Bonn, Germany, December 5th, 2013 - While the human brain is in a resting state, patterns of neuronal activity which are associated to specific memories may spontaneously reappear. Such recurrences contribute to memory consolidation - i.e. to the stabilization of memory contents. Scientists of the DZNE and the University of Bonn are reporting these findings in the current issue of The Journal of Neuroscience. The researchers headed by Nikolai Axmacher performed a memory test on a series of persons while monitoring their brain activity by functional magnetic resonance imaging (fMRI). The experimental setup comprised several resting states including a nap inside a neuroimaging scanner. The study indicates that resting periods can generally promote memory performance.
Depending on one’s mood and activity different regions are active in the human brain. Perceptions and thoughts also influence this condition and this results in a pattern of neuronal activity which is linked to the experienced situation. When it is recalled, similar patterns, which are slumbering in the brain, are reactivated. How this happens, is still largely unknown.
The prevalent theory of memory formation assumes that memories are stored in a gradual manner. At first, the brain stores new information only temporarily. For memories to remain in the long term, a further step is required. „We call it consolidation“, Dr. Nikolai Axmacher explains, who is a researcher at the Department of Epileptology of the University of Bonn and at the Bonn site of the DZNE. “We do not know exactly how this happens. However, studies suggest that a process we call reactivation is of importance. When this occurs, the brain replays activity patterns associated with a particular memory. In principle, this is a familiar concept. It is a fact that things that are actively repeated and practiced are better memorized. However, we assume that a reactivation of memory contents may also happen spontaneously without there being an external trigger.”
A vaccine normally used to thwart the respiratory illness tuberculosis also might help prevent the development of multiple sclerosis, a disease of the central nervous system, a new study suggests.
In people who had a first episode of symptoms that indicated they might develop multiple sclerosis (MS), an injection of the tuberculosis vaccine lowered the odds of developing MS, Italian researchers report.
“It is possible that a safe, handy and cheap approach will be available immediately following the first [episode of symptoms suggesting MS],” said study lead author Dr. Giovanni Ristori, of the Center for Experimental Neurological Therapies at Sant’Andrea Hospital in Rome.
But, the study authors cautioned that much more research is needed before the tuberculosis vaccine could possibly be used against multiple sclerosis.
Swedish researchers at Uppsala University have, together with Brazilian collaborators, discovered a new group of nerve cells that regulate processes of learning and memory. These cells act as gatekeepers and carry a receptor for nicotine, which can explain our ability to remember and sort information.
The discovery of the gatekeeper cells, which are part of a memory network together with several other nerve cells in the hippocampus, reveal new fundamental knowledge about learning and memory. The study is published today in Nature Neuroscience.
The hippocampus is an area of the brain that is important for consolidation of information into memories and helps us to learn new things. The newly discovered gatekeeper nerve cells, also called OLM-alpha2 cells, provide an explanation to how the flow of information is controlled in the hippocampus.
“It is known that nicotine improves cognitive processes including learning and memory, but this is the first time that an identified nerve cell population is linked to the effects of nicotine”, says Professor Klas Kullander at Scilifelab and Uppsala University.
In this week’s PLoS Medicine, Jay Berry of Harvard Medical School, USA and colleagues report findings from an analysis of hospitalization data in the United States, examining the proportion of inpatient resources attributable to care for children with neurological impairment (NI). Their results indicate that children with NI account for a substantial proportion of inpatient resources and that the impact of these children is growing within children’s hospitals, necessitating adequate clinical care and a coordination of efforts to ensure that the needs of children with NI are met.
The authors state: “We must ensure that the current health care system is staffed, educated, and equipped to serve, with efficiency and quality, this growing segment of vulnerable children.”
Funding: AP was supported by the Harvard Medical School Eleanor & Miles Shore Scholar/Children’s Hospital Boston Junior Faculty Career Development Fellowship. RS and JGB were supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development career development awards K23 HD052553 and K23 HD58092-02, respectively. JLB was supported by NIH K08 DA024753. This project was supported in part by the Children’s Health Research Center at the University of Utah and Primary Children’s Medical Center Foundation. The funders and sponsors were not involved in the design and conduct of the study; collection, management, analysis, and interpretation of the data; or preparation, review, or approval of the manuscript.
Because of care advances, more infants and children with previously lethal health problems are surviving. Many, however, are left with lifelong neurologic impairment. A Children’s Hospital Boston study of more than 25 million pediatric hospitalizations in the U.S. now shows that neurologically impaired children, though still a relatively small part of the overall population, account for increasing hospital resources, particularly within children’s hospitals. Their analysis, based on data from the Agency for Healthcare Research and Quality Kids’ Inpatient Database (KID), was published online January 17th in PLoS Medicine.
The researchers analyzed KID data from 1997, 2000, 2003 and 2006, encompassing 25.7 million hospitalizations of children age 0 to 18. Of these, 1.3 million hospitalizations were for children with neurologic conditions, primarily cerebral palsy and epilepsy.
During the 10-year period, children with neurologic diagnoses were admitted more to children’s hospitals and less to community hospitals. At non-children’s hospitals, they made up a falling share of admissions (from 3 percent in 1997 to 2.5 percent in 2006); at children’s hospitals, they made up a rising share (from 11.7 percent of admissions in 1997 to 13.5 percent in 2006).
New research reveals how we make decisions. Birds choosing between berry bushes and investors trading stocks are faced with the same fundamental challenge - making optimal choices in an environment featuring varying costs and benefits. A neuroeconomics study from the Montreal Neurological Institute and Hospital – The Neuro, McGill University, shows that the brain employs two separate regions and two distinct processes in valuing ‘stimuli’ i.e. ‘goods’ (for example, berry bushes), as opposed to valuing the ‘actions,’ needed to obtain the desired option (for example flight paths to the berry bushes). The findings, published in the most recent issue of the Journal of Neuroscience and funded by the Canadian Institutes of Health Research, are vital not only for improving knowledge of brain function, but also for treating and understanding the effects of frontal lobe damage, which can be a feature of common neurological conditions ranging from stroke to traumatic brain injury to dementia.
Decision making - selecting the most valuable option, typically by taking an action - requires value comparisons, but there has been debate about how these comparisons occur in the brain: is value linked to the object itself , or to the action required to get that object. Are choices made between the things we want, or between the actions we take? The dominant model of decision making proposes that value comparisons occur in series, with stimulus value information feeding into actions (the body’s motor system). “So, in this study we wanted to understand how the brain uses value information to make decisions between different actions, and between different objects,” said the study’s lead investigator Dr. Lesley Fellows, neurologist and researcher at The Neuro. “The surprising and novel finding is that in fact these two mechanisms of choice are independent of one another. There are distinct processes in the brain by which value information guides decisions, depending on whether the choice is between objects or between actions.” Dr. Fellows often sees patients with damage to the frontal lobe, where decision making areas of the brain are located. “This finding gives me more insight into what is happening in the brain of my patients, and may lead to new treatments and new ways to care for them and manage their symptoms.”
“Despite the ubiquity and importance of decision making, we have had, until now, a limited understanding of its basis in the brain,” said Fellows. “Psychologists, economists, and ecologists have studied decision making for decades, but it has only recently become a focus for neuroscientists.
With a new application developed by a U-M neurologist, better understanding of the anatomy of the peripheral nervous system can be found right on your iPhone.
Nerve Whiz is a free application for medical professionals interested in learning the complex anatomy of nerve roots, plexuses, and peripheral nerves. It can work on Apple personal devices such as iPhones, iPads and iPods, and will soon be available for Android devices.
The application goes beyond simple nerve charts to help medical professionals interpret clinical examinations. Users select which muscles are weak or point to where the patient has sensory loss and the application provides a differential diagnosis, complete with relevant pictures and diagrams.
Scientists and educators alike have long known that cramming is not an effective way to remember things. With their latest findings, researchers at the RIKEN Brain Science Institute in Japan, studying eye movement response in trained mice, have elucidated the neurological mechanism explaining why this is so. Published in the Journal of Neuroscience, their results suggest that protein synthesis in the cerebellum plays a key role in memory consolidation, shedding light on the fundamental neurological processes governing how we remember.
The “spacing effect”, first discovered over a century ago, describes the observation that humans and animals are able to remember things more effectively if learning is distributed over a long period of time rather than performed all at once. The effect is believed to be closely connected to the process of memory consolidation, whereby short-term memories are stabilized into long-term ones, yet the underlying neural mechanism involved has long remained unclear.
To clarify this mechanism, the researchers developed a technique based around the phenomenon of horizontal optokinetic response (HOKR), a compensatory eye movement which can be used to quantify the effects of motor learning. Studying HOKR in mice, they found that the long-term effects of learning are strongly dependent on whether training is performed all at once (“massed training”), or in spaced intervals (“spaced training”): whereas gains incurred in massed training disappeared within 24 hours, those gained in spaced training were sustained longer.
A new study may explain why only 50% of patients experiencing chronic nerve pain achieve even partial relief from existing therapeutics. The study, published in the June 6 online version of the international research journal PAIN, reveals that certain types of chronic pain may be caused by signals from the skin itself, rather than damage to nerves within the skin, as previously thought.
A Medical Mystery
For years, researchers have known that increased amounts of a molecule called Calcitonin Gene-Related Peptide (CGRP) is found in the skin of chronic pain patients. The source of the increased CGRP was thought to be certain types of sensory nerve fibers in the skin that normally make and release a type or “isoform” called CGRP-alpha. Curiously, however, the authors of the current study found that nerve fibers containing CGRP-alpha are actually reduced under painful conditions – leading them to investigate where the increased CGRP in the skin came from.
The answer, surprisingly, was that the skin cells themselves generate increased amounts of a lesser-known “beta” isoform of CGRP. This skin cell-derived CGRP-beta is increased in painful conditions and may be sending pain signals to remaining sensory nerve fibers in the skin. The discovery of CGRP-beta as a therapeutic target presents a potentially important new treatment approach.
A new treatment that treats a subset of stroke patients by combining minimally invasive surgery, an imaging technique likened to “GPS for the brain,” and the clot-busting drug t-PA appears to be safe and effective, according to a multicenter clinical trial led by Johns Hopkins researchers.
The novel treatment, detailed for the first time at this week’s European Stroke Conference in Hamburg, Germany, was developed for patients with intracerebral hemorrhage (ICH), a bleed in the brain that causes a clot to form within brain tissue. This clot builds up pressure and leaches inflammatory chemicals that can cause irreversible brain damage, often leading to death or extreme disability. The usual treatments for ICH - either general supportive care such as blood pressure control and ventilation, which is considered the current standard of care, or invasive surgeries that involve taking off portions of the skull to remove the clot - have similar mortality rates, ranging from 30 to 80 percent depending on the size of the clot.
Seeking to improve these mortality rates and surviving ICH patients’ quality of life, Daniel Hanley, M.D., professor of neurology at the Johns Hopkins University School of Medicine, and his colleagues developed and tested the new treatment on 60 patients at 12 hospitals in the United States, Canada, the United Kingdom and Germany. They compared their results to those of 11 patients who received only supportive care.
A team led by developmental biologist Professor Christophe Marcelle has nailed the mechanism that causes stem cells in the embryo to differentiate into specialised cells that form the skeletal muscles of animals’ bodies. The scientists published their results in the British journal Nature on Monday (May 16).
Scientists world wide are racing to pin down the complex molecular processes that cause stem cells in the early embryo to differentiate into specialist cells such as muscle or nerve cells. The field has the potential to revolutionise medicine by delivering therapies to regenerate tissue damaged by disease or injury.
Differentiation happens soon after fertilisation, when embryonic cells are dividing rapidly and migrating as the animal’s body takes shape.
Reporting in Nature Immunology, Jefferson neuroscientists have identified a driving force behind autoimmune diseases such as multiple sclerosis (MS), and suggest that blocking this cell-signaling molecule is the first step in developing new treatments to eradicate these diseases.
Researchers led by Abdolmohamad Rostami, M.D., Ph.D., Professor and Chairman of the Department of Neurology at Jefferson Medical College of Thomas Jefferson University, found that GM-CSF, which stands for Granulocyte-macrophage colony-stimulating factor, appears to be the key culprit in the onset of MS, because without it, T helper 17 cells (Th17) cells did not induce the MS-like disease in an experimental animal model.
Th17 cells have been shown to play an important pathogenic role in humans and experimental models of autoim¬mune diseases, but the mechanisms behind this have remained elusive until now.
Endless hours of piano practice can be the bane of a child’s life - but there might be an added benefit of sticking with it.
A study has found that learning a musical instrument as a child could keep you sharp into old age.
Pensioners who had piano, flute, clarinet or other lessons as a youngster, did better on intelligence tests than others.
A retrovirus that inserted itself into the human genome thousands of years ago may be responsible for some cases of the neurodegenerative disease amyotrophic lateral sclerosis (ALS), also known as Lou Gherig’s disease. The finding, made by Johns Hopkins scientists, may eventually give researchers a new way to attack this universally fatal condition.
While roughly 20 percent of ALS cases appear to have a genetic cause, the vast majority of cases appear to arise sporadically, with no known trigger. Research groups searching for a cause of this so-called sporadic form had previously spotted a protein known as reverse transcriptase, a product of retroviruses such as HIV, in ALS patients’ serum samples, suggesting that a retrovirus might play a role in the disease. However, these groups weren’t able to trace this reverse transcriptase to a specific retrovirus, leaving some scientists in doubt whether retroviruses are involved in ALS.
Seeking to verify whether a culprit retrovirus indeed exists, Avindra Nath, M.D., a professor of neurology at the Johns Hopkins University School of Medicine, and colleagues examined brain samples from 62 people: 28 who died from ALS, 12 who died from chronic, systemic diseases such as cancer, 10 who died from accidental causes and 12 who had another neurodegenerative disease, Parkinson’s disease, at the time of their deaths. Using a technique known as polymerase chain reaction, the researchers searched for messenger RNA (mRNA) transcripts from retroviruses, a chemical signature that retroviruses were active in these patients.
The population of aged persons worldwide is expanding rapidly, and it is becoming increasingly clear that there are many different diseases that affect the minds of these individuals. Researchers at the University of Kentucky are breaking new ground in the ongoing project of identifying and defining those diseases most likely to affect an aged population. Dr. Peter Nelson of the University of Kentucky Sanders-Brown Center on Aging is the lead author on a paper soon to be published in the journal BRAIN; the paper deals with the little-understood but serious condition hippocampal sclerosis (HS-AGING). He is also the recipient of a newly approved grant from the National Institutes of Health (NIH) to conduct a study of HS-AGING genetics.
Many different diseases may produce symptoms of dementia - defined as cognitive decline and impaired memory - in aged persons. Although Alzheimer’s disease is probably the most recognized cause of dementia, HS-AGING also causes serious cognitive impairment in older adults. In those who live to a very advanced age (beyond the age of 95) HS-AGING is roughly as prevalent as Alzheimer’s.
It is important for physicians and scientists to understand the unique pathology of HS-AGING, and to be able to differentiate it from other diseases, as it is only by making an accurate diagnosis that clinicians can hope to treat people who present with signs of cognitive decline.