Posts tagged neuroscience
Articles and news from the latest research reports.
Although images in textbooks generally represent phylogenetic trees with trunks angling up and to the right, research shows that students have better comprehension when the trunks angle down to the right.
New Findings on Protein Misfolding
Misfolded proteins can cause various neurodegenerative diseases such as spinocerebellar ataxias (SCAs) or Huntington’s disease, which are characterized by a progressive loss of neurons in the brain. Researchers of the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch, Germany, together with their colleagues of the Université Paris Diderot, Paris, France, have now identified 21 proteins that specifically bind to a protein called ataxin-1. Twelve of these proteins enhance the misfolding of ataxin-1 and thus promote the formation of harmful protein aggregate structures, whereas nine of them prevent the misfolding (PLoS Genetics).
Proteins only function properly when the chains of amino acids, from which they are built, fold correctly. Misfolded proteins can be toxic for the cells and assemble into insoluble aggregates together with other proteins. Ataxin-1, the protein that the researchers have now investigated, is very prone to misfolding due to inherited gene defects that cause neurodegenerative diseases. The reason for this is that the amino acid glutamine is repeated in the amino acid chain of ataxin-1 very often - the more glutamine, the more toxic the protein. Approximately 40 repeats of glutamine are considered to be toxic for the cells.
Now, Dr. Spyros Petrakis, Dr. Miguel Andrade, Professor Erich Wanker and colleagues have identified 21 proteins that mainly interact with ataxin-1 and influence its folding or misfolding. Twelve of these proteins enhance the toxicity of ataxin-1 for the nerve cells, whereas nine of the identified proteins reduce its toxicity.
Furthermore, the researchers detected a common feature in the structure of those proteins that enhances toxicity and aggregation. It is a special structure scientists call “coiled-coil-domain” because it resembles a double twisted spiral or helix. Apparently this structure promotes aggregation, because proteins that interact with ataxin-1 and have this domain enhance the toxic effect of mutated ataxin-1. As the researchers said, this structure could be a potential target for therapy: “A careful analysis of the molecular details could help to discover drugs that suppress toxic processes.”
(Source: mdc-berlin.de)
Confirming earlier scientific doubts, a new study concludes that chronic fatigue syndrome is not caused by two viruses known as XMRV and pMLV.
Researchers from the U.S. National Institutes of Health, the U.S. Centers for Disease Control and Prevention, Columbia University and other institutions, including some scientists who did the original research, examined 147 patients with chronic fatigue syndrome from sites across the country and compared them to 146 healthy patients.
Bottom line? “This analysis reveals no evidence of either XMRV or pMLV infection,” the authors wrote. The study is published in the September/October issue of the journal mBio.
Alzheimer’s breaks brain networks’ coordination
Scientists at Washington University School of Medicine in St. Louis have taken one of the first detailed looks into how Alzheimer’s disease disrupts coordination among several of the brain’s networks. The results, reported in The Journal of Neuroscience, include some of the earliest assessments of Alzheimer’s effects on networks that are active when the brain is at rest.
“Until now, most research into Alzheimer’s effects on brain networks has either focused on the networks that become active during a mental task, or the default mode network, the primary network that activates when a person is daydreaming or letting the mind wander,” says senior author Beau Ances, MD, assistant professor of neurology. “There are, however, a number of additional networks besides the default mode network that become active when the brain is idling and could tell us important things about Alzheimer’s effects.”
Ances and his colleagues analyzed brain scans of 559 subjects. Some of these subjects were cognitively normal, while others were in the early stages of very mild to mild Alzheimer’s disease. Scientists found that all of the networks they studied eventually became impaired during the initial stages of Alzheimer’s.
“Communications within and between networks are disrupted, but it doesn’t happen all at once,” Ances says. “There’s even one network that has a momentary surge of improved connections before it starts dropping again. That’s the salience network, which helps you determine what in your environment you need to pay attention to.”
Other networks studied by the researchers included:
- the dorsal attention network, which directs attention toward things in the environment that are salient;
- the control network, believed to be active in consciousness and decision-making; and
- the sensory-motor network, which integrates the brain’s control of body movements with sensory feedback (e.g., did the finger that just moved strike the right piano key?).
Scientists also examined Alzheimer’s effects on a brain networking property known as anti-correlations. Researchers identify networks by determining which brain areas frequently become active at the same time, but anti-correlated networks are noteworthy for the way their activities fluctuate: when one network is active, the other network is quiet. This ability to switch back-and-forth between networks is significantly diminished in participants with mild to moderate Alzheimer’s disease.
The default mode network, previously identified as one of the first networks to be impaired by Alzheimer’s, is a partner in two of the three pairs of anti-correlated networks scientist studied.
“While we can’t prove this yet, one hypothesis is that as things go wrong in the processing of information in the default mode network, that mishandled data is passed on to other networks, where it creates additional problems,” Ances says.
It’s not practical to use these network breakdowns to clinically diagnose Alzheimer’s disease, Ances notes, but they may help track the development of the disease and aid efforts to better understand its spread through the brain.
Ances plans to look at other markers for Alzheimer’s disease in the same subjects, such as levels in the cerebrospinal fluid of amyloid beta, a major component of Alzheimer’s plaques.
(Source: news.wustl.edu)
A child who suffers a moderate or severe traumatic brain injury (TBI) may still have substantial functional disabilities and reduced quality of life 2 years after the injury. After those first 2 years, further improvement may be minimal. Better interventions are needed to prevent long-lasting consequences of TBI in children conclude the authors of a study published in Journal of Neurotrauma, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers.
Frederick Rivara and colleagues from University of Washington, Seattle, and Mary Bridge Children’s Hospital, Tacoma, WA, and Children’s Hospital of Philadelphia and the University of Pennsylvania, Philadelphia, PA, describe the functional and quality of life outcomes of children who experienced a moderate or severe TBI when they were 0-17 years of age. In the article “Persistence of Disability 24 to 36 Months after Pediatric Traumatic Brain Injury: A Cohort Study” they follow up on a previous report that found improvement in some areas of functioning for up to 24 months. In this expanded study, the authors showed no significant improvement in the children’s ability to function, participate in activities, or in their quality of life between 24 and 36 months post-injury, and they suggest that a plateau is reached in the recovery.
"This important communication by Rivara and colleagues reinforces the concept that pediatric traumatic brain injury is associated with significant enduring morbidity, with recovery plateauing over time," says John T. Povlishock, PhD, Editor-in-Chief of Journal of Neurotrauma and Professor, VCU Neuroscience Center, Medical College of Virginia, Richmond. “This finding also reinforces emerging thought that pediatric traumatic brain injury must be viewed in another context, rather than the current perception that the course of such injury parallels that found in the adult population.”
Imaging the network traffic in our brains
MRI brain scans no longer just show the various regions of brain activity; nowadays the networks in the brain can now be imaged with ever greater precision. This will make functional MRI (fMRI) increasingly powerful in the coming years, leading to tools that can be used in cognitive neuroscience. This is the claim made by Prof. David Norris in his inaugural lecture as Professor of Neuroimaging at the University of Twente on 13 September.
During the twenty years since the invention of fMRI (functional Magnetic Resonance Imaging) developments have come thick and fast, from initially identifying active brain regions to more complex analysis of the connections and hubs in the brain. In his inaugural lecture Norris describes how this has been achieved thanks to not only a growing understanding of the underlying biophysics but also rapid technological developments: scanners with larger magnetic fields, better image-processing techniques and algorithms. His aim is to go beyond merely localizing which parts of the brain are active. The challenge is to answer two questions: How are the various regions interconnected, structurally and functionally? What do the networks in our brains look like?
Faster and more powerful
Back in the 19th century scientists observed increased blood flow in brain regions that are functionally active. fMRI enables the change in oxygen content to be seen. Haemoglobin, the substance that transports oxygen in the blood, can take the form of oxyhaemoglobin (when it is still combined with oxygen) and deoxyhaemoglobin (when the oxygen has been released), each of which has different magnetic properties. One of the complicating factors when interpreting the scans is that various physiological mechanisms are at work simultaneously, causing the deoxyhaemoglobin level to rise and fall. One of the remedies to increase accuracy, Norris explains, has been to increase the magnetic field strength: there are now MRI scanners operating at 7 Tesla. At the same time the speed at which laminae can be imaged has gone up by leaps and bounds: the entire brain can be scanned in three seconds with a precision of 1 millimetre.
Hubs
The functional connections between parts of the brain can be registered by means of blood flow, but MRI also enables the structural and anatomical connections to be seen. This involves measuring the movement of water molecules caused by the ‘white matter’ in nerve fibres. This technology is known as diffusion-weighted imaging (DWI). Combining these technologies provides a wealth of fresh information on the networks in the brain and the places where many connections come together, the ‘hubs’. Not only have ‘known networks’ thus been proven, so have networks that neuroscience posits as plausible but that have never been measured.
Image showing the distribution of connector hubs on the surface of a flattened brain. The top two figures show the medial views of each hemisphere, the bottom two show the external views.
CMI
The new Centre for Medical Imaging that is to come to the University of Twente campus will soon provide extensive facilities for collaborating in the field of fMRI, says Norris, who is also on the staff of the Donders Institute in Nijmegen.
(Source: utwente.nl)
A ‘can do’ attitude is the key to a healthy lifestyle, University of Melbourne economists have determined.
Researchers from the Melbourne Institute of Applied Economic and Social Research analysed data on the diet, exercise and personality type of more than 7,000 people. The study found those who believe their life can be changed by their own actions ate healthier food, exercised more, smoked less and avoided binge drinking.
Professor Deborah Cobb-Clark, Director of the Melbourne Institute of Applied Economic and Social Research, said those who have a greater faith in ‘luck’ or ‘fate’ are more likely to live an unhealthy life. “Our research shows a direct link between the type of personality a person has and a healthy lifestyle,“ she said.
Professor Cobb-Clark hoped the study would help inform public health policies on conditions such as obesity. “The main policy response to the obesity epidemic has been the provision of better information, but information alone is insufficient to change people’s eating habits,” she said.
“Understanding the psychological underpinning of a person’s eating patterns and exercise habits is central to understanding obesity.” The study also found men and women hold different views on the benefits of a healthy lifestyle.
Men wanted physical results from their healthy choices, while women were more receptive to the everyday enjoyment of leading a healthy lifestyle. Professor Cobb-Clarke said the research demonstrated the need for more targeted policy responses. “What works well for women may not work well for men,” she said. “Gender specific policy initiatives which respond to these objectives may be particularly helpful in promoting healthy lifestyles.”
CAMH illuminates roles of novel epigenetic chemical in the brain
Researchers from the Centre for Addiction and Mental Health (CAMH) have identified a new role of a chemical involved in controlling the genes underlying memory and learning.
"The brain is a plastic tissue, and we know that learning and memory require various genes to be expressed,” says CAMH Senior Scientist Dr. Art Petronis, who is a senior author on the new study. “Our research has identified how the chemical 5-hmC may be involved in the epigenetic processes allowing this plasticity.” Dr. Petronis is head of the Krembil Family Epigenetics Laboratory in CAMH’s Campbell Family Mental Health Research Institute.
5-hmC is an epigenetic modification of DNA, and was discovered in humans and mice in 2009. DNA modifications are chemical changes to DNA. They flag genes to be turned “on” - signalling the genome to make a protein - or turned “off.” As the overwhelming majority of cells in an individual contain the same genetic code, this pattern of flags is what allows a neuron to use the same genome as a blood or liver cell, but create a completely different and specialized cellular environment.
The research, published online in Nature Structural & Molecular Biology, sheds light on the role of 5-hmC. Intriguingly, it is more abundant in the brain than in other tissues in the body, for reasons not clear to date.
The CAMH team of scientists examined DNA from a variety of tissues, including the mouse and human brain, and looked at where 5-hmC was found in the genome. They detected that 5-hmC had a unique distribution in the brain: it was highly enriched in genes related to the synapse, the dynamic tips of brain cells. Growth and change in the synapse allow different brain cells to “wire” together, which allows learning and memory.
"This enrichment of 5-hmC in synapse-related genes suggests a role for this epigenetic modification in learning and memory," says Dr. Petronis.
The team further showed that 5-hmC had a special distribution even within the gene. The code for one gene can be edited and “spliced” to create several different proteins. Dr. Petronis found that 5-hmC is located at “splice junctions,” the points where the gene is cut before splicing.
"5-hmC may signal the cell’s splicing machinery to generate the diverse proteins that, in turn, give rise to the unprecedented complexity of the brain," he says.
The research team is continuing to investigate the role of 5-hmC in more detail, and to determine whether 5-hmC function is different in people with bipolar disorder and schizophrenia compared to people without these diagnoses.
This research was funded by the U.S National Institutes of Health, the Canadian Institutes of Health Research, and the Tapscott Chair in Schizophrenia Studies at the University of Toronto.
The Centre for Addiction and Mental Health (CAMH) is Canada’s largest mental health and addiction teaching hospital, as well as one of the world’s leading research centres in the area of addiction and mental health. CAMH combines clinical care, research, education, policy development and health promotion to help transform the lives of people affected by mental health and addiction issues.
(Source: Yahoo!)
By studying how birds master songs used in courtship, scientists at Duke University have found that regions of the brain involved in planning and controlling complex vocal sequences may also be necessary for memorizing sounds that serve as models for vocal imitation.
In a paper appearing in the September 2012 issue of the journal Nature Neuroscience, researchers at Duke and Harvard universities observed the imitative vocal learning habits of male zebra finches to pinpoint which circuits in the birds’ brains are necessary for learning their songs.
Knowing which brain circuits are involved in learning by imitation could have broader implications for diagnosing and treating human developmental disorders, the researchers said. The finding shows that the same circuitry used for vocal control also participates in auditory learning, raising the possibility that vocal circuits in our own brain also help encode auditory experience important to speech and language learning.
EnChroma glasses designed to compensate for color-blindness
While many people may think that being color blind means seeing everything in black-and-white, such a condition is in fact quite rare. Instead, the majority of people who are classified as color blind are capable of color vision, but they have difficulty distinguishing red and green as distinct colors. EnChroma’s Cx sunglasses are designed to help in these cases, by selectively reducing the transmission of given wavelengths of light, thus allowing red and green to stand out.
The key to the sunglasses’ performance is a proprietary coating on the lenses. Said to be harder and more scratch-resistant than glass, it can be tweaked in production to filter certain wavelengths that cause “color confusion.” The result is an improved signal-to-noise ratio in the perception of colors, in which red and green don’t just appear as variations of yellowy-brown – as an example.
Depending on their specific type of red-green color vision deficiency, users can choose between two different models of the sunglasses, designed to filter different wavelengths of light. There are also models that simply boost the intensity of all colors (for use by normally-sighted users), and that boost colors while also blocking UV rays.
People who are completely incapable of seeing any colors will unfortunately not be helped by any of the models. Also, because they are sunglasses, their color correction feature only works in bright light.
EnChroma’s Cx sunglasses should be available as of the middle of next month. Expect to pay at least US$800 for a complete set of glasses, or $700 for the lenses alone.