Posts tagged brain
Articles and news from the latest research reports.
Learning faster with neurodegenerative disease
People who bear the genetic mutation for Huntington’s disease learn faster than healthy people. The more pronounced the mutation was, the more quickly they learned. This is reported by researchers from the Ruhr-Universität Bochum and from Dortmund in the journal Current Biology. The team has thus demonstrated for the first time that neurodegenerative diseases can go hand in hand with increased learning efficiency. “It is possible that the same mechanisms that lead to the degenerative changes in the central nervous system also cause the considerably better learning efficiency” says Dr. Christian Beste, head of the Emmy Noether Junior Research Group “Neuronal Mechanisms of Action Control” at the RUB.
Passive learning through repeated stimulus presentation
In a previous study, the Bochum psychologists reported that the human sense of vision can be changed in the long term by repeatedly exposing subjects to certain visual stimuli for short periods (we reported in May 2011). The task of the participants was to detect changes in the brightness of stimuli. They performed better if they had viewed the stimuli passively for a while first. In the current study, the researchers presented the same task to 29 subjects with the genetic mutation for Huntington’s disease, who, however, did not yet show any symptoms. They also tested 45 control subjects without such mutations in the genome. In both groups, the learning efficiency was better after passive stimulus presentation than without the passive training. Subjects with the Huntington’s mutation, however, increased their performance twice as fast as those without the mutation.
Glutamate may have paradoxical effect
Degenerative diseases of the nervous system are based on complex changes. A key mechanism is an increased release of the neurotransmitter glutamate. However, since glutamate is also important for learning, in some cases it could lead to the paradoxical effect: better learning efficiency despite degeneration of the nerve cells.
Detecting differences in brightness under aggravated conditions
In each experimental run, the subjects saw two consecutive small bars on a computer screen that either had the same or different brightness. Sometimes, however, not only the brightness changed from bar one to bar two, but also the orientation of the bar (vertical or horizontal). “Normally, the distraction stimulus, i.e. the change in orientation, draws all the attention” Christian Beste explains. “But after the passive training with the visual stimuli, the distraction stimulus has no effect at all.” The shift of attention from the non-relevant to the relevant properties of the stimulus was also visible in the electroencephalogram (EEG) in brain areas for early visual processing.
Better performance with stronger mutation
In Huntington’s disease, a short segment of a gene is repeated. The number of repetitions determines when the disease breaks out. In the present study, a greater number of repetitions was, however, also associated with higher learning efficiency. “This shows that neurodegenerative changes can cause paradoxical effects” says Christian Beste. “The everyday view that neurodegenerative changes fundamentally entail deterioration of various functions can no longer be maintained in this dogmatic form.”
(Source: aktuell.ruhr-uni-bochum.de)
A new study shows that newborns that have been exposed to nicotine from both active and passive smoking mothers show poor physiological, sensory, motor and attention responses.
"Newborns who have had intrauterine exposure to nicotine, whether in an active or passive way, show signs of being more affected in terms of their neurobehavioural development. This could be an indicator of pathologies, independently of sociodemographic, obstetric and paediatric factors," as explained to SINC by Josefa Canals and Carmen Hernández, the lead authors of the study.
The most common form of strokes are caused by a sudden reduction in blood flow to the brain (ischemia) that leads to an inadequate supply of oxygen and nutrients. These so-called ischemic strokes are one of the leading causes of death and disability in industrialized nations. If they are not immediately remedied by medical intervention, areas of the brain may die off. In the journal Angewandte Chemie, Korean researchers have now proposed a new approach for supplemental treatment: Ceria nanoparticles could trap the reactive oxygen compounds that result from ischemia and cause cells to die.
Nanoengineers at the University of California, San Diego have developed a novel technology that can fabricate, in mere seconds, microscale three dimensional (3D) structures out of soft, biocompatible hydrogels. Near term, the technology could lead to better systems for growing and studying cells, including stem cells, in the laboratory. Long-term, the goal is to be able to print biological tissues for regenerative medicine. For example, in the future, doctors may repair the damage caused by heart attack by replacing it with tissue that rolled off of a printer.
The biofabrication technique uses a computer projection system and precisely controlled micromirrors to shine light on a selected area of a solution containing photo-sensitive biopolymers and cells. This photo-induced solidification process forms one layer of solid structure at a time, but in a continuous fashion.
A syndrome called “post-operative cognitive decline” has been coined to refer to the commonly reported loss of cognitive abilities, usually in older adults, in the days to weeks after surgery. In fact, some patients time the onset of their Alzheimer’s disease symptoms from a surgical procedure. Exactly how the trio of anesthesia, surgery, and dementia interact is clinically inconclusive, yet of great concern to patients, their families and physicians.
A year ago, researchers at the Perelman School of Medicine at the University of Pennsylvania reported that Alzheimer’s pathology, as reflected by cerebral spinal fluid biomarkers, might be increased in patients after surgery and anesthesia. However, it is not clear whether the anesthetic drugs or the surgical procedure itself was responsible. To separate these possibilities, the group turned to a mouse model of Alzheimer’s disease.
The results, published online this month in the Annals of Surgery, show that surgery itself, rather than anesthesia, has the more profound impact on a dementia-vulnerable brain.
Mark Mallman plans to create music for seven straight days and nights by wiring himself up to sensors that translate his brain waves into music around the clock.
(Source: wired.co.uk)
During the 1980s, thousands of infants in Romanian orphanages spent up to 20 hours a day lying untouched in their cribs, deprived of human contact. As they grew up, neurological and psychological tests confirmed a haunting phenomenon observed in other species, such as mice and rhesus monkeys: Early isolation and neglect can produce lasting cognitive damage, ranging from severe emotional instability to mental retardation. Now, researchers say they have discovered a possible explanation for why early neglect wreaks such havoc—isolation may stunt the growth of the brain cells that insulate neurons, resulting in slower communication between different areas of the brain.
Scientists have known for 50 years that the strength and arrangement of connections between neurons changes as we learn and experience new things, says Gabriel Corfas, senior author of the paper published online today in Science and a neuroscientist at Harvard Medical School in Boston and Boston Children’s Hospital. But the role of the brain’s non-neuronal cells in creating, strengthening, and shaping these neural circuits is more mysterious. The brain’s “white matter”—as opposed to its gray matter, which is composed of neurons—consists mostly of glial cells, which produce the fat and protein myelin sheaths that insulate a neuron’s branching axons, the slender fibers that conduct electrical impulses to other cells. One purpose of myelin, scientists think, is to reduce “leakage” of electric current as electrochemical signals zip to and fro. When the myelin is thin or damaged, the signals can’t travel as fast; that slowdown can impair many different brain functions, including motor control, language, and memory.
Rewiring the Autistic Brain
Signs of autism—such as impaired social skills and repetitive, ritualistic movements—usually begin to appear when a child is about 18 months old. Autism is thought to result from miswired connections in the developing brain, and many experts believe that therapies must begin during a “critical window,” before the faulty circuits become fixed in place. But a new study online today in Science shows that at least one malfunctioning circuit can be repaired after that window closes, holding out hope that in some forms of autism, abnormal circuits in the brain can be corrected even after their development is complete.
Faulty wiring. Shutting off the Nlgn3 gene in mice (right panel) results in miswired synaptic connections, which may be fixable. Credit: S. J. Baudouin et al., Science
According to developmental neurobiologist Peter Scheiffele of the University of Basel in Switzerland, autism doesn’t result from a handful of “culprit” genes that point to a treatable flaw. Instead, patients appear to carry mutations in one out of dozens, even hundreds of risk genes. “This genetic complexity is a huge issue with respect to developing treatments [for autism],” Scheiffele says. To complicate the picture further, autism is not always an isolated disorder; it’s often a common feature in syndromes that otherwise differ drastically. For example, in fragile X syndrome, a form of mental retardation, about 25% of patients are also autistic.
Scheiffele and colleagues were studying a gene called neuroligin-3 (Nlgn3), involved in building the contact points, called synapses, between neurons. Many researchers believe that autism begins at the synapse, and mutations in Nlgn3 have appeared in some forms of the disorder. Sheiffele’s team was focusing on synapses in the cerebellum, a part of the brain that controls movement, but, according to recent research, may also be involved in social behavior. Abnormalities in this region may contribute to both the unusual movements and the social problems seen in autistic patients.
To get a better handle on the role of Nlgn3, the scientists studied mice whose Nlgn3 genes were engineered with an on-off switch, called a promoter region, that is controlled by the antibiotic doxycycline. The animals were raised with the drug in their drinking water, which kept the switch in the off position. With the Nlgn3 gene disabled in the mice, neurons in their cerebellum made the abnormal connections seen in the autistic brain.
Specifically, and much to the researchers’ surprise, the lack of Nlgn3 led to the overactivation of a receptor abbreviated as mGluR1α. This receptor is a component of a pathway that is also disrupted in fragile X syndrome, though it results from mutations in an entirely different gene. In the mice, the overabundance of these receptors led the neurons to make synaptic connections in the wrong places.
To see if turning Nlgn3 gene back on would correct these problems, the researchers withdrew the doxycycline. It worked: With Nlgn3 functioning once more, levels of the extraneous receptor receded back to normal, and the misplaced synapses began to disappear.
"Our finding demonstrates that there is still flexibility after the ‘critical window’ of brain development,” Scheiffele says. “It raises the question: To what extent can a miswired brain be corrected?” The next step, he says, is to see whether motor abnormalities, such as ladder-climbing difficulties, and social interactions can be corrected with similar treatment in the engineered mice. His team is also studying whether drugs that block the mGluR1α receptor can have the same effect as genetically controlling the Nlgn3 gene, which isn’t a treatment option for humans.
"This study holds out hope for children and even adults with developmental disorders. Maybe their conditions aren’t set in stone and can be treated," says neuroscientist Kimberly Huber of the University of Texas Southwestern Medical Center in Dallas. Huber adds that drugs that block a similar receptor, mGluR5, are in clinical trials to treat fragile X syndrome.
(Source: news.sciencemag.org)
How to shrink Berlusconi’s head
To perceive the effect, fix your eyes on the cross in the center of the video. Once the motion stops and the head pictures are flashed on-screen, the image on the left should appear smaller than the one on the right. If you pause the video, you’ll notice that in fact both heads are the same size.
Created by Tim Meese and colleagues at Aston University in Birmingham, UK, the illusion was presented last week at the European Conference on Visual Perception in Alghero, Italy.
(Source: newscientist.com)