual disability - the gene regulatory landscape is much bigger than the protein coding landscape. We have already found, and I would expect to continue finding, a number of other intellectual disabilities linked with protein regulation over the next 20 years or so."
Professor Gecz and his team have published their findings in this month’s issue of the American Journal of Human Genetics.
(Source: adelaide.edu.au)
Filed under intellectual disabilities genetics mutation protein neuroscience science
Same neurons at work in sleep and under anesthesia
Anesthesiologists aren’t totally lying when they say they’re going to put you to sleep. Some anesthetics directly tap into sleep-promoting neurons in the brain, a study in mice reveals.
The results may help clarify how drugs that have been used around the world for decades actually put someone under. “It’s kind of shocking that after 170 years, we still don’t understand why they work,” says study coauthor Max Kelz of the University of Pennsylvania in Philadelphia.
Most neurons in the brain appear to be calmed by anesthetics, says neuropharmacologist and anesthesiologist Hugh Hemmings Jr. of Weill Cornell Medical College in New York City. But the new results, published online October 25 in Current Biology, show that two common anesthetics actually stimulate sleep-inducing neurons. “It’s unusual for neurons to be excited by anesthetics,” Hemmings says.
In the study, Kelz, Jason Moore, also of the University of Pennsylvania, and colleagues studied the effects of the anesthetics isoflurane and halothane. Mice given the drugs soon became sleepy, as expected. Along with this drowsiness came a jump in nerve cell activity in a part of the brain’s hypothalamus called the ventrolateral preoptic nucleus, or VLPO.
Filed under brain neuron anesthetics sleep brain stimulation neuroscience psychology science
Everyone feels refreshed after a good night’s sleep, but sleep does more than just rejuvenate, it can also consolidate memories. ‘The rapid eye movement form of sleep and slow wave sleep are involved in cognitive forms of memory such as learning motor skills and consciously accessible memory’, explains Randolf Mezel from the Freie Universtät Berlin, Germany. According to Menzel, the concept that something during sleep reactivates a memory for consolidation is a basic theory in sleep research. However, the human brain is far too complex to begin dissecting the intricate neurocircuits that underpin our memories, which is why Menzel has spent the last four decades working with honey bees: they are easy to train, well motivated and it is possible to identify the miniaturised circuits that control specific behaviours in their tiny brains. Intrigued by the role of sleep in memory consolidation and knowing that a bee is sleeping well when its antennae are relaxed and collapsed down, Menzel decided to focus on the role of sleep in one key memory characteristic: relearning (p. 3981). The challenge that Menzel set the bees was to learn a new route home after being displaced from a familiar path.
Menzel and his colleague Lisa Beyaert provided a hive with a well-stocked feeder and trained the bees to visit the feeder and return home fully laden. Then, when the duo were convinced that the bees had memorized the routine, they cunningly intercepted the bees at the feeder and transported them to a new location before releasing the insects to find their way home. According to Menzel, foragers learn the general lay of the land as novices before specialising in a few well-travelled routes later in their careers. He explains that the displaced bees had to rely on their earlier experiences to learn their new way home. How would loss of sleep affect the bee’s ability to learn the new route? To determine this, Menzel and Beyeart first had to check that the bees could learn the new route and that sleep deprivation hadn’t made them too tired or altered their motivation to forage.
Teaming up with electrical engineer Uwe Greggers, Menzel kitted the bees out with tiny RADAR transponders; the RADAR technology was particularly demanding to operate. Tracking the insects’ progress as they tried to learn the alternative route home, Menzel and his colleagues saw that by the second run home, the displaced bees had learned the new route. And when the trio disturbed the insects’ sleep during the night before the initial displacement by shaking them awake every 5 min, they found that the bees were unfazed. In fact they didn’t seem to need sleep to maintain their foraging energy levels and the foragers that were deprived of sleep before the first displacement run had no problems learning the new route home.
However, when the team disrupted the bees’ sleep after they had allowed the bees a single run along the new displaced route, the lack of sleep played havoc with their memories on the following day. Fewer than half of the sleep-deprived foragers made it home successfully, and those that did took more than twice as long as bees that had enjoyed an uninterrupted night’s sleep.
Sleep deprivation had dramatically affected the bees’ ability to alter a well-established memory and the team is now keen to see whether they can identify characteristic activity patterns in the slumbering insects’ brains that could represent memory formation.
Filed under sleep sleep deprivation memory learning relearning bees neuroscience science
Speed-Learning a New Language May Help Brain Grow
Learning a new language over a short period of time appears to make the brain grow, new research suggests. The new study included young recruits at the Swedish Armed Forces Interpreter Academy who went from having no knowledge of a new language to speaking it fluently within 13 months. The recruits studied at a furious pace: from morning to evening, weekdays and weekends.
The recruits were compared to medicine and cognitive science students at a university (the “control” group), who also studied hard, but weren’t learning a new language. Both groups underwent MRI brain scans before and after a three-month period of intensive study. The scans showed that the brain structure of the control group remained unchanged, but certain parts of the brain of the language students grew.
This growth occurred in the hippocampus, a structure involved in learning new material and spatial navigation, and in three areas of the cerebral cortex. Among the recruits, those who took naturally to learning a new language had greater growth in the hippocampus and areas of the cerebral cortex related to language learning, while those who had to put more effort into learning a new language had greater growth in an area of the motor region of the cerebral cortex, the investigators found.
"We were surprised that different parts of the brain developed to different degrees depending on how well the students performed and how much effort they had had to put in to keep up with the course," Johan Martensson, a researcher in psychology at Lund University in Sweden, said in a university news release.
Martensson noted that previous research has indicated that bilingual and multilingual people develop Alzheimer’s disease at a later age. “Even if we cannot compare three months of intensive language study with a lifetime of being bilingual, there is a lot to suggest that learning languages is a good way to keep the brain in shape,” Martensson said.
The study appeared in the Oct. 15 issue of the journal NeuroImage.
Filed under brain language learning neuroimaging neuroscience psychology science
When the era of regenerative medicine dawned more than three decades ago, the potential to replenish populations of cells destroyed by disease was seen by many as the next medical revolution. However, what followed turned out not to be a sprint to the clinic, but rather a long tedious slog carried out in labs across the globe required to master the complexity of stem cells and then pair their capabilities and attributes with specific diseases.
In a review article appearing today in the journal Science, University of Rochester Medical Center scientists Steve Goldman, M.D., Ph.D., Maiken Nedergaard, Ph.D., and Martha Windrem, Ph.D., contend that researchers are now on the threshold of human application of stem cell therapies for a class of neurological diseases known as myelin disorders – a long list of diseases that include conditions such as multiple sclerosis, white matter stroke, cerebral palsy, certain dementias, and rare but fatal childhood disorders called pediatric leukodystrophies.
"Stem cell biology has progressed in many ways over the last decade, and many potential opportunities for clinical translation have arisen," said Goldman. "In particular, for diseases of the central nervous system, which have proven difficult to treat because of the brain’s great cellular complexity, we postulated that the simplest cell types might provide us the best opportunities for cell therapy."
The common factor in myelin disorders is a cell called the oligodendrocyte. These cells arise, or are created, by another cell found in the central nervous system called the glial progenitor cell. Both oligodendrocytes and their “sister cells” – called astrocytes – share this same parent and serve critical support functions in the central nervous systems.
(Source: eurekalert.org)
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Filed under nervous system nerve cells neurological disorders oligodendrocytes stem cells neuroscience science
Five scientists, including two from Simon Fraser University, have discovered that 30 per cent of our likelihood of developing Multiple Sclerosis (MS) can be explained by 475,806 genetic variants in our genome. Genome-wide Association Studies (GWAS) commonly screen these variants, looking for genetic links to diseases.
Corey Watson, a recent SFU doctoral graduate in biology, his thesis supervisor SFU biologist Felix Breden and three scientists in the United Kingdom have just had their findings published online in Scientific Reports. It’s a sub-publication of the journal Nature.
An inflammatory disease of the central nervous system, MS is the most common neurological disorder among young adults. Canada has one of the highest MS rates in the world.
Watson and his colleagues recently helped quantify MS genetic susceptibility by taking a closer look at GWAS-identified variants in the major histocompatibility complex (MHC) region in 1,854 MS patients. The region has long been associated with MS susceptibility.
The MS patients’ variants were compared to those of 5,164 controls, people without MS.
They noted that eight percent of our 30-per-cent genetic susceptibility to MS is linked to small DNA variations on chromosome 6, which have also long been associated with MS susceptibility.
The MHC encodes proteins that facilitate communication between certain cells in the immune system. Outside of the MHC, a good majority of genetic susceptibility can’t be nailed down because current studies don’t allow for all variants in our genome to be captured.
“Much of the liability is unaccounted for because current research methods don’t enable us to fully interrogate our genome in the context of risk for MS or other diseases,” says Watson.
The researchers believe that one place to look for additional genetic causes of MS may be in genes that have variants that are rare in the population. “The importance of rare gene variants in MS has been illustrated in two recent studies,” notes Watson, now a postdoctoral researcher at the Mount Sinai School of Medicine in New York.
“But these variants, too, are generally poorly represented by genetic markers captured in GWAS, like the one our study was based on.”
(Source: sfu.ca)
Filed under MS genetics genomics GWAS neurological disorders CNS neuroscience science
