Posts tagged brain
Articles and news from the latest research reports.
Tripping the switches on brain growth to treat depression
Depression takes a substantial toll on brain health. Brain imaging and post-mortem studies provide evidence that the wealth of connections in the brain are reduced in individuals with depression, with the result of impaired functional connections between key brain centers involved in mood regulation. Glial cells are one of the cell types that appear to be particularly reduced when analyzing post-mortem brain tissue from people who had depression. Glial cells support the growth and function of nerve cells and their connections.
Over the past several years, it has become increasingly recognized that antidepressants produce positive effects on brain structure that complement their effects on symptoms of depression. These structural effects of antidepressants appear to depend, in large part, on their ability to raise the levels of growth factors in the brain.
In a new study, Elsayed and colleagues from the Yale University School of Medicine report their findings on a relatively novel growth factor named fibroblast growth factor-2 or FGF2. They found that FGF2 can increase the number of glial cells and block the decrease caused by chronic stress exposure by promoting the generation of new glial cells.
Senior author Dr. Ronald Duman said, “Our study uncovers a new pathway that can be targeted for treating depression. Our research shows that we can increase the production and maintenance of glial cells that are important for supporting neurons, providing an enriched environment for proper neuronal function.”
To study whether FGF2 can treat depression, the researchers used rodent models where animals are subjected to various natural stressors, which can trigger behaviors that are similar to those expressed by depressed humans, such as despair and loss of pleasure. FGF2 infusions restored the deficit in glial cell number caused by chronic stress. An underlying molecular mechanism was also identified when the data showed that antidepressants increase glial generation and function via increasing FGF2 signaling.
"Although more research is warranted to explore the contribution of glial cells to the antidepressant effects of FGF2, the results of this study present a fundamental new mechanism that merits attention in the quest to find more efficacious and faster-acting antidepressant drugs," concluded Duman.
"The deeper that science digs into the biology underlying antidepressant action, the more complex it becomes. Yet understanding this complexity increases the power of the science, suggesting reasons for the limitations of antidepressant treatment and pointing to novel approaches to the treatment of depression," commented Dr. John Krystal, Editor of Biological Psychiatry and Chairman of the Department of Psychiatry at the Yale University School of Medicine.
Source: Bio-Medicine
Low-Power Chips to Model a Billion Neurons
It’s a little sobering, actually. The average human brain packs a hundred billion or so neurons—connected by a quadrillion (1015) constantly changing synapses—into a space the size of a cantaloupe. It consumes a paltry 20 watts, much less than a typical incandescent lightbulb. But simulating this mess of wetware with traditional digital circuits would require a supercomputer that’s a good 1000 times as powerful as the best ones we have available today. And we’d need the output of an entire nuclear power plant to run it.
Fortunately, we don’t have to rely on traditional, power-hungry computers to get us there. Scattered around the world are at least half a dozen projects dedicated to building brain models using specialized analog circuits. Unlike the digital circuits in traditional computers, which could take weeks or even months to model a single second of brain operation, these analog circuits can model brain activity as fast as or even faster than it really occurs, and they consume a fraction of the power. But analog chips do have one serious drawback—they aren’t very programmable. The equations used to model the brain in an analog circuit are physically hardwired in a way that affects every detail of the design, right down to the placement of every analog adder and multiplier. This makes it hard to overhaul the model, something we’d have to do again and again because we still don’t know what level of biological detail we’ll need in order to mimic the way brains behave.
To help things along, my colleagues and I are building something a bit different: the first low-power, large-scale digital model of the brain. Dubbed SpiNNaker, for Spiking Neural Network Architecture, our machine looks a lot like a conventional parallel computer, but it boasts some significant changes to the way chips communicate. We expect it will let us model brain activity with speeds matching those of biological systems but with all the flexibility of a supercomputer.
Another team, led by Dharmendra Modha at IBM Almaden Research Center, in San Jose, Calif., works on supercomputer models of the cortex, the outer, information-processing layer of the brain, using simpler neuron models. In 2009, team members at IBM and Lawrence Livermore National Laboratory showed they could simulate the activity of 900 million neurons connected by 9 trillion synapses, more than are in a cat’s cortex. But as has been the case for all such models, its simulations were quite slow. The computer needed many minutes to model a second’s worth of brain activity.
One way to speed things up is by using custom-made analog circuits that directly mimic the operation of the brain. Traditional analog circuits—like the chips being developed by the BrainScaleS project at the Kirchhoff Institute for Physics, in Heidelberg, Germany—can run 10 000 times as fast as the corresponding parts of the brain. They’re also fabulously energy efficient. A digital logic circuit may need thousands of transistors to perform a multiplication, but analog circuits need only a few. When you break it down to the level of modeling the transmission of a single neural signal, these circuits consume about 0.001 percent as much energy as a supercomputer would need to perform the same task. Considering you’d need to perform that operation 10 quadrillion times a second, that translates into some significant energy savings. While a whole brain model built using today’s digital technology could easily consume more than US $10 billion a year in electricity, the power bill for a similar-scale analog system would likely come to less than $1 million.
Long-Term Methadone Treatment Can Affect Nerve Cells in Brain
ScienceDaily (Aug. 15, 2012) — Long-term methadone treatment can cause changes in the brain, according to recent studies from the Norwegian Institute of Public Health. The results show that treatment may affect the nerve cells in the brain. The studies follow on from previous studies where methadone was seen to affect cognitive functioning, such as learning and memory.
Since it is difficult to perform controlled studies of methadone patients and unethical to attempt in healthy volunteers, rats were used in the studies. Previous research has shown that methadone can affect cognitive functioning in both humans and experimental animals.
Sharp decrease in key signaling molecule
Rats were given a daily dose of methadone for three weeks. Once treatment was completed, brain areas which are central for learning and memory were removed and examined for possible neurobiological changes or damage.
In one study, on the day after the last exposure to methadone, there was a significant reduction (around 70 per cent) in the level of a signal molecule which is important in learning and memory, in both the hippocampus and in the frontal area of the brain. This reduction supports findings from a previous study (Andersen et al., 2011) where impaired attention in rats was found at the same time. At this time, methadone is no longer present in the brain. This indicates that methadone can lead to cellular changes that affect cognitive functioning after the drug has left the body, which may be cause for concern.
No effect on cell generation
The second study, a joint project with Southwestern University in Texas, investigated whether methadone affects the formation of nerve cells in the hippocampus. Previous research has shown that new nerve cells are generated in the hippocampus in both adult humans and rats, and that this formation is probably important for learning and memory. Furthermore, it has been shown that other opiates such as morphine and heroin can inhibit this formation. It was therefore reasonable to assume that methadone, which is also an opiate, would have the same effect.
However, the researchers did not find any change in the generation of new nerve cells after long-term methadone treatment. If the same is true in humans, this is probably more positive for methadone patients than continuing with heroin. However, the researchers do not know what effect methadone has on nerve cells that have previously been exposed to heroin.
Large gaps in knowledge
Since the mid-1960s, methadone has been used to treat heroin addiction. This is considered to be a successful treatment but, despite extensive and prolonged use, little is known about possible side effects. There are large knowledge gaps in this field.
Our studies show that prolonged methadone treatment can affect the nerve cells, and thus behaviour, but the results are not always as expected. Many more pre-clinical and clinical studies are needed to understand methadone’s effect on the brain, how this can result in altered cognitive function, and, if so, how long these changes last. Knowledge of this is important — both for the individual methadone patient and the outcome of treatment.
Source: Science Daily
Brain scans have revealed distinctive features in the brain structure of karate experts that are associated with how well they performed in a test of punching ability.
Researchers from Imperial College London and UCL looked for differences in brain structure between 12 karate practitioners with a black belt rank and an average of 13.8 years’ karate experience, and 12 people of similar age who exercised regularly but did not have any martial arts experience.
Dr Ed Roberts, from the Department of Medicine at Imperial College London, who led the study, explained: "The karate black belts were able to repeatedly coordinate their punching action with a level of coordination that novices can’t produce. We think that ability might be related to fine-tuning of neural connections in the cerebellum, allowing them to synchronise their arm and trunk movements very accurately."
The scans used in this study, called diffusion tensor imaging (DTI), detected structural differences in the white matter of parts of the brain called the cerebellum and the primary motor cortex, which are known to be involved in controlling movement. The differences measured by DTI in the cerebellum correlated with the synchronicity of the subjects’ wrist and shoulder movements when punching.
The DTI signal also correlated with the age at which karate experts began training and their total experience of the discipline. These findings suggest that the structural differences in the brain are related to the black belts’ punching ability.
(Image credit: Adam J. Merton on Flickr)
Scientists Discover Previously Unknown Cleansing System in Brain
A previously unrecognized system that drains waste from the brain at a rapid clip has been discovered by neuroscientists at the University of Rochester Medical Center. The findings were published online August 15 in Science Translational Medicine.
The highly organized system acts like a series of pipes that piggyback on the brain’s blood vessels, sort of a shadow plumbing system that seems to serve much the same function in the brain as the lymph system does in the rest of the body – to drain away waste products.
“Waste clearance is of central importance to every organ, and there have been long-standing questions about how the brain gets rid of its waste,” said Maiken Nedergaard, M.D., D.M.Sc., senior author of the paper and co-director of the University’s Center for Translational Neuromedicine. This work shows that the brain is cleansing itself in a more organized way and on a much larger scale than has been realized previously.
Acute Stress Alters Control of Gene Activity: Researchers Examine DNA Methylation
ScienceDaily (Aug. 15, 2012) — Acute stress alters the methylation of the DNA and thus the activity of certain genes. This is reported by researchers at the Ruhr-Universität Bochum together with colleagues from Basel, Trier and London for the first time in the journal Translational Psychiatry. “The results provide evidence how stress could be related to a higher risk of mental or physical illness,” says Prof. Dr. Gunther Meinlschmidt from the Clinic of Psychosomatic Medicine and Psychotherapy at the LWL University Hospital of the RUB. The team looked at gene segments which are relevant to biological stress regulation.
In stressful social situations, the methylation patterns (bright spheres) of the DNA change. (Credit: Illustration: Christoph Unternährer and Christian Horisberger)
Epigenetics — the “second code” — regulates gene activity
Our genetic material, the DNA, provides the construction manual for the proteins that our bodies need. Which proteins a cell produces depends on the cell type and the environment. So-termed epigenetic information determines which genes are read, acting quasi as a biological switch. An example of such a switch is provided by methyl (CH3) groups that attach to specific sections of the DNA and can remain there for a long time — even when the cell divides. Previous studies have shown that stressful experiences and psychological trauma in early life are associated with long-term altered DNA methylation. Whether the DNA methylation also changes after acute psychosocial stress, was, however, previously unknown.
Two genes tested
To clarify this issue, the research group examined two genes in particular: the gene for the oxytocin receptor, i.e. the docking site for the neurotransmitter oxytocin, which has become known as the “trust hormone” or “anti-stress hormone”; and the gene for the nerve growth factor Brain-Derived Neurotrophic Factor (BDNF), which is mainly responsible for the development and cross-linking of brain cells. The researchers tested 76 people who had to participate in a fictitious job interview and solve arithmetic problems under observation — a proven means for inducing acute stress in an experiment. For the analysis of the DNA methylation, they took blood samples from the subjects before the test as well as ten and ninety minutes afterwards.
DNA methylation changes under acute psychosocial stress
Stress had no effect on the methylation of the BDNF gene. In a section of the oxytocin receptor gene, however, methylation already increased within the first ten minutes of the stressful situation. This suggests that the cells formed less oxytocin receptors. Ninety minutes after the stress test, the methylation dropped below the original level before the test. This suggests that the receptor production was excessively stimulated.
Possible link between stress and disease
Stress increases the risk of physical or mental illness. The stress-related costs in Germany alone amount to many billions of Euros every year. In recent years, there have been indications that epigenetic processes are involved in the development of various chronic diseases such as cancer or depression. “Epigenetic changes may well be an important link between stress and chronic diseases” says Prof. Meinlschmidt, Head of the Research Department of Psychobiology, Psychosomatics and Psychotherapy at the LWL University Hospital. “We hope to identify more complex epigenetic stress patterns in future and thus to be able to determine the associated risk of disease. This could provide information on new approaches to treatment and prevention.” The work originated within the framework of an interdisciplinary research consortium with the University of Trier, the University of Basel and King’s College London. The German Research Foundation and the Swiss National Science Foundation supported the study.
Source: Science Daily
In a major breakthrough, an international team of scientists has proven that addiction to morphine and heroin can be blocked, while at the same time increasing pain relief.
The team from the University of Adelaide and University of Colorado has discovered the key mechanism in the body’s immune system that amplifies addiction to opioid drugs. Laboratory studies have shown that the drug (+)-naloxone will selectively block the immune-addiction response. The results - which could eventually lead to new co-formulated drugs that assist patients with severe pain, as well as helping heroin users to kick the habit - will be published in the Journal of Neuroscience.
"Our studies have shown conclusively that we can block addiction via the immune system of the brain, without targeting the brain’s wiring," says the lead author of the study, Dr Mark Hutchinson, ARC Research Fellow in the University of Adelaide’s School of Medical Sciences.
"Both the central nervous system and the immune system play important roles in creating addiction, but our studies have shown we only need to block the immune response in the brain to prevent cravings for opioid drugs."
Watch a video of Dr Mark Hutchinson talking about this study.
Yale researchers studying epileptic seizures have shed new light on the neurological origins of consciousness.
When epileptics lose consciousness during a variety of types of seizures, the signals converge on the same brain structures, but through different pathways, says Dr. Hal Blumenfeld, professor of neurology, neurobiology, and neurosurgery.
“Understanding of these mechanisms could lead to improved treatment strategies to prevent impairment of consciousness and improve the quality of life of people with epilepsy,” he said.
Blumenfeld’s research is described in the current issue of the journal Lancet Neurology.
(Image: The fMRI images are different viewpoints of the brain of a child experiencing an epileptic seizure. Areas in yellow and orange represent increased brain activity compared to its normal state, while areas in blue show decreased activity. These are the areas of the brain needed for normal consciousness.)
The stalked eyes of mantis shrimp species that live in shallow water can have up to 16 kinds of photoreceptor cells, 12 of which are specialized for different colors. People make do with four kinds, three of which pick up colors.
Hanne Thoen of the University of Queensland in Brisbane, Australia, tested the color vision of mantis shrimp by training them to scoot out of their burrows toward a pair of optical fibers and punch at the one glowing a particular color. As she narrowed the color gap between the two fibers, she could tell when the animals no longer discerned a difference.
So far, Thoen has tested her mantis shrimp on six target colors ranging from a 425-nanometer purple to a 628-nanometer red. If the animals perform just as poorly at distinguishing colors in other wavelengths, then mantis shrimp may be using some unknown system of color perception.
People and other animals studied so far distinguish colors through brainpower by interpreting competing activity in different kinds of light-receptor cells. Instead of doing such fancy brainwork, mantis shrimp may just rely on what a particular specialized cell responds to strongly. Wavelengths that tickle the purple-sensitive cells may be just plain purple regardless of whether they’re more toward the blue or the ultraviolet.
Unlocking a major secret of the brain
McGill researchers uncover crucial link between hippocampus and prefrontal cortex
A clue to understanding certain cognitive and mental disorders may involve two parts of the brain which were previously thought to have independent functions, according to a McGill University team of researchers led by Prof. Yogita Chudasama, of the Laboratory of Brain and Behavior, Department of Psychology. The McGill team discovered a critical interaction between two prominent brain areas: the hippocampus, a well-known memory structure made famous by Dr. Brenda Milner’s patient H.M., and the prefrontal cortex, which is involved in decision-making and inhibiting inappropriate behaviours.
“We had always thought that the hippocampus and the prefrontal cortex functioned independently,” says Prof. Chudasama. “Our latest study provides the first indication that that is not the case.”
The team’s finding, just published in the Journal of Neuroscience, reveals a critical interaction between these two brain areas and the control of behavior, and may advance the treatment of some cognitive and mental disorders including schizophrenia, and depression. The interaction between the hippocampus and the prefrontal cortex shows that brain circuits function not just as specific parts of the brain, but are linked together and work as a system.
“Although the prefrontal cortex has long been known to be the driving force that steers our behavior, pushing us to make good decisions and withhold improper actions, it turns out that it can’t do this unless it interacts with the hippocampus,” added Prof. Chudasama. “We found that when we prevented these two structures from communicating with each other, like humans with compulsive disorders, rats persisted with behaviours that were not good for them; they didn’t correct their errant behaviours and could not control their natural urges.
The ability to control impulsive urges or inhibit our actions allows us to interact normally in personal or social situations, and this type of behaviour depends on the normal interaction of the hippocampus and the prefrontal cortex. This result provides a means for understanding the neural basis for social and cognitive deficits in disorders of brain and behaviour, such as those with frontotemporal dementia”, concludes Prof. Chudasama.