Posts tagged science
Articles and news from the latest research reports.
Leptin also influences brain cells that control appetite
Twenty years after the hormone leptin was found to regulate metabolism, appetite, and weight through brain cells called neurons, Yale School of Medicine researchers have found that the hormone also acts on other types of cells to control appetite.
Published in the June 1 issue of Nature Neuroscience, the findings could lead to development of treatments for metabolic disorders such as obesity and diabetes.
"Up until now, the scientific community thought that leptin acts exclusively in neurons to modulate behavior and body weight," said senior author Tamas Horvath, the Jean and David W. Wallace Professor of Biomedical Research and chair of comparative medicine at Yale School of Medicine. "This work is now changing that paradigm."
Leptin, a naturally occurring hormone, is known for its hunger-blocking effect on the hypothalamus, a region in the brain. Food intake is influenced by signals that travel from the body to the brain. Leptin is one of the molecules that signal the brain to modulate food intake. It is produced in fat cells and informs the brain of the metabolic state. If animals are missing leptin, or the leptin receptor, they eat too much and become severely obese.
Leptin’s effect on metabolism has been found to control the brain’s neuronal circuits, but no previous studies have definitively found that leptin could control the behavior of cells other than neurons.
To test the theory, Horvath and his team selectively knocked out leptin receptors in the adult non-neuronal glial cells of mice. The team then recorded the water and food intake, as well as physical activity every five days. They found that animals responded less to feeding reducing effects of leptin but had heightened feeding responses to the hunger hormone ghrelin.
"Glial cells provide the main barrier between the periphery and the brain," said Horvath. "Thus glial cells could be targeted for drugs that treat metabolic disorders, including obesity and diabetes."
(Source: eurekalert.org)
Speaking 2 languages benefits the aging brain
New research reveals that bilingualism has a positive effect on cognition later in life. Findings published in Annals of Neurology, a journal of the American Neurological Association and Child Neurology Society, show that individuals who speak two or more languages, even those who acquired the second language in adulthood, may slow down cognitive decline from aging.
Bilingualism is thought to improve cognition and delay dementia in older adults. While prior research has investigated the impact of learning more than one language, ruling out “reverse causality” has proven difficult. The crucial question is whether people improve their cognitive functions through learning new languages or whether those with better baseline cognitive functions are more likely to become bilingual.
"Our study is the first to examine whether learning a second language impacts cognitive performance later in life while controlling for childhood intelligence," says lead author Dr. Thomas Bak from the Centre for Cognitive Aging and Cognitive Epidemiology at the University of Edinburgh.
For the current study, researchers relied on data from the Lothian Birth Cohort 1936, comprised of 835 native speakers of English who were born and living in the area of Edinburgh, Scotland. The participants were given an intelligence test in 1947 at age 11 years and retested in their early 70s, between 2008 and 2010. Two hundred and sixty two participants reported to be able to communicate in at least one language other than English. Of those, 195 learned the second language before age 18, 65 thereafter.
Findings indicate that those who spoke two or more languages had significantly better cognitive abilities compared to what would be expected from their baseline. The strongest effects were seen in general intelligence and reading. The effects were present in those who acquired their second language early as well as late.
The Lothian Birth Cohort 1936 forms the Disconnected Mind project at the University of Edinburgh, funded by Age UK. The work was undertaken by The University of Edinburgh Centre for Cognitive Ageing and Cognitive Epidemiology, part of the cross council Lifelong Health and Wellbeing Initiative (MR/K026992/1) and has been made possible thanks to funding from the Biotechnology and Biological Sciences Research Council (BBSRC) and Medical Research Council (MRC).
"The Lothian Birth Cohort offers a unique opportunity to study the interaction between bilingualism and cognitive aging, taking into account the cognitive abilities predating the acquisition of a second language" concludes Dr. Bak. "These findings are of considerable practical relevance. Millions of people around the world acquire their second language later in life. Our study shows that bilingualism, even when acquired in adulthood, may benefit the aging brain."
After reviewing the study, Dr. Alvaro Pascual-Leone, an Associate Editor for Annals of Neurology and Professor of Medicine at Harvard Medical School in Boston, Mass. said, “The epidemiological study by Dr. Bak and colleagues provides an important first step in understanding the impact of learning a second language and the aging brain. This research paves the way for future causal studies of bilingualism and cognitive decline prevention.”
(Source: eurekalert.org)
Newly Identified Brain Cancer Mutation Will Aid Drug Development
A collaborative effort between Duke Medicine researchers and neurosurgeons and scientists in China has produced new genetic insights into a rare and deadly form of childhood and young adult brain cancer called brainstem glioma.
The researchers identified a genetic mutation in the tumor cells that plays a role in both the growth and the death of a cell. Additionally, the mutation to the newly identified gene may also contribute to the tumor’s resistance to radiation.
The findings, published online in the journal Nature Genetics on June 1, 2014, provide both immediate and long-term benefits. Knowing that this mutation may render radiation ineffective, patients could be spared that therapy. The mutation would also serve as a strong candidate for drug development.
The researchers conducted genetic tests and found that many of the tumor cells had a mutation in a gene called PPM1D, which causes cells to proliferate and avoid natural death. It is the first time this mutation has been found to be a major driving force in the development of brainstem gliomas; it is not evident in other brain tumors.
If tumors have this PPM1D mutation, they do not have another more common genetic mutation to the TP53 gene, a tumor suppressor that, when defective, is linked to half of all cancers.
“This finding has immediate clinical applications, because either mutation - PPM1D or TP53 – cause the tumor cells to be resistant to radiation,” said senior author Hai Yan, M.D., Ph.D., a professor of pathology at Duke University School of Medicine. “Knowing that could spare patients from an ineffective treatment approach.”
Additionally, the PPM1D genetic mutation is a strong candidate for new drug development.
“This finding gives us a clue as to why these particular tumors are growing inappropriately,” said co-author Zachary Reitman, M.D., Ph.D., a research associate at Duke. “These clues may help us to design better treatments for this type of cancer.”
Yan said his lab is working to identify new treatments that could target the PPM1D genetic mutation and shut down its cancer-growing capabilities.
“PPM1D is itself a target for drug development, because the gene mutation causes cells to avoid death and proliferate,” Yan said. “In drug development, it’s easier to turn that growth function off than it is to switch on the cell’s defective tumor suppression mechanism.”
(Source: corporate.dukemedicine.org)
How to Erase a Memory – And Restore It
Researchers at the University of California, San Diego School of Medicine have erased and reactivated memories in rats, profoundly altering the animals’ reaction to past events.
The study, published in the June 1 advanced online issue of the journal Nature, is the first to show the ability to selectively remove a memory and predictably reactivate it by stimulating nerves in the brain at frequencies that are known to weaken and strengthen the connections between nerve cells, called synapses.
“We can form a memory, erase that memory and we can reactivate it, at will, by applying a stimulus that selectively strengthens or weakens synaptic connections,” said Roberto Malinow, MD, PhD, professor of neurosciences and senior author of the study.
Scientists optically stimulated a group of nerves in a rat’s brain that had been genetically modified to make them sensitive to light, and simultaneously delivered an electrical shock to the animal’s foot. The rats soon learned to associate the optical nerve stimulation with pain and displayed fear behaviors when these nerves were stimulated.
Analyses showed chemical changes within the optically stimulated nerve synapses, indicative of synaptic strengthening.
In the next stage of the experiment, the research team demonstrated the ability to weaken this circuitry by stimulating the same nerves with a memory-erasing, low-frequency train of optical pulses. These rats subsequently no longer responded to the original nerve stimulation with fear, suggesting the pain-association memory had been erased.
In what may be the study’s most startlingly discovery, scientists found they could re-activate the lost memory by re-stimulating the same nerves with a memory-forming, high-frequency train of optical pulses. These re-conditioned rats once again responded to the original stimulation with fear, even though they had not had their feet re-shocked.
“We can cause an animal to have fear and then not have fear and then to have fear again by stimulating the nerves at frequencies that strengthen or weaken the synapses,” said Sadegh Nabavi, a postdoctoral researcher in the Malinow lab and the study’s lead author.
In terms of potential clinical applications, Malinow, who holds the Shiley Endowed Chair in Alzheimer’s Disease Research in Honor of Dr. Leon Thal, noted that the beta amyloid peptide that accumulates in the brains of people with Alzheimer’s disease weakens synaptic connections in much the same way that low-frequency stimulation erased memories in the rats. “Since our work shows we can reverse the processes that weaken synapses, we could potentially counteract some of the beta amyloid’s effects in Alzheimer’s patients,” he said.
Εngineer invents safe way to transfer energy to medical chips in the body
A Stanford electrical engineer has invented a way to wirelessly transfer power deep inside the body, and then use this power to run tiny electronic medical gadgets such as pacemakers, nerve stimulators or new sensors and devices yet to be developed.
The discoveries reported May 19 in the Proceedings of the National Academy of Sciences culminate years of efforts by Ada Poon, assistant professor of electrical engineering, to eliminate the bulky batteries and clumsy recharging systems that prevent medical devices from being more widely used.
The technology could provide a path toward a new type of medicine that allows physicians to treat diseases with electronics rather than drugs.
"We need to make these devices as small as possible to more easily implant them deep in the body and create new ways to treat illness and alleviate pain," said Poon.
Poon’s team built an electronic device smaller than a grain of rice that acts as a pacemaker. It can be powered or recharged wirelessly by holding a power source about the size of a credit card above the device, outside the body.
Using thoughts to control airplanes
Pilots of the future could be able to control their aircraft by merely thinking commands. Scientists of the Technische Universität München and the TU Berlin have now demonstrated the feasibility of flying via brain control – with astonishing accuracy.
The pilot is wearing a white cap with myriad attached cables. His gaze is concentrated on the runway ahead of him. All of a sudden the control stick starts to move, as if by magic. The airplane banks and then approaches straight on towards the runway. The position of the plane is corrected time and again until the landing gear gently touches down. During the entire maneuver the pilot touches neither pedals nor controls.
This is not a scene from a science fiction movie, but rather the rendition of a test at the Institute for Flight System Dynamics of the Technische Universität München (TUM). Scientists working for Professor Florian Holzapfel are researching ways in which brain controlled flight might work in the EU-funded project “Brainflight”.
"A long-term vision of the project is to make flying accessible to more people," explains aerospace engineer Tim Fricke, who heads the project at TUM. "With brain control, flying, in itself, could become easier. This would reduce the work load of pilots and thereby increase safety. In addition, pilots would have more freedom of movement to manage other manual tasks in the cockpit."
Surprising accuracy
The scientists have logged their first breakthrough: They succeeded in demonstrating that brain-controlled flight is indeed possible – with amazing precision. Seven subjects took part in the flight simulator tests. They had varying levels of flight experience, including one person without any practical cockpit experience whatsoever. The accuracy with which the test subjects stayed on course by merely thinking commands would have sufficed, in part, to fulfill the requirements of a flying license test. “One of the subjects was able to follow eight out of ten target headings with a deviation of only 10 degrees,” reports Fricke. Several of the subjects also managed the landing approach under poor visibility. One test pilot even landed within only few meters of the centerline.
The TU München scientists are now focusing in particular on the question of how the requirements for the control system and flight dynamics need to be altered to accommodate the new control method. Normally, pilots feel resistance in steering and must exert significant force when the loads induced on the aircraft become too large. This feedback is missing when using brain control. The researchers are thus looking for alternative methods of feedback to signal when the envelope is pushed too hard, for example.
Electrical potentials are converted into control commands
In order for humans and machines to communicate, brain waves of the pilots are measured using electroencephalography (EEG) electrodes connected to a cap. An algorithm developed by scientists from Team PhyPA (Physiological Parameters for Adaptation) of the Technische Universität Berlin allows the program to decipher electrical potentials and convert them into useful control commands.
Only the very clearly defined electrical brain impulses required for control are recognized by the brain-computer interface. “This is pure signal processing,” emphasizes Fricke. Mind reading is not possible.
A Mexican Scientist Just Invented a ‘Telekinesis’ Helmet
A researcher just made a remarkable breakthrough in the area of brain-computer interfaces—creating a rig that allows a user to operate machines with thought alone, almost literally granting a form of ‘telekinesis’ over attached devices.
Brain-computer interfaces are a rapidly expanding area of research and industry. Though the technology to read brainwaves from the head’s surface has been around for decades, scientists and engineers have only recently created numerous systems to read signals directly from the brain and translate them into commands that control computers.
In the future, these technologies could allow people with physical disabilities to control their environment through thought alone—the brain-computer interface effectively grants users a form of telekinesis. With an increasingly digital world, brain-computer interfaces (BCIs) could allow future generations to interact with technology telepathically. Many of the early BCI studies were promising, but the technology was difficult to use and mentally exhausting.
Environmental Influences May Cause Autism in Some Cases
Research by scientists at Albert Einstein College of Medicine of Yeshiva University may help explain how some cases of autism spectrum disorder (ASD) can result from environmental influences rather than gene mutations. The findings, published online today in PLOS Genetics, shed light on why older mothers are at increased risk for having children with ASD and could pave the way for more research into the role of environment on ASD.
The U.S. Centers for Disease Control and Prevention announced in March that one in 68 U.S. children has an ASD—a 30 percent rise from 1 in 88 two years ago. A significant number of people with an ASD have gene mutations that are responsible for their condition. But a number of studies—particularly those involving identical twins, in which one twin has ASD and the other does not—show that not all ASD cases arise from mutations.
In fact, a major study of more than 14,000 children with ASDs published earlier this month in the Journal of the American Medical Association concluded that gene abnormalities could explain only half the risk for developing ASD. The other half of the risk was attributable to “nongenetic influences,” meaning environmental factors that could include the conditions in the womb or a pregnant woman’s stress level or diet.
(Source: einstein.yu.edu)
Exceptional Evolutionary Divergence of Human Muscle and Brain Metabolomes Parallels Human Cognitive and Physical Uniqueness
Metabolite concentrations reflect the physiological states of tissues and cells. However, the role of metabolic changes in species evolution is currently unknown. Here, we present a study of metabolome evolution conducted in three brain regions and two non-neural tissues from humans, chimpanzees, macaque monkeys, and mice based on over 10,000 hydrophilic compounds. While chimpanzee, macaque, and mouse metabolomes diverge following the genetic distances among species, we detect remarkable acceleration of metabolome evolution in human prefrontal cortex and skeletal muscle affecting neural and energy metabolism pathways. These metabolic changes could not be attributed to environmental conditions and were confirmed against the expression of their corresponding enzymes. We further conducted muscle strength tests in humans, chimpanzees, and macaques. The results suggest that, while humans are characterized by superior cognition, their muscular performance might be markedly inferior to that of chimpanzees and macaque monkeys.
Research details how developing neurons sense a chemical cue
Symmetry is an inherent part of development. As an embryo, an organism’s brain and spinal cord, like the rest of its body, organize themselves into left and right halves as they grow. But a certain set of nerve cells do something unusual: they cross from one side to the other. New research in mice delves into the details of the molecular interactions that help guide these neurons toward this anatomical boundary.
In an embryo, a neuron’s branches, or axons, have special structures on their tips that sense chemical cues telling them where to grow. The new findings, by researchers at Memorial Sloan Kettering Cancer Center and The Rockefeller University, reveal the structural details of how one such cue, Netrin-1, interacts with two sensing molecules on the axons, DCC and a previously less well characterized player known as neogenin, as a part of this process.
“Our work provides the first high-resolution view of the molecular complexes that form on the surface of a developing axon and tell it to move in one direction or another,” says Dimitar Nikolov, a structural biologist at Memorial Sloan Kettering. “This detailed understanding of these assemblies helps us better understand neural wiring, and may one day be useful in the development of drugs to treat spinal cord or brain injuries.”
In a developing nervous system, the signaling molecule, Netrin-1, identified by Rockefeller University Professor Marc Tessier-Lavigne and colleagues, can guide neurons by attracting or repulsing them. In the case of axons that cross from one side to the other, extended by so-called commissural neurons, Netrin-1 attracts them toward the middle.
With a technique that uses X-rays to visualize the structure of crystalized proteins, research scientist Kai Xu and colleagues in Nikolov’s laboratory revealed that Netrin-1 has two separate binding sites on opposite ends, enabling it to simultaneously bind to different receptors. This may explain how Netrin-1, which is an important axon-guiding molecule, can affect in different ways neurons that express different combinations of receptors, Nikolov says.
For some time, scientists have known commissural neurons used the receptor molecule DCC to detect Netrin-1. Neogenin has a structure similar to DCC, and this research, described today in Science, confirms neogenin too acts as a sensing molecule for commissural neurons in mammals.
In experiments that complemented the structural work, conducted by Nicolas Renier and Zhuhao Wu in Tessier-Lavigne’s lab, the researchers confirmed that, like DCC, neogenin senses Netrin-1 for the growing commissural neurons in mice.
These neurons are part of the system by which one side of the brain controls movement on the opposite side of the body. As a result, a mutation in the gene responsible for DCC interferes with this coordination, causing congenital mirror movement disorder. People with this disorder cannot move one side of the body in isolation; for example, a right-handed wave is mirrored by a similar gesture by the left hand.
The work also has implications for understanding why DCC, neogenin and other cell-surface receptors come in slightly different forms, called splice isoforms. The structural research revealed these isoforms bind differently to Netrin-1. However, it is not yet clear what this means for neuron wiring, Nikolov says.
“With this structural knowledge, and with the identification of an additional receptor involved in axon guidance in the spinal cord, we are gaining deeper insight into the mechanisms through which neurons make connections that produce a functioning nervous system, as well as the dysfunction that arises from miswiring of connections” says Tessier-Lavigne.
(Source: newswire.rockefeller.edu)