Posts tagged science
Articles and news from the latest research reports.
Innovative system for the rehabilitation of people with brain damage
The Biomechanics Institute of Valencia (IBV) is currently taking part in the European project WALKX with the aim of developing an innovative rehabilitation system to improve the quality of life of people who have suffered brain damage. This system will allow home rehabilitation and improve patient’s autonomy.
WALKX is a two-year research project for the benefit of small and medium sized enterprises (SMEs), co-funded by the European Commission through the Seventh Framework Programme.
The user friendly walking training device the partners are designing will support the patient in raising from sitting to standing position and enable the patient to perform walking training and improve his/her manoeuvrability. “An upper body stabilizing and controllable supporting vest will be developed. Early in the rehabilitation process it will be used under supervision of a therapist, but with greatly reduced need for physical support from the therapists. This is intended to reduce the need for help from others and increase freedom of movement and personal autonomy of the patient”, said Ignacio Bermejo, Market Innovation Director at IBV.
One of the novelties of this device consists of a vest with attachment points on the patient’s waist in order to regulate the mobility of the trunk. Also, the device will be modular and low cost. The role of IBV in this initiative has been to define the design specifications and preclinical testing to validate the prototype. Preclinical tests are done in collaboration with the Department of Physical Medicine and Rehabilitation at the Hospital Universitari i Politècnic La Fe of Valencia.
The project is coordinated by the Norwegian company Made for Movement Group. Besides Biomechanics Institute, other members of the consortium are Innovatsiooni Eesti Instituut (Estonia), INNORA ROBOTICS (Greece), Newtrim and MCT (UK), ENIX (France), Motus (Italy) and MOBILE ROBOTICS SWEDEN (Sweden).
Stroke (cerebrovascular accident) is the most common cause of adult disability in Europe. Roughly 75% of victims survive, but about half of these lose the ability to live independently in their own home. As strokes often result in long term disability rather than death, the rehabilitation and hospitalisation represent a major economic burden for the EU of about €34 Bn annually. Currently, the annual incidence is approximately 2 per 1,000 inhabitants in the EU, and the number is predicted to double over the next 50 years due to the aging of the population.
Machine Perception Lab Shows Robotic One-Year-Old on Video
The world is getting a long-awaited first glimpse at a new humanoid robot in action mimicking the expressions of a one-year-old child. The robot will be used in studies on sensory-motor and social development – how babies “learn” to control their bodies and to interact with other people.
Diego-san’s hardware was developed by leading robot manufacturers: the head by Hanson Robotics, and the body by Japan’s Kokoro Co. The project is led by University of California, San Diego full research scientist Javier Movellan.
Movellan directs the Institute for Neural Computation’s Machine Perception Laboratory, based in the UCSD division of the California Institute for Telecommunications and Information Technology (Calit2). The Diego-san project is also a joint collaboration with the Early Play and Development Laboratory of professor Dan Messinger at the University of Miami, and with professor Emo Todorov’s Movement Control Laboratory at the University of Washington.
Movellan and his colleagues are developing the software that allows Diego-san to learn to control his body and to learn to interact with people.
"We’ve made good progress developing new algorithms for motor control, and they have been presented at robotics conferences, but generally on the motor-control side, we really appreciate the difficulties faced by the human brain when controlling the human body," said Movellan, reporting even more progress on the social-interaction side. "We developed machine-learning methods to analyze face-to-face interaction between mothers and infants, to extract the underlying social controller used by infants, and to port it to Diego-san. We then analyzed the resulting interaction between Diego-san and adults." Full details and results of that research are being submitted for publication in a top scientific journal.
While photos and videos of the robot have been presented at scientific conferences in robotics and in infant development, the general public is getting a first peak at Diego-san’s expressive face in action. On January 6, David Hanson (of Hanson Robotics) posted a new video on YouTube.
“This robotic baby boy was built with funding from the National Science Foundation and serves cognitive A.I. and human-robot interaction research,” wrote Hanson. “With high definition cameras in the eyes, Diego San sees people, gestures, expressions, and uses A.I. modeled on human babies, to learn from people, the way that a baby hypothetically would. The facial expressions are important to establish a relationship, and communicate intuitively to people.”
Diego-san is the next step in the development of “emotionally relevant” robotics, building on Hanson’s previous work with the Machine Perception Lab, such as the emotionally responsive Albert Einstein head.
Networking Ability a Family Trait in Monkeys
Two years of painstaking observation on the social interactions of a troop of free-ranging monkeys and an analysis of their family trees has found signs of natural selection affecting the behavior of the descendants.
Rhesus macaques who had large, strong networks tended to be descendants of similarly social macaques, according to a Duke University team of researchers. And their ability to recognize relationships and play nice with others also won them more reproductive success.
"If you are a more social monkey, then you’re going to have greater reproductive success, meaning your babies are more likely to survive their first year," said post-doctoral research fellow Lauren Brent, who led the study. "Natural selection appears to be favoring pro-social behavior."
The analysis, which appears in Nature Scientific Reports, combined sophisticated social network maps with 75 years of pedigree data and some genetic analysis.
Stem Cells May Hold Promise for Lou Gehrig’s Disease (ALS)
Apparent stem cell transplant success in mice may hold promise for people with amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease. The results of the study were released today and will be presented at the American Academy of Neurology’s 65th Annual Meeting in San Diego, March 16 to 23, 2013. “There have been remarkable strides in stem cell transplantation when it comes to other diseases, such as cancer and heart failure,” said study author Stefania Corti, MD, PhD, with the University of Milan in Italy and a member of the American Academy of Neurology. “ALS is a fatal, progressive, degenerative disease that currently has no cure. Stem cell transplants may represent a promising avenue for effective cell-based treatment for ALS and other neurodegenerative diseases.”
For the study, mice with an animal model of ALS were injected with human neural stem cells taken from human induced pluripotent stem cells (iPSCs). iPSC are adult cells such as skin cells that have been genetically reprogrammed to an embryonic stem cell-like state. Neurons are a basic building block of the nervous system, which is affected by ALS. After injection, the stem cells migrated to the spinal cord of the mice, matured and multiplied.
The study found that stem cell transplantation significantly extended the lifespan of the mice by 20 days and improved their neuromuscular function by 15 percent. “Our study shows promise for testing stem cell transplantation in human clinical trials,” said Corti.
(Image: ALAMY)
Eliminating useless information important to learning, making new memories
As we age, it just may be the ability to filter and eliminate old information – rather than take in the new stuff – that makes it harder to learn, scientists report.
“When you are young, your brain is able to strengthen certain connections and weaken certain connections to make new memories,” said Dr. Joe Z. Tsien, neuroscientist at the Medical College of Georgia at Georgia Regents University and Co-Director of the GRU Brain & Behavior Discovery Institute.
It’s that critical weakening that appears hampered in the older brain, according to a study in the journal Scientific Reports.
The NMDA receptor in the brain’s hippocampus is like a switch for regulating learning and memory, working through subunits called NR2A and NR2B. NR2B is expressed in higher percentages in children, enabling neurons to talk a fraction of a second longer; make stronger bonds, called synapses; and optimize learning and memory. This formation of strong bonds is called long-term potentiation. The ratio shifts after puberty, so there is more NR2A and slightly reduced communication time between neurons.
When Tsien and his colleagues genetically modified mice that mimic the adult ratio – more NR2A, less NR2B – they were surprised to find the rodents were still good at making strong connections and short-term memories but had an impaired ability to weaken existing connections, called long-term depression, and to make new long-term memories as a result. It’s called information sculpting and adult ratios of NMDA receptor subunits don’t appear to be very good at it.
“If you only make synapses stronger and never get rid of the noise or less useful information then it’s a problem,” said Tsien, the study’s corresponding author. While each neuron averages 3,000 synapses, the relentless onslaught of information and experiences necessitates some selective whittling. Insufficient sculpting, at least in their mouse, meant a reduced ability to remember things short-term – like the ticket number at a fast-food restaurant – and long-term – like remembering a favorite menu item at that restaurant. Both are impacted in Alzheimer’s and age-related dementia.
All long-term depression was not lost in the mice, rather just response to the specific electrical stimulation levels that should induce weakening of the synapse. Tsien expected to find the opposite: that long-term potentiation was weak and so was the ability to learn and make new memories. “What is abnormal is the ability to weaken existing connectivity.”
Acknowledging the leap, this impaired ability could also help explain why adults can’t learn a new language without their old accent and why older people tend to be more stuck in their ways, the memory researcher said.
“We know we lose the ability to perfectly speak a foreign language if we learn than language after the onset of sexual maturity. I can learn English but my Chinese accent is very difficult to get rid of. The question is why,” Tsien said.
Tsien and his colleagues already have learned what happens when NR2B is overexpressed. He and East China Normal University researchers announced in 2009 the development of Hobbie-J, a smarter than average rat. A decade earlier, Tsien reported in the journal Nature the development of a smart mouse dubbed Doogie using the same techniques to over-express the NR2B gene in the hippocampus.
Doogie, Hobbie-J and their descendants have maintained superior memory as they age. Now Tsien is interested in following the NR2A over-expressing mouse to see what happens.
(Source: news.georgiahealth.edu)
Newly found ‘volume control’ in the brain promotes learning, memory
Scientists have long wondered how nerve cell activity in the brain’s hippocampus, the epicenter for learning and memory, is controlled — too much synaptic communication between neurons can trigger a seizure, and too little impairs information processing, promoting neurodegeneration. Researchers at Georgetown University Medical Center say they now have an answer. In the January 10 issue of Neuron, they report that synapses that link two different groups of nerve cells in the hippocampus serve as a kind of “volume control,” keeping neuronal activity throughout that region at a steady, optimal level.
"Think of these special synapses like the fingers of God and man touching in Michelangelo’s famous fresco in the Sistine Chapel," says the study’s senior investigator, Daniel Pak, PhD, an associate professor of pharmacology. "Now substitute the figures for two different groups of neurons that need to perform smoothly. The touching of the fingers, or synapses, controls activity levels of neurons within the hippocampus."
The hippocampus is a processing unit that receives input from the cortex and consolidates that information in terms of learning and memory. Neurons known as granule cells, located in the hippocampus’ dentate gyrus, receive transmissions from the cortex. Those granule cells then pass that information to the other set of neurons (those in the CA3 region of the hippocampus, in this study) via the synaptic fingers.
Those fingers dial up, or dial down, the volume of neurotransmission from the granule cells to the CA3 region to keep neurotransmission in the learning and memory areas of the hippocampus at an optimal flow — a concept known as homeostatic plasticity. “If granule cells try to transmit too much activity, we found, the synaptic junction tamps down the volume of transmission by weakening their connections, allowing the proper amount of information to travel to CA3 neurons,” says Pak. “If there is not enough activity being transmitted by the granule cells, the synapses become stronger, pumping up the volume to CA3 so that information flow remains constant.”
There are many such touching fingers in the hippocampus, connecting the so-called “mossy fibers” of the granule cells to neurons in the CA3 region. But importantly, not every one of the billions of neurons in the hippocampus needs to set its own level of transmission from one nerve cell to the other, says Pak.
To explain, he uses another analogy. “It had previously been thought that neurons act separately like cars, each working to keep their speed at a constant level even though signal traffic may be fast or slow. But we wondered how these neurons could process learning and memory information efficiently, while also regulating the speed by which they process and communicate that information.
"We believe, based on our study, that only the mossy fiber synapses on the CA3 neurons control the level of activity for the hippocampus — they are like the engine on a train that sets the speed for all the other cars, or neurons, attached to it," Pak says. "That frees up the other neurons to do the job they are tasked with doing — processing and encoding information in the forms of learning and memory."
Not only does the study offer a new model for how homeostatic plasticity in the hippocampus can co-exist with learning and memory, it also suggests a new therapeutic avenue to help patients with uncontrollable seizures, he says.
"The CA3 region is highly susceptible to seizures, so if we understand how homeostasis is maintained in these neurons, we could potentially manipulate the system. When there is an excessive level of CA3 neuronal activity in a patient, we could learn how to therapeutically turn it down."
(Source: eurekalert.org)
Pannexins are abundant in the central nervous system of vertebrates
Pannexins traverse the cell membrane of vertebrate animals and form large pored channels. They are permeable for certain signalling molecules, such as the energy storage molecule ATP (adenosine triphosphate). The best known representative is Pannexin1, which occurs in abundance in the brain and spinal cord and among others in the hippocampus - a brain structure that is critical for long-term memory. Malfunctions of the pannexins play a role in the development of epilepsy and strokes.
No more scope in long-term potentiation
The research team studied mice in which the gene for Pannexin1 was lacking. Using cell recordings carried out on isolated brain sections, they analysed the long-term potentiation in the hippocampus. Long-term potentiation usually occurs when new memory content is built - the contacts between nerve cells are strengthened; they communicate more effectively with each other. In mice without Pannexin1, the long-term potentiation occurred earlier and was more prolonged than in mice with Pannexin1. “It looks at first glance like a gain in long-term memory”, says Nora Prochnow. “But precise analysis shows that there was no more scope for upward development.” Due to the lack of Pannexin1, the cell communication in general was increased to such an extent that a further increase through the learning of new knowledge was no longer possible. The synaptic plasticity was thus extremely restricted. “The plasticity is essential for learning processes in the brain”, Nora Prochnow explains. “It helps you to organise, keep or even to forget contents in a positive sense, to gain room for new inputs.”
Autistic-like behaviour without Pannexin1
The absence of Pannexin1 also had an impact on behaviour: when solving simple problems, the animals were quickly overwhelmed in terms of content. Their spatial orientation was limited, their attention impaired and an increased probability for seizure generation occurred. “The behavioural patterns are reminiscent of autism. We should therefore consider the Pannexin1 channel more closely with regard to the treatment of such diseases”, says the neurobiologist from Bochum.
Theory: feedback regulation gets out of hand without Pannexin1
According to the scientists’ theory, nerve cells lack a feedback mechanism without Pannexin1. Normally the channel protein releases ATP, which binds to specific receptors and thus reduces the release of the neurotransmitter glutamate. Without Pannexin1 more glutamate is released, which leads to increased long-term potentiation. This causes the cell to lose its dynamic equilibrium, which is needed for an efficient learning process.
A landmark discovery about how insulin docks on cells could help in the development of improved types of insulin for treating both type 1 and type 2 diabetes.
For the first time, researchers have captured the intricate way in which insulin uses the insulin receptor to bind to the surface of cells. This binding is necessary for the cells to take up sugar from the blood as energy.
The research team was led by the Walter and Eliza Hall Institute and used the Australian Synchrotron in Melbourne. The study was published in the journal Nature.
For more than 20 years scientists have been trying to solve the mystery of how insulin binds to the insulin receptor. A research team led by Associate Professor Mike Lawrence, Dr Colin Ward and Dr John Menting have now found the answer.
Associate Professor Lawrence from the institute’s Structural Biology division said the team was excited to reveal for the first time a three-dimensional view of insulin bound to its receptor. “Understanding how insulin interacts with the insulin receptor is fundamental to the development of novel insulins for the treatment of diabetes,” Associate Professor Lawrence said. “Until now we have not been able to see how these molecules interact with cells. We can now exploit this knowledge to design new insulin medications with improved properties, which is very exciting.”
The Australian Synchrotron’s MX2 microcrystallography beamline was critical to the project’s success. “If we did not have this fantastic facility in Australia and their staff available to help us, we would simply not have been able to complete this project,” Associate Professor Lawrence said.
Associate Professor Lawrence assembled an international team of project collaborators, including researchers from Case Western Reserve University, the University of Chicago, the University of York and the Institute of Organic Chemistry and Biochemistry in Prague. “Collaborations in this field are essential,” he said. “No one laboratory has all the resources, expertise and experience to take on a project as difficult as this one.”
“We have now found that the insulin hormone engages its receptor in a very unusual way,” Associate Professor Lawrence said. “Both insulin and its receptor undergo rearrangement as they interact – a piece of insulin folds out and key pieces within the receptor move to engage the insulin hormone. You might call it a ‘molecular handshake’.”
Australia is facing an increasing epidemic of type 2 diabetes. There are now approximately one million Australians living with diabetes and around 100,000 new diagnoses each year.
“Insulin controls when and how glucose is used in the human body,” Associate Professor Lawrence said. “The insulin receptor is a large protein on the surface of cells to which the hormone insulin binds. The generation of new types of insulin have been limited by our inability to see how insulin docks into its receptor in the body.
“Insulin is a key treatment for diabetics, but there are many ways that its properties could potentially be improved,” Associate Professor Lawrence said. “This discovery could conceivably lead to new types of insulin that could be given in ways other than injection, or an insulin that has improved properties or longer activity so that it doesn’t need to be taken as often. It may also have ramifications for diabetes treatment in developing nations, by creating insulin that is more stable and less likely to degrade when not kept cold, an angle being pursued by our collaborators. Our findings are a new platform for developing these kinds of medications.”
Mass. Eye and Ear Researchers Regenerate Sensory Hair Cells, Restore Hearing to Noise-Damaged Ears
Hearing loss is a significant public health problem affecting almost 50 million people in the United States alone. Sensorineural hearing loss is the most common form and is caused by the loss of sensory hair cells in the cochlea. Hair cell loss results from a variety of factors including noise exposure, aging, toxins, infections, and certain antibiotics and anti-cancer drugs. Although hearing aids and cochlear implants can ameliorate the symptoms somewhat, there are no known treatments to restore hearing, because auditory hair cells in mammals, unlike those in birds or fish, do not regenerate once lost. Auditory hair cell replacement holds great promise as a treatment that could restore hearing after loss of hair cells.
In the Jan. 10 issue of Neuron, Massachusetts Eye and Ear and Harvard Medical School researchers demonstrate for the first time that hair cells can be regenerated in an adult mammalian ear by using a drug to stimulate resident cells to become new hair cells, resulting in partial recovery of hearing in mouse ears damaged by noise trauma. This finding holds great potential for future therapeutic application that may someday reverse deafness in humans.
“Hair cells are the primary receptor cells for sound and are responsible for the sense of hearing,” explains senior author, Dr. Albert Edge, of Harvard Medical School and Mass. Eye and Ear. “We show that hair cells can be generated in a damaged cochlea and that hair cell replacement leads to an improvement in hearing.”
In the experiment, the researchers applied a drug to the cochlea of deaf mice. The drug had been selected for its ability to generate hair cells when added to stem cells isolated from the ear. It acted by inhibiting an enzyme called gamma-secretase that activates a number of cellular pathways. The drug applied to the cochlea inhibited a signal generated by a protein called Notch on the surface of cells that surround hair cells. These supporting cells turned into new hair cells upon treatment with the drug. Replacing hair cells improved hearing in the mice, and the improved hearing could be traced to the areas in which supporting cells had become new hair cells.
“The missing hair cells had been replaced by new hair cells after the drug treatment, and analysis of their location allowed us to correlate the improvement in hearing to the areas where the hair cells were replaced,” Dr. Edge said.
This is the first demonstration of hair cell regeneration in an adult mammal. “We’re excited about these results because they are a step forward in the biology of regeneration and prove that mammalian hair cells have the capacity to regenerate,” Dr. Edge said. “With more research, we think that regeneration of hair cells opens the door to potential therapeutic applications in deafness.”
First Alzheimer’s case has full diagnosis 106 years later
More than a hundred years after Alois Alzheimer identified Alzheimer’s disease in a patient an analysis of that original patient’s brain has revealed the genetic origin of their condition.
The brain specimen tested was discovered in a university basement late last century after a search by rival teams of academics.
"It is extremely satisfying to place this last piece in the medical puzzle that Auguste Deter, the first ever Alzheimer patient, presented us with,” said Professor Manuel Graeber, from the University of Sydney.
"It is not only of historical interest, however, as it ends any speculation about whether the disease is correctly named after Alois Alzheimer. Alzheimer’s ability to recognise this dementia more than a century ago provides compelling support for specialisation in medicine. Alzheimer was a founding father of neuropathology, an important medical specialty that is still underrepresented."
Professor Graeber, from the University’s Brain and Mind Research Institute, Sydney Medical School and the Faculty of Health Sciences, collaborated with Professor Ulrich Müller’s team from the Institute of Human Genetics of the University of Giessen in Germany to produce the molecular diagnosis recently published in Lancet Neurology.
For years scientists have been wondering whether the first case of Alzheimer’s disease had a genetic cause. In 1901 Auguste Deter, a middle-aged female patient at the Frankfurt Asylum with unusual symptoms, including short-term memory loss, came to the attention of Dr Alzheimer. When she died, Dr Alzheimer examined her brain and described the distinctive damage indicating a form of presenile dementia.
For decades the more than 200 slides that Alzheimer prepared from Deter’s brain were lost. Then in 1992, after Professor Graeber uncovered new information pointing to their location, two teams of medical researchers began a dramatic race to find them.
One team searched in Frankfurt but it was a team headed by Professor Graeber, then working at the Max Planck Institute for Neurobiology that finally located the material at the University of Munich in 1997.
The slides were examined and confirmed beyond doubt that Deter was suffering from Alzheimer’s disease, with large numbers of amyloid plaques and neurofribrillary tangles in the brain that are hallmarks of the disease. Until now a more sophisticated DNA analysis of the small amount of fragile material in single slides has not been possible.
Since their rediscovery, a significant number of brain slides have been under the official custodianship of Professor Graeber who has been at the University of Sydney since 2010. He is preparing a book on the material.
"We found a mutation whose ultimate effect is the formation of amyloid plaques. These plaques, which form between nerve cells and seem to suffocate them are the key diagnostic landmark of the disease."
Alzheimer’s disease represents one of the greatest health problems in industrialised societies today. An estimated 100 million dementia sufferers are predicted worldwide by 2050, the vast majority of whom will have Alzheimer’s disease.
95 percent of Alzheimer’s patients suffer late onset of the illness after they turn 65. Five percent fall ill before that age (early onset) and Auguste Deter belongs to this group.
"We have revealed that Auguste Deter is one of those in which early onset of the disease is caused by mutation in a single gene," said Professor Graeber.