SMART Arm helps stroke survivors recover faster
A non-robotic device that helps stroke survivors regain upper limb movement is expected to be commercially available in Australia within the next 12 months.
Sensory-Motor Active Rehabilitation Training Arm (SMART Arm) is a device developed by researchers from The University of Queensland and James Cook University.
The device enables stroke survivors with upper limb weakness to drive their own rehabilitation through feedback on performance via an interactive computer program and incremental increases in load and reaching range.
Filed under stroke SMART Arm rehabilitation neural plasticity neuroscience science
Research shows binge drinking inhibits brain development
Teenagers who binge drink risk inhibiting part of their brain’s development and many are laying the groundwork for alcoholism down the track a Queensland University of Technology (QUT) researcher has found.
Professor Selena Bartlett, from QUT’s Institute for Health and Biomedical Innovation (IHBI), studied the effect excessive binge drinking during adolescence had on a particular receptor in the brain and discovered teen bingeing altered it irreversibly, keeping the brain in an adolescent state.
"The human brain doesn’t fully develop until around age 25 and bingeing during adolescence modifies its circuits, preventing the brain from reaching maturity," she said.
"During adolescence, the brain undergoes massive changes in the prefrontal cortex and areas linked to drug reward but alcohol disrupts this.
"The research, which was carried out on rats, suggests that during ageing, the brain’s delta opioid peptide receptor (DOP-R) activity turns down, but binge drinking causes the receptors to stay on, keeping it in an adolescent stage.
"The younger a child or teenager starts binge drinking and the more they drink, the worse the possible outcome for them."
Professor Bartlett said recent trends to mix high-caffeine drinks such as Red Bull with alcohol were making the binge drinking problem worse.
Filed under binge drinking adolescents brain prefrontal cortex alcohol neuroscience psychology science
Two heads are better than one
Dramatic expansion of the human cerebral cortex, over the course of evolution, accommodated new areas for specialized cognitive function, including language. Understanding the genetic mechanisms underlying these changes, however, remains a challenge to neuroscientists.
A team of researchers in Japan, led by Hideyuki Okano of Keio University School of Medicine and Tomomi Shimogori of the RIKEN Brain Science Institute, has now elucidated the mechanisms of cortical evolution. They used molecular techniques to compare the gene expression patterns in mouse and monkey brains.
Using the technique called in situ hybridization to visualize the distribution of mRNA transcripts, Okano, Shimogori and their colleagues examined the expression patterns of genes that are known to regulate development of the mouse brain. They compared these patterns to those of the same genes in the brain of the common marmoset. They found that most of the genes had similar expression patterns in mice and marmosets, but that some had strikingly different patterns between the two species. Notably, some areas of the visual and prefrontal cortices showed expression patterns that were unique to marmosets.
The researchers also found differences in gene expression within regions that connect the prefrontal cortex and hippocampus, a structure that is critical for learning and memory.
Filed under visual cortex cognitive functioning brain structure neuron genes gene expression neuroscience science
Scientists from the Florida campus of The Scripps Research Institute (TSRI) have defined the molecular structure of an enzyme as it interacts with several proteins involved in outcomes that can influence neurodegenerative disease and insulin resistance. The enzymes in question, which play a critical role in nerve cell (neuron) survival, are among the most prized targets for drugs to treat brain disorders such as Parkinson’s disease, Alzheimer’s disease and amyotrophic lateral sclerosis (ALS).
The study was published online ahead of print on November 8, 2012, by the journal Structure.
The new study reveals the structure of a class of enzymes called c-jun-N-terminal kinases (JNK) when bound to three peptides from different protein families; JNK is an important contributor to stress-induced apoptosis (cell death), and several studies in animal models have shown that JNK inhibition protects against neurodegeneration.
"Our findings have long-range implications for drug discovery," said TSRI Professor Philip LoGrasso, who, along with TSRI Associate Professor Kendall Nettles, led the study. "Knowing the structure of JNK bound to these proteins will allow us to make novel substrate competitive inhibitors for this enzyme with even greater specificity and hopefully less toxicity."
The scientists used what they called structure class analysis, looking at groups of structures, which revealed subtle differences not apparent looking at them individually.
"From a structural point of view, these different proteins appear to be very similar, but the biochemistry shows that the results of their binding to JNK were very different," he said.
LoGrasso and his colleagues were responsible for creating and solving the crystal structures of the three peptides (JIP1, SAB, and ATF-2) with JNK3 using a technique called x-ray crystallography, while Nettles handled much of the data analysis.
All three peptides have important effects, LoGrasso said, inducing two distinct inhibitory mechanisms—one where the peptide caused the activation loop to bind directly in the ATP pocket, and another with allosteric control (that is, using a location on the protein other than the active site). Because JNK signaling needs to be tightly controlled, even small changes in it can alter a cell’s fate.
"Solving the crystal structures of these three bound peptides gives us a clearer idea of how we can block each of these mechanisms related to cell death and survival," LoGrasso said. "You have to know their structure to know how to deal with them."
(Source: medicalxpress.com)
Filed under neurodegenerative diseases insulin resistance nerve cells enzyme neuroscience science
Sugar boosts self-control
To boost self-control, gargle sugar water. According to a study co-authored by University of Georgia professor of psychology Leonard Martin published Oct. 22 in Psychological Science, a mouth rinse with glucose improves self-control.
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Filed under sugar glucose self-control cognitive tasks neuroscience psychology science
Extra chromosome 21 removed from Down syndrome cell line
University of Washington scientists have succeeded in removing the extra copy of chromosome 21 in cell cultures derived from a person with Down syndrome, a condition in which the body’s cells contain three copies of chromosome 21 rather than the usual pair.
A triplicate of any chromosome is a serious genetic abnormality called a trisomy. Trisomies account for almost one-quarter of pregnancy loss from spontaneous miscarriages, according to the research team. Besides Down syndrome (trisomy 21), some other human trisomies are extra Y or X chromosomes, and Edwards syndrome (trisomy 18) and Patau syndrome (trisomy 13), both of which have extremely high newborn fatality rates.
In their report appearing in the Nov. 2 edition of Cell Stem Cell, a team led by Dr. Li B. Li of the UW Department of Medicine described how they corrected trisomy 21 in human cell lines they grew in the lab. The senior scientists on the project were gene therapy researchers Dr. David W. Russell, professor of medicine and biochemistry, and Dr. Thalia Papayannopoulou, professor of medicine.
The targeted removal of a human trisomy, they noted, could have both clinical and research applications.
Filed under Down syndrome trisomy trisomy 21 chromosomes genetics medicine science
Scripps Research Institute Scientists Uncover a New Pathway that Regulates Information Processing in the Brain
Scientists at The Scripps Research Institute (TSRI) have identified a new pathway that appears to play a major role in information processing in the brain. Their research also offers insight into how imbalances in this pathway could contribute to cognitive abnormalities in humans.
The study, published in the November 9, 2012 issue of the journal Cell, focuses on the actions of a protein called HDAC4. The researchers found that HDAC4 is critically involved in regulating genes essential for communication between neurons.
“We found that HDAC4 represses these genes, and its function in a given neuron is controlled by activity of other neurons forming a circuit,” said TSRI Assistant Professor Anton Maximov, senior investigator for the study.
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Filed under brain informaton processing neuron synapses learning memory neuroscience science
Sanford-Burnham researchers discovered that the protein appoptosin prompts neurons to commit suicide in several neurological conditions—giving them a new therapeutic target for Alzheimer’s disease and traumatic brain injury.
Dying neurons lead to cognitive impairment and memory loss in patients with neurodegenerative disorders–conditions like Alzheimer’s disease and traumatic brain injury. To better diagnose and treat these neurological conditions, scientists first need to better understand the underlying causes of neuronal death.
Enter Huaxi Xu, Ph.D., professor in Sanford-Burnham’s Del E. Webb Neuroscience, Aging, and Stem Cell Research Center. He and his team have been studying the protein appoptosin and its role in neurodegenerative disorders for the past several years. Appoptosin levels in the brain skyrocket in conditions like Alzheimer’s and stroke, and especially following traumatic brain injury.
Appoptosin is known for its role in helping the body make heme, the molecule that carries iron in our blood (think “hemoglobin,” which makes blood red). But what does heme have to do with dying brain cells? As Xu and his group explain in a paper they published recently in the Journal of Neuroscience, excess heme leads to the overproduction of reactive oxygen species, which include cell-damaging free radicals and peroxides, and triggers apoptosis, the carefully regulated process of cellular suicide. This means that more appoptosin and more heme cause neurons to die.
Not only did Xu and his team unravel this whole appoptosin-heme-neurodegeneration mechanism, but when they inhibited appoptosin in laboratory cell cultures, they noticed that the cells didn’t die. This finding suggests that appoptosin might make an interesting new therapeutic target for neurodegenerative disorders.
What’s next? Xu and colleagues are now probing appoptosin’s function in mouse models. They’re also looking for new therapies that target the protein.
“Since the upregulation of appoptosin is important for cell death in diseases such as Alzheimer’s, we’re now searching for small molecules that modulate appoptosin expression or activity. We’ll then determine whether these compounds may be potential drugs for Alzheimer’s or other neurodegenerative diseases,” Xu explains.
Putting a stop to runaway appoptosin won’t be easy, though. That’s because we still need the heme-building protein to operate at normal levels for our blood to carry iron. In a previous study, researchers found that a mutation in the gene that encodes appoptosin causes anemia. “Too much of anything is bad, but so is too little,” Xu says.
New therapies that target neurodegenerative disorders and traumatic brain injury are sorely needed. According to the CDC, approximately 1.7 million people sustain a traumatic brain injury each year. It’s an acute injury, but one that can also lead to long-term problems, causing epilepsy and increasing a person’s risk for Alzheimer’s and Parkinson’s diseases. Not only has traumatic brain injury become a worrisome problem in youth and professional sports in recent years, the Department of Defense calls traumatic brain injury “one of the signature injuries of troops wounded in Afghanistan and Iraq.”
(Source: beaker.sanfordburnham.org)
Filed under neurodegenerative diseases TBI appoptosin neuron cognitive impairment neuroscience science
ADHD medicine affects the brain’s reward system
A group of scientists from the University of Copenhagen has created a model that shows how some types of ADHD medicine influence the brain’s reward system. The model makes it possible to understand the effect of the medicine and perhaps in the longer term to improve the development of medicine and dose determination. The new research results have been published in the Journal of Neurophysiology.
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Filed under ADHD ADHD medicine Ritalin reward-punishment dopamine neuroscience science
A scientific explanation to why people perform better after receiving a compliment
A team of Japanese scientists have found scientific proof that people doing exercises appear to perform better when another person compliments them. The research was carried out by a group lead by National Institute for Physiological Sciences Professor Norihiro Sadato, Graduate University for Advanced Studies graduate student Sho Sugawara, Nagoya Institute of Technology Tenure-Track Associate Professor Satoshi Tanaka, and in collaboration with Research Center for Advanced Science and Technology Associate Professor Katsumi Watanabe. The team had previously discovered that the same area of the brain, the striatum, is activated when a person is rewarded a compliment or cash. Their latest research could suggest that when the striatum is activated, it seems to encourage the person to perform better during exercises. The paper is published online in PLOS ONE
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According to Professor Sadato, “To the brain, receiving a compliment is as much a social reward as being rewarded money. We’ve been able to find scientific proof that a person performs better when they receive a social reward after completing an exercise. There seems to be scientific validity behind the message ‘praise to encourage improvement’. Complimenting someone could become an easy and effective strategy to use in the classroom and during rehabilitation.”
Filed under brain striatum compliments performance reward neuroscience psychology science
