Posts tagged neuroscience
Articles and news from the latest research reports.
New merciful treatment method for children with brain tumours
Children who undergo brain radiation therapy run a significant risk of suffering from permanent neurocognitive adverse effects. These adverse effects are due to the fact that the radiation often encounters healthy tissue. This reduces the formation of new cells, particularly in the hippocampus – the part of the brain involved in memory and learning.
Researchers at the University of Gothenburg’s Sahlgrenska Academy have used a model study to test newer radiation therapy techniques which could reduce these harmful adverse effects. The researchers based their study on a number of paediatric patients who had undergone conventional radiation treatment for medulloblastoma, a form of brain tumour that almost exclusively affects children, and simulated treatment plans using proton therapy techniques and newer photon therapy techniques.
Each treatment plan was personalised by physician Malin Blomstrand, physicist Patrik Brodin and their colleagues. The results show that the risk of neurocognitive adverse effects can be reduced significantly using the new radiation treatment techniques, particularly proton therapy.
“This could mean a better quality of life for children who are forced to undergo brain radiation therapy,” says Malin Blomstrand.
A Future Without Seizures
Five-year-old Nathan Kalina of Naperville will enter kindergarten this fall after spending the summer in day camp: playing games, enjoying field trips, and romping in the pool. He loves playing with action figures and acting out scenes from his favorite movies.
The scene two years ago was very different. After getting a few reports from daycare about unexplained falls, Nathan’s parents started to notice him having minor seizures. His mother, Megan, wasn’t too concerned at first; both she and her father had had childhood seizures and recovered from them without incident. Then came Nathan’s first tonic-clonic seizure (formerly known as a “grand mal” seizure), a major event involving his whole brain and body. A trip to a local emergency room for basic tests led to an electroencephalogram a few days later. All the while Nathan was having more seizures, large and small.
"We went from zero to crazy in a matter of days," Megan said.
Medication helped some. Nathan’s father David, a teacher in the Naperville schools, devoted his summer to adjusting Nathan’s regimen. But in the fall, the seizures ramped up again. One specialist suggested a high-fat ketogenic diet, which has been shown to help some children with epilepsy — but it didn’t help Nathan. “Feeding a 4-year-old picky eater on meat, cheese and cream was hard on us and started making him sick,” Megan said.
PNAS Study: Language Structure Arises from Balance of Clear and Effective Communication
When learning a new language, we automatically organize words into sentences that will be both clearly understood and efficient (quick) to communicate. That’s the finding of a new study reported today in the Proceedings of the National Academy of Sciences (PNAS) which challenges opposing theories on why and how languages come to be organized the way they are.
With more than 5000 languages in the world, it would be easy to assume all vary endlessly, but, in fact, there is great commonality: languages follow only a few recurrent patterns. These commonalities are called “language universals,” a notion suggested in the 1960’s by Noam Chomsky and Joseph Greenberg. A team of researchers from the University of Rochester and Georgetown University Medical Center set out to investigate how these language universals come to be.
Linguists and cognitive scientists have opposing ideas on how a language is developed and shaped. Some believe that languages all derived from a common ancestor; others think that languages vary quite widely and universals do not exist at all. Some have suggested that language universals are an arbitrary evolutionary outcome. The position of the Rochester-Georgetown team is that the human mind shapes a language, even while learning it, based on the need for robust and effective information transfer.
“The thousands of natural languages in our world only have a couple of formats in which they appear, and we are good at understanding and learning languages that have just these formats. Otherwise we could never succeed in learning something so complicated as human languages,” says one of the study’s authors, Elissa L. Newport, Ph.D., a professor in the department of neurology at Georgetown University Medical Center.
Evolution Mostly Driven by Brawn, Not Brains, Analysis Finds
The most common measure of intelligence in animals, brain size relative to body size, may not be as dependent on evolutionary selection on the brain as previously thought, according to a new analysis by scientists.
Brain size relative to body size has been used by generations of scientists to predict an animal’s intelligence. For example, although the human brain is not the largest in the animal kingdom in terms of volume or mass, it is exceptionally large considering our moderate body mass.
Now, a study by a team of scientists at UCL, the University of Konstanz, and the Max Planck Institute of Ornithology has found that the relationship between the two traits is driven by different evolutionary mechanisms in different animals.
Crucially, researchers have found that the most significant factor in determining relative brain size is often evolutionary pressure on body size, and not brain size. For example, the evolutionary history of bats reveals they decreased body size much faster than brain size, leading to an increase in relative brain size. As a result, small bats were able to evolve improved flying maneuvrability while maintaining the brainpower to handle foraging in cluttered environments.
This shows that relative brain size can not be used unequivocally as evidence of selection for intelligence. The study is published in the Proceedings of the National Academy of Sciences.
Theresa Klein talks about Achilles, the first machine to move in a biologically accurate way.
"Our robot, named Achilles, is the first to walk in a biologically accurate way. That means it doesn’t just move like a person, but also sends commands to the legs like the human nervous system does.
Each leg has eight muscles—Kevlar straps attached to a motor on one end and to the plastic skeleton on the other. As the motor turns, it pulls the strap, mimicking the way our muscles contract. Some of Achilles’ muscles extend from the hip or thigh to the lower leg so they can project forces all the way down the limb. This allows us to put most of the motors in the hips and thighs. Placing them up high keeps the lower leg light, so that it can swing quickly like a human’s lower leg.
In people, neurons in the spinal column send out rhythmic signals that control our legs. It’s like a metronome, and sensory feedback from the legs alters the pace. Your brain can step in to make corrections, but it doesn’t explicitly control every muscle, which is essentially why you can walk without thinking about it. For our robot, a computer program running off an external PC controls movement in a similar way. With each step, the computer sends a signal to flex one hip muscle and extend the other. The computer changes the timing of those signals based on feedback from the legs’ load and angle sensors. A similar control system handles the lower muscles.
Modeling human movement has applications outside of robotics. It could also help us understand how people recover after spinal-cord injuries, for example. But our robot is still a very simplified model—it has no torso and can’t handle complex terrain. Initially, we also had a problem with its feet slipping. We thought about different types of rubber to give its feet more grip but eventually realized a solution already exists. Now, the robot wears a pair of Keds.”
An immunosuppressive drug could delay the onset of neurodegenerative diseases
Rapamycin, a drug used to prevent rejection in transplants, could delay the onset of neurodegenerative diseases such as Alzheimer’s and Parkinson’s. This is the main conclusion of a study published in the Nature in which has collaborated the researcher Isidro Ferrer, head of the group of Neuropathology at the Bellvitge Biomedical Research Institute (IDIBELL) and the Bellvitge University Hospital and Full Professor of Pathological Anatomy at the University of Barcelona. The research was led by researchers from the International School for Advanced Studies (SISSA) in Trieste (Italy).
The collaboration of the research group led by Dr. Ferrer with SISSA researchers began five years ago when they observed that Parkinson’s patients showed a deficit in UCHL1 protein. At that time, researchers didn’t know what mechanism produced this deficit. To discover it a European project was launched. It was coordinated by the Italian researchers and participated by other European research groups, including the group led by Dr. Ferrer. The project, called Dopaminet, focused on how dopaminergic neurons (brain cells whose neurotransmitter is dopamine) are involved in Parkinson’s disease.
Contrary to most common hypothesis that a DNA fragment encodes a protein through a messenger RNA molecule, the researchers found that it also works in reverse. They found a balance between the protein and its mirror protein, which is configured in reverse, and they are mutually controlled. If the protein mirror is located in the nucleus of the cell, it does not interact with the protein, while if it is in the cytoplasm, then both of them interact.
In the case of Parkinson’s disease the protein UCHL1 appears reduced and also its mirror protein is localized in the nucleus, and in the cytoplasm. Thus, the researchers sought a method to extract the mirror protein from the nucleus and made it interact with the original UCHL1 protein. The authors found that rapamycin was able to extract them from the nucleus. The drug allows the two proteins, the UCHL1 and its mirror, hold together in the cytoplasm, which would correct the mistakes that occur in Parkinson’s disease.
This in vitro research has allowed describing a new unknown mechanism. It is necessary that the UCHL1 mirror protein should accumulate in the nucleus and escape from the cytoplasm and join the UCLH1 protein. The combination of both makes the system work.
"The rapamycin can not cure Parkinson’s disease, but it may delay the onset of neurodegenerative diseases such as Alzheimer’s and Parkinson’s itself. Rapamycin can protect and delay the beginning of these diseases. It can complete the treatment, but it should be combined with other existing treatments", explains Isidro Ferrer.
Anyway, it is still far its application in patients. The next step is to validate these results in animal models and study the effects of rapamycin in combination with other drugs.
(Source: idibell.cat)
Replicating Risk Genes in Bipolar Disorder
One of the biggest challenges in psychiatric genetics has been to replicate findings across large studies.
Scientists at King’s College London, Institute of Psychiatry have now performed one of the largest ever genetic replication studies of bipolar affective disorder, with 28,000 subjects recruited from 36 different research centers. Their findings provide compelling evidence that the chromosome 3p21.1 locus contains a common genetic risk for bipolar disorder, the PBRM1 gene.
The locus at 3p21.1 has also been previously associated with depression and schizophrenia. Using a separate dataset of over 34,000 subjects, they did not confirm association of this same variant with schizophrenia.
Thus, they replicated the association of the marker with bipolar disorder, but not with schizophrenia. This is an interesting finding, in that it distinguishes the heritable risk for bipolar disorder and schizophrenia. It contrasts with the majority of studies that have found that schizophrenia risk genes also contribute to the risk for bipolar disorder.
"This study adds to the recent rapid progress in identifying genes for mental illness. The last few years have seen the identification of about two dozen genetic loci for bipolar disorder and schizophrenia," commented first author Evangelos Vassos. "About half of these are shared between these two disorders, indicating they share some, but not all, genetic causes."
Due to the conflicting results, it is clear that more work is needed to determine the role this locus plays in psychosis, but the evidence seems solid that it is associated with bipolar disorder.
Researchers reveal first brain study of Temple Grandin
Temple Grandin, perhaps the world’s most famous person with autism, has exceptional nonverbal intelligence and spatial memory, and her brain has a host of structural and functional differences compared with the brains of controls, according to a presentation Saturday at the 2012 Society for Neuroscience annual meeting in New Orleans.
Grandin, professor of animal sciences at Colorado State University, is an outspoken advocate for autism research and awareness. She is known as a ‘savant,’ or a person who shows characteristic social deficits of autism and yet also has some exceptional abilities. For instance, she has extremely sharp visual acuity.
This is the first study to take a close look at Grandin’s brain, and one of the first to look at the brains of savants.
Developing brain is source of stability and instabilty in adolescence
Scientists are presenting new research on how the brain develops during the dynamic and vulnerable transition period from childhood to adulthood. The findings underscore the uniqueness of adolescence, revealing factors that may influence depression, decision-making, learning, and social relationships.
The findings were presented at Neuroscience 2012, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health.
The brain’s “reward system,” those brain circuits and structures that mediate the experience and pursuit of pleasure, figured prominently in several studies. The studies shed light on adolescents’ ability to control impulsivity and think through problems; reveal physical changes in the “social brain;” document connections between early home life and brain function in adolescence; and examine the impact of diet on depressive-like behavior in rodents.
Today’s new findings show that:
- Adolescents can throw impulsivity out the window when big rewards are at stake. The bigger the reward, the more thoughtful they can be, calling on important brain regions to gather and weigh evidence, and make decisions that maximize gains (BJ Casey, PhD).
- Rodents that receive an omega-3 fatty acid in their diets, from gestation through their early development, appear less vulnerable to depressive-like behaviors during adolescence (Christopher Butt, PhD).
- Depression in older adolescent boys may be associated with changes in communication between regions of the brain that process reward. At the same time, the study found possible connections between early emotional attachments — particularly with mothers — and later reward system function (Erika Forbes, PhD).
- Early cognitive stimulation appears to predict the thickness of parts of the human cortex in adolescence, and experiences at age four appear to have a greater impact than those at age eight (Martha Farah, PhD).
- During the span of adolescence, the volume of the “social brain” — those areas that deal with understanding other people — changes substantially, with notable gender differences (Kathryn Mills, BA).
"Advances in neuroscience continue to delve deeper and deeper into the unique and dynamically changing biology of the adolescent brain," said press conference moderator Jay Giedd, MD, of the National Institute of Mental Health, an expert on childhood and adolescent brain development. "The insights are beginning to elucidate the mechanisms that make the teen years a time of particular vulnerabilities but also a time of great opportunity."
(Source: sciencedaily.com)
Neuroscientists find the molecular “When” and “Where” of memory formation
Neuroscientists from New York University and the University of California, Irvine have isolated the “when” and “where” of molecular activity that occurs in the formation of short-, intermediate-, and long-term memories. Their findings, which appear in the journal the Proceedings of the National Academy of Sciences, offer new insights into the molecular architecture of memory formation and, with it, a better roadmap for developing therapeutic interventions for related afflictions.
“Our findings provide a deeper understanding of how memories are created,” explained the research team leader Thomas Carew, a professor in NYU’s Center for Neural Science and dean of NYU’s Faculty of Arts and Science. “Memory formation is not simply a matter of turning molecules on and off; rather, it results from a complex temporal and spatial relationship of molecular interaction and movement.”
Neuroscientists have previously uncovered different aspects of molecular signaling relevant to the formation of memories. But less understood is the spatial relationship between molecules and when they are active during this process.
To address this question, the researchers studied the neurons in Aplysia californica, the California sea slug. Aplysia is a model organism that is quite powerful for this type of research because its neurons are 10 to 50 times larger than those of higher organisms, such as vertebrates, and it possesses a relatively small network of neurons—characteristics that readily allow for the examination of molecular signaling during memory formation. Moreover, its coding mechanism for memories is highly conserved in evolution, and thus is similar to that of mammals, making it an appropriate model for understanding how this process works in humans.
The scientists focused their study on two molecules, MAPK and PKA, which earlier research has shown to be involved in many forms of memory and synaptic plasticity—that is, changes in the brain that occur after neuronal interaction. But less understood was how and where these molecules interacted.
To explore this, the researchers subjected the sea slugs to sensitization training, which induces increased behavioral reflex responsiveness following mild tail shock, or in this study, mild activation of the nerve form the tail. They then examined the subsequent molecular activity of both MAPK and PKA. Both molecules have been shown to be involved in the formation of memory for sensitization, but the nature of their interaction is less clear.
What they found was MAPK and PKA coordinate their activity both spatially and temporally in the formation of memories. Specifically, in the formation of intermediate-term (i.e., hours) and long-term (i.e., days) memories, both MAPK and PKA activity occur, with MAPK spurring PKA action. By contrast, for short-term memories (i.e., less than 30 minutes), only PKA is active, with no involvement of MAPK.
(Source: nyu.edu)