Posts tagged neuroscience
Articles and news from the latest research reports.
Simulations improve predictability of aneurysm development
Using new computer models of blood flow in the vicinity of cerebral aneurysms (dilated sections of blood vessels in the brain), it is now possible to calculate every detail of the patient-specific situation. This has resulted in powerful new techniques for predicting a further weakening or even rupture of the blood vessel’s wall, and for effective intervention. Julia Mikhal was awarded a PhD on this topic by the University of Twente.
Bacteria yield clues about why proteins go bad in ALS and Alzheimer’s
Scientists are unsure why proteins form improperly and cluster together in bunches, a hallmark of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), Alzheimer’s and Mad Cow Disease. In the Nov. 1 issue of the journal Molecular Cell, Yale scientists shed light on protein aggregate formation by studying the process in bacteria.
“The question we are all asking is what happens when protein synthesis goes wrong?” said Jesse Rinehart, assistant professor of cellular and molecular physiology at Yale’s West Campus and co-senior author of the paper.
Proteins are created from instructions encoded in DNA and assembled in ribosomes within the cells. However, sometimes they are not assembled correctly, and these misfolded proteins tend to aggregate, a process typified by the plaques that form in the brains of Alzheimer’s patients.
The Yale team — led by Rinehart and Dieter Söll, Sterling Professor of Molecular Biophysics and Biochemistry and professor of chemistry — showed that the antibiotic streptomycin can trigger protein aggregations in the bacterium E. coli. Using large-scale proteomics and genetic screens, they analyzed the aggregates and searched for bacterial proteins that make E. coli cells resistant to antibiotics and other threats. The researchers discovered how one of these proteins protecting the bacteria from hydrogen peroxide also suppressed the aggregation of proteins triggered by streptomycin.
Making a Game Out of Improving the ‘Sticky’ Brain
UCSF neuroscientists have found that by training on attention tests, people young and old can improve brain performance and multitasking skills.
Anyone who tries to perform two tasks at once is likely to do worse on both. Why that is so at the neurological level has largely been terra incognita. But research now is starting to reveal the impact of multitasking on short-term memory and attention.
Adam Gazzaley, MD, PhD, associate professor of neurology, physiology and psychiatry, and researchers at the UCSF Neuroscience Imaging Center use EEG, MRI and other non-invasive tools to study cognitive processes while people try their best on drills that test short-term memory.
UCSB Scientists Report ‘New Beginning’ in Split-Brain Research, Using New Analytical Tools
UC Santa Barbara has reported an important discovery in the interdisciplinary study of split-brain research. The findings uncover dynamic changes in brain coordination patterns between left and right hemispheres.
Split-brain research has been conducted for decades, and scientists have long ago shown that language processing is largely located in the left side of the brain. When words appear only in the left visual field –– an area processed by the right side of the brain –– the right brain must transfer that information to the left brain, in order to interpret it. The new study at UCSB shows that healthy test subjects respond less accurately when information is shown only to the right brain.
While hemispheric specialization is considered accurate, the new study sheds light on the highly complex interplay –– with neurons firing back and forth between distinct areas in each half of the brain. The findings rely on extremely sensitive neuroscience equipment and analysis techniques from network science, a fast-growing field that draws on insights from sociology, mathematics, and physics to understand complex systems composed of many interacting parts. These tools can be applied to systems as diverse as earthquakes and brains.
Fifty years ago, UC Santa Barbara neuroscientist Michael S. Gazzaniga moved the field forward when he was a graduate student at the California Institute of Technology and first author of a groundbreaking report on split-brain patients. The study, which became world-renowned, was published in the Proceedings of the National Academy of Sciences (PNAS) in August 1962. This week, in the very same journal, Gazzaniga and his team announced major new findings in split-brain research. The report is an example of the interdisciplinary science for which UCSB is well known.
"The occasion of this paper is on the 50th anniversary of the first report on human split-brain research reported in PNAS," said Gazzaniga. "That study showed how surgically dividing the two hemispheres of the human brain –– in an attempt to control epilepsy –– allowed for studying how each isolated half-brain was specialized for cognitive function.
"In the present study, new techniques –– not present 50 years ago –– begin to allow for an understanding of how the normal, undivided brain integrates the special functions of each half brain. It is a new beginning and very exciting," said Gazzaniga, professor of psychology in UCSB’s Department of Psychological and Brain Sciences, and director of UCSB’s SAGE Center for the Study of Mind.
(Source: ia.ucsb.edu)
Brain’s Code for Visual Working Memory Deciphered in Monkeys
The brain holds in mind what has just been seen by synchronizing brain waves in a working memory circuit, an animal study supported by the National Institutes of Health suggests. The more in-sync such electrical signals of neurons were in two key hubs of the circuit, the more those cells held the short-term memory of a just-seen object.
Charles Gray, Ph.D., of Montana State University, Bozeman, a grantee of NIH’s National Institute of Mental Health (NIMH), and colleagues, report their findings Nov. 1, 2012, online, in the journal Science Express.
“This work demonstrates, for the first time, that there is information about short term memories reflected in in-sync brainwaves,” explained Gray.
“The Holy Grail of neuroscience has been to understand how and where information is encoded in the brain. This study provides more evidence that large scale electrical oscillations across distant brain regions may carry information for visual memories,” said NIMH director Thomas R. Insel, M.D.
Prior to the study, scientists had observed synchronous patterns of electrical activity between the two circuit hubs after a monkey saw an object, but weren’t sure if the signals actually represent such short-term visual memories in the brain. Rather, it was thought that such neural oscillations might play the role of a traffic cop, directing information along brain highways.
Not Just Parroting Back: Alex the Parrot Knew His Numbers
Alex, an African grey parrot who died 5 years ago and was known for his ability to use English words, also understood a great deal about numbers. In a new study in this month’s Cognition, scientists show that Alex correctly inferred the relationship between cardinal and ordinal numbers, an ability that has not previously been found in any species other than humans. After learning the cardinal numbers—or exact values—of one to six, Alex was taught the ordinal values (the position of a number in a list) of seven and eight—that is, he learned that six is less than seven, and seven is less than eight. He was never taught the cardinal values of seven and eight—but when tested on this, he passed with flying colors, apparently inferring, for instance, that the sound “seven” meant six plus one. In the video above of one of these experiments, comparative psychologist Irene Pepperberg of Harvard University asks Alex to pick out the set of colored blocks that equal the number seven. Play the video to hear his answer.
Inflammation and Cognition in Schizophrenia
There are a growing number of clues that immune and inflammatory mechanisms are important for the biology of schizophrenia. In a new study in Biological Psychiatry, Dr. Mar Fatjó-Vilas and colleagues explored the impact of the interleukin-1β gene (IL1β) on brain function alterations associated with schizophrenia.
Fatjó-Vilas said that “this study is a contribution to the relatively new field of ‘functional imaging genetics’ which appears to be potentially powerful for the study of schizophrenia, where genetic factors are of established importance and cognitive impairment – affecting particularly executive function and long-term memory – is increasingly recognized as a core feature of the disorder.”
To conduct this study, they recruited patients with schizophrenia and healthy volunteers, all of whom completed a working memory task while undergoing a functional magnetic resonance imaging scan in the laboratory. This allowed the researchers to determine which areas of the brain became activated during the task. Each participant was also genotyped to determine which allelic combination of the -511C/T polymorphism at the promoter region of the IL1β gene they carry: CC, TT, or CT.
Patients who were homozygous for the C allele (CC) showed reduced prefrontal cortex activation associated with working memory than patients who had at least one copy of the T allele. Among the healthy volunteers, frontal brain activation did not differ according to genotype.
“The analyzed genetic variant exerts an influence on prefrontal cortex function and this influence is different in healthy subjects and patients with schizophrenia,” summarized Fatjó-Vilas.
An important issue is that the -511C/T seems to have a role in regulating the levels of IL1B expression, in which case it would influence neuronal activity dependent on the protein availability. This means that the T allele has been reported to be more active than the C allele, suggesting that a tendency for greater expression of IL1β is associated with greater compromise of frontal cortical functions underlying cognition.
Interleukin-1β is released in the blood under stressful conditions and its release is one of the ways that stress promotes inflammation. IL-1β levels in the blood are altered, for example, in patients with depression and other neuropsychiatric disorders.
Apart from having a role in the immune system, interleukins are also involved in a variety of developmental and functioning processes of the central nervous system. Thus, this study provides further clues for identifying specific biological mechanisms of the disorder associated with both neurodevelopmental processes and immunological and stress response functions.
Dr. John Krystal, Editor of Biological Psychiatry, commented, “We are just beginning to explore the functional impact of inflammatory mechanisms in schizophrenia and the current findings increase our curiosity about these novel mechanisms.”
(Source: alphagalileo.org)
Researchers identify gene required for nerve regeneration
A gene that is associated with regeneration of injured nerve cells has been identified by scientists at Penn State and Duke University. The team, led by Melissa Rolls, an assistant professor of biochemistry and molecular biology at Penn State, has found that a mutation in a single gene can entirely shut down the process by which axons — the parts of the nerve cell that are responsible for sending signals to other cells — regrow themselves after being cut or damaged. “We are hopeful that this discovery will open the door to new research related to spinal-cord and other neurological disorders in humans,” Rolls said. The journal Cell Reports published an early online copy of the paper (Nov. 1), and also will include the paper in the monthly issue of the journal, which will be published Nov. 29.
LSUHSC research identifies new therapeutic target for Alzheimer’s disease
Research led by Chu Chen, PhD, Associate Professor of Neuroscience at LSU Health Sciences Center New Orleans, has identified an enzyme called Monoacylglycerol lipase (MAGL) as a new therapeutic target to treat or prevent Alzheimer’s disease. The study was published online November 1, 2012 in the Online Now section of the journal Cell Reports.
The research team found that inactivation of MAGL, best known for its role in degrading a cannabinoid produced in the brain, reduced the production and accumulation of beta amyloid plaques, a pathological hallmark of Alzheimer’s disease. Inhibition of this enzyme also decreased neuroinflammation and neurodegeneration, and improved plasticity of the brain, learning and memory.
"Our results suggest that MAGL contributes to the cause and development of Alzheimer’s disease and that blocking MAGL represents a promising therapeutic target," notes Dr. Chu Chen, who is also a member of the Department of Otolaryngology at LSU Health Sciences Center New Orleans.
The researchers blocked MAGL with a highly selective and potent inhibitor in mice using different dosing regimens and found that inactivation of MAGL for eight weeks was sufficient to decrease production and deposition of beta amyloid plaques and the function of a gene involved in making beta amyloid toxic to brain cells. They also measured indicators of neuroinflammation and neurodegeneration and found them suppressed when MAGL was inhibited. The team discovered that not only did the integrity of the structure and function of synapses associated with cognition remain intact in treated mice, but MAGL inactivation appeared to promote spatial learning and memory, measured with behavioral testing.
Alzheimer’s disease is a neurodegenerative disorder characterized by accumulation and deposition of amyloid plaques and neurofibrillary tangles, neuroinflammation, synaptic dysfunction, progressive deterioration of cognitive function and loss of memory in association with widespread nerve cell death. The most common cause of dementia among older people, more than 5.4 million people in the United States and 36 million people worldwide suffer with Alzheimer’s disease in its various stages. Unfortunately, the few drugs that are currently approved by the Food and Drug Administration have demonstrated only modest effects in modifying the clinical symptoms for relatively short periods, and none has shown a clear effect on disease progression or prevention.
"There is a great public health need to discover new therapies to prevent and treat this devastating disorder," Dr. Chen concludes. The research was supported by grants from the National Institutes of Health. In addition to scientists from LSU Health Sciences Center New Orleans, the research team also included investigators from the Massachusetts Institute of Technology.
(Source: eurekalert.org)
Berkeley Lab Scientists Help Develop Promising Therapy for Huntington’s Disease
There’s new hope in the fight against Huntington’s disease. A group of researchers that includes scientists from the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) have designed a compound that suppresses symptoms of the devastating disease in mice.
The compound is a synthetic antioxidant that targets mitochondria, an organelle within cells that serves as a cell’s power plant. Oxidative damage to mitochondria is implicated in many neurodegenerative diseases including Alzheimer’s, Parkinson’s, and Huntington’s.
The scientists administered the synthetic antioxidant, called XJB-5-131, to mice that have a genetic mutation that triggers Huntington’s disease. The compound improved mitochondrial function and enhanced the survival of neurons. It also inhibited weight loss and stopped the decline of motor skills, among other benefits. In short, the Huntington’s mice looked and behaved like normal mice.
Based on their findings, the scientists believe that XJB-5-131 is a promising therapeutic compound that deserves further investigation as a way to fight neurodegenerative diseases.
They report their research in a paper that appears online Nov. 1 in the journal Cell Reports.