Posts tagged neuroscience
Articles and news from the latest research reports.
Brain may flush out toxins during sleep
NIH-funded study suggests sleep clears brain of molecules associated with neurodegeneration
A good night’s rest may literally clear the mind. Using mice, researchers showed for the first time that the space between brain cells may increase during sleep, allowing the brain to flush out toxins that build up during waking hours. These results suggest a new role for sleep in health and disease. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the NIH.
“Sleep changes the cellular structure of the brain. It appears to be a completely different state,” said Maiken Nedergaard, M.D., D.M.Sc., co-director of the Center for Translational Neuromedicine at the University of Rochester Medical Center in New York, and a leader of the study.
For centuries, scientists and philosophers have wondered why people sleep and how it affects the brain. Only recently have scientists shown that sleep is important for storing memories. In this study, Dr. Nedergaard and her colleagues unexpectedly found that sleep may be also be the period when the brain cleanses itself of toxic molecules.
Their results, published in Science, show that during sleep a “plumbing” system, called the glymphatic system, may open, letting fluid flow rapidly through brain. Dr. Nedergaard’s lab recently discovered the glymphatic system helps control whether cerebrospinal fluid (CSF), a clear liquid surrounding the brain and spinal cord, flows through the brain.
“It’s as if Dr. Nedergaard and her colleagues have uncovered a network of hidden caves and these exciting results highlight the potential importance of the network in normal brain function,” said Roderick Corriveau, Ph.D., a program director at NINDS.
Initially the researchers studied the system by injecting dye into the CSF of mice and watching it flow through their brains while simultaneously monitoring electrical brain activity. The dye flowed rapidly when the mice were unconscious, either asleep or anesthetized. In contrast, the dye barely flowed when the same mice were awake.
“We were surprised by how little flow there was into the brain when the mice were awake,” said Dr. Nedergaard. “It suggested that the space between brain cells changed greatly between conscious and unconscious states.”
To test this idea, the researchers inserted electrodes into the brain to directly measure the space between brain cells. They found that the space inside the brains increased by 60 percent when the mice were asleep or anesthetized.
“These are some dramatic changes in extracellular space,” said Charles Nicholson, Ph.D., a professor at New York University’s Langone Medical Center and an expert in measuring the dynamics of brain fluid flow and how it influences nerve cell communication.
Certain brain cells, called glia, control flow through the glymphatic system by shrinking or swelling. Noradrenaline is an arousing hormone that is also known to control cell volume. Treating awake mice with drugs that block noradrenaline induced sleep and increased brain fluid flow and the space between cells, further supporting the link between the glymphatic system and sleep.
Previous studies suggest that toxic molecules involved in neurodegenerative disorders accumulate in the space between brain cells. In this study, the researchers tested whether the glymphatic system controls this by injecting mice with radiolabeled beta-amyloid, a protein associated with Alzheimer’s disease, and measuring how long it lasted in their brains when they were asleep or awake. Beta-amyloid disappeared faster in mice brains when the mice were asleep, suggesting sleep normally clears toxic molecules from the brain.
“These results may have broad implications for multiple neurological disorders,” said Jim Koenig, Ph.D., a program director at NINDS. “This means the cells regulating the glymphatic system may be new targets for treating a range of disorders.”
The results may also highlight the importance of sleep.
“We need sleep. It cleans up the brain,” said Dr. Nedergaard.
(Source: ninds.nih.gov)
Brain scans show unusual activity in retired American football players
A new study has discovered profound abnormalities in brain activity in a group of retired American football players
Although the former players in the study were not diagnosed with any neurological condition, brain imaging tests revealed unusual activity that correlated with how many times they had left the field with a head injury during their careers.
Previous research has found that former American football players experience higher rates of neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease. The new findings, published in Scientific Reports, suggest that players also face a risk of subtle neurological deficits that don’t show up on normal clinical tests.
Hidden problems
The study involved 13 former National Football League (NFL) professionals who believed they were suffering from neurological problems affecting their everyday lives as a consequence of their careers.
The former players and 60 healthy volunteers were given a test that involved rearranging coloured balls in a series of tubes in as few steps as possible. Their brain activity was measured using functional magnetic resonance imaging (fMRI) while they did the test.
The NFL group performed worse on the test than the healthy volunteers, but the difference was modest. More strikingly, the scans showed unusual patterns of brain activity in the frontal lobe. The difference between the two groups was so marked that a computer programme learned to distinguish NFL alumni and controls at close to 90 per cent accuracy based just on their frontal lobe activation patterns.
“The NFL alumni showed some of the most pronounced abnormalities in brain activity that I have ever seen, and I have processed a lot of patient data sets in the past,” said Dr Adam Hampshire, lead author of the study, from the Department of Medicine at Imperial College London.
The frontal lobe is responsible for executive functions: higher-order brain activity that regulates other cognitive processes. The researchers think the differences seen in this study reflect deficits in executive function that might affect the person’s ability to plan and organise their everyday lives.
“The critical fact is that the level of brain abnormality correlates strongly with the measure of head impacts of great enough severity to warrant being taken out of play. This means that it is highly likely that damage caused by blows to the head accumulate towards an executive impairment in later life.”
Early detection
Dr Hampshire and his colleagues at the University of Western Ontario, Canada suggest that fMRI could be used to reveal potential neurological problems in American football players that aren’t picked up by standard clinical tests. Brain imaging results could be useful to retired players who are negotiating compensation for neurological problems that may be related to their careers. Players could also be scanned each season to detect problems early.
The findings also highlight the inadequacy of standard cognitive tests for detecting certain types of behavioural deficit.
“Researchers have put a lot of time into developing tests to pick up on executive dysfunction, but none of them work at all well. It’s not unusual for an individual who has had a blow to the head to perform relatively well on a neuropsychological testing battery, and then go on to struggle in everyday life.
“The results tell us something very interesting about the human brain, which is that after damage, it can work harder and bring extra areas on line in order to cope with cognitive tasks. It is likely that in more complicated real world scenarios, this plasticity is insufficient and consequently, the executive impairment is no longer masked. In this respect, the results are also of relevance to other patients who suffer from multiple head injuries.
“Of course, this is a relatively preliminary study. We really need to test more players and to track players across seasons using brain imaging.”
Researcher Reveals the Brain Connections Underlying Accurate Introspection
The human mind is not only capable of cognition and registering experiences but also of being introspectively aware of these processes. Until now, scientists have not known if such introspection was a single skill or dependent on the object of reflection. Also unclear was whether the brain housed a single system for reflecting on experience or required multiple systems to support different types of introspection.
A new study by UC Santa Barbara graduate student Benjamin Baird and colleagues suggest that the ability to accurately reflect on perceptual experience and the ability to accurately reflect on memories were uncorrelated, suggesting that they are distinct introspective skills. The findings appear in the Journal of Neuroscience.
The researchers used classic perceptual decision and memory retrieval tasks in tandem with functional magnetic resonance imaging to determine connectivity to regions in the front tip of the brain, commonly referred to as the anterior prefrontal cortex. The study tested a person’s ability to reflect on his or her perception and memory and then examined how individual variation in each of these capacities was linked to the functional connections of the medial and lateral parts of the anterior prefrontal cortex.
"Our results suggest that metacognitive or introspective ability may not be a single thing," Baird said. "We actually find a behavioral dissociation between the two metacognitive abilities across people, which suggests that you can be good at reflecting on your memory but poor at reflecting on your perception, or vice versa."
The newly published research adds to the literature describing the role of the medial and lateral areas of the anterior prefrontal cortex in metacognition and suggests that specific subdivisions of this area may support specific types of introspection. The findings of Baird’s team demonstrate that the ability to accurately reflect on perception is associated with enhanced connectivity between the lateral region of the anterior prefrontal cortex and the anterior cingulate, a region involved in coding uncertainty and errors of performance.
In contrast, the ability to accurately reflect on memory is linked to enhanced connectivity between the medial anterior prefrontal cortex and two areas of the brain: the precuneus and the lateral parietal cortex, regions prior work has shown to be involved in coding information pertaining to memories.
The experiment assessed the metacognitive abilities of 60 participants at the Max Planck Institute for Human Cognitive and Brain Sciences in Leipzig, Germany, where Baird was a visiting researcher. The perceptual decision task consisted of visual displays with six circles of vertical alternating light and dark bars –– called Gabor gratings –– arranged around a focal point. Participants were asked to identify whether the first or second display featured one of the six areas with a slight tilt, not always an easy determination to make.
A classic in psychology literature, the memory retrieval task consisted of two parts. First, participants were shown a list of 145 words. They were then shown a second set of words and asked to distinguish those they had seen previously. After each stimulus in both the perceptual decision and the memory retrieval task, participants rated their confidence in the accuracy of their responses on a scale of 1 (low confidence) to 6 (high confidence).
"Part of the novelty of this study is that it is the first to examine how connections between different regions of the brain support metacognitive processes," Baird said. "Also, prior means of computing metacognitive accuracy have been shown to be confounded by all kinds of things, like how well you do the primary task or your inherent bias toward high or low confidence.
"Using these precise measures, we’re now beginning to drill down and see how different types of introspection are actually housed in the real human brain," Baird concluded. "So it’s pretty fascinating from that perspective."
‘Individualized’ Therapy for the Brain Targets Specific Gene Mutations Causing Dementia and ALS
Johns Hopkins scientists have developed new drugs that — at least in a laboratory dish — appear to halt the brain-destroying impact of a genetic mutation at work in some forms of two incurable diseases, amyotrophic lateral sclerosis (ALS) and dementia.
They made the finding by using neurons they created from stem cells known as induced pluripotent stem cells (iPS cells), which are derived from the skin of people with ALS who have a gene mutation that interferes with the process of making proteins needed for normal neuron function.
“Efforts to treat neurodegenerative diseases have the highest failure rate for all clinical trials,” says Jeffrey D. Rothstein, M.D., Ph.D., a professor of neurology and neuroscience at the Johns Hopkins University School of Medicine and leader of the research described online in the journal Neuron. “But with this iPS technology, we think we can target an exact subset of patients with a specific mutation and succeed. It’s individualized brain therapy, just the sort of thing that has been done in cancer, but not yet in neurology.”
Scientists in 2011 discovered that more than 40 percent of patients with an inherited form of ALS and at least 10 percent of patients with the non-inherited sporadic form have a mutation in the C9ORF72 gene. The mutation also occurs very often in people with frontotemporal dementia, the second-most-common form of dementia after Alzheimer’s disease. The same research appeared to explain why some people develop both ALS and the dementia simultaneously and that, in some families, one sibling might develop ALS while another might develop dementia.
In the C9ORF72 gene of a normal person, there are up to 30 repeats of a series of six DNA letters (GGGGCC); but in people with the genetic glitch, the string can be repeated thousands of times. Rothstein, who is also director of the Johns Hopkins Brain Science Institute and the Robert Packard Center for ALS Research, used his large bank of iPS cell lines from ALS patients to identify several with the C9ORF72 mutation, then experimented with them to figure out the mechanism by which the “repeats” were causing the brain cell death characteristic of ALS.
In a series of experiments, Rothstein says, they discovered that in iPS neurons with the mutation, the process of using the DNA blueprint to make RNA and then produce protein is disrupted. Normally, RNA-binding proteins facilitate the production of RNA. Instead, in the iPS neurons with the C9ORF72 mutation, the RNA made from the repeating GGGGCC strings was bunching up, gumming up the works by acting like flypaper and grabbing hold of the extremely important RNA binding proteins, including one known as ADARB2, needed for the proper production of many other cellular RNAs. Overall, the C9ORF72 mutation made the cell produce abnormal amounts of many other normal RNAs and made the cells very sensitive to stress.
To counter this effect, the researchers developed a number of chemical compounds targeting the problem. This compound behaved like a coating that matches up to the GGGGCC repeats like velcro, keeping the flypaper-like repeats from attracting the bait, allowing the RNA-binding protein to properly do its job.
Rothstein says Isis Pharmaceuticals helped develop many of the studied compounds and, by working closely with the Johns Hopkins teams, could begin testing it in human ALS patients with the C9ORF72 mutation in the next several years. In collaboration with the National Institutes of Health, plans are already underway to begin to identify a group of patients with the C9ORF72 mutation for future research.
Rita Sattler, Ph.D., an assistant professor of neurology at Johns Hopkins and the co-investigator of the study, says without iPS technology, the team would have had a difficult time studying the C9ORF72 mutation. “Typically, researchers engineer rodents with mutations that mimic the human glitches they are trying to research and then study them,” she says. “But the nature of the multiple repeats made that nearly impossible.” The iPS cells did the job just as well or even better than an animal model, Sattler says, in part because the experiments could be done using human cells.
“An iPS cell line can be used effectively and rapidly to understand disease mechanisms and as a tool for therapy development,” Rothstein adds. “Now we need to see if our findings translate into a valuable treatment for humans.”
The researchers also analyzed brain tissue from people with the C9ORF72 mutation who died of ALS. They saw evidence of this bunching up and found that the many genes that were altered as a consequence of this mutation in the iPS cells were also abnormal in the brain tissue, thereby showing that iPS cells can be a faithful tool to study the human disease and discover effective therapies.
In the future, the scientists will look at cerebral spinal fluid from ALS patients with the C9ORF72 mutation, searching for proteins that were found both in the fluid and the iPS cells. These may pave the way to develop markers that can be studied by clinicians to see if the treatment is working once the drug therapy is moved to clinical trials.
ALS, sometimes known as Lou Gehrig’s disease, named for the Yankee baseball great who died from it, destroys nerve cells in the brain and spinal cord that control voluntary muscle movement. The nerve cells waste away or die, and can no longer send messages to muscles, eventually leading to muscle weakening, twitching and an inability to move the arms, legs and body. Onset is typically around age 50 and death often occurs within three to five years of diagnosis. Some 10 percent of cases are hereditary. There is no cure for ALS and there is only one FDA-approved drug treatment, which has just a small effect in slowing disease progression and increasing survival, Rothstein notes.
(Source: hopkinsmedicine.org)
When neurons have less to say, they say it with particular emphasis
The brain is an extremely adaptable organ – but it is also very conservative according to scientists from the Max Planck Institute of Neurobiology in Martinsried in collaboration with colleagues from the Friedrich Miescher Institute in Basel and the Ruhr Institute Bochum. The researchers succeeded in demonstrating that neurons in the brain regulate their own excitability so that the activity level in the network remains as constant as possible. Even in the event of major changes, for example the complete absence of information from a sensory organ, the almost silenced neurons re-establish levels of activity similar to their previous ones after only 48 hours. The mean activity level thus achieved is a basic prerequisite for a healthy brain and the formation of new connections between neurons – an essential capacity for regeneration following injury to the brain or a sensory organ, for example.
Neurons communicate using electrical signals. They transmit these signals to neighbouring cells via special contact points known as the synapses. When a new item of information presents for processing, the cells can develop new synaptic contacts with their neighbouring cells or strengthen existing ones. To enable forgetting, these processes are also reversible. The brain is consequently in a constant state of reorganisation, through which individual neurons are prevented from becoming either too active or too inactive. The aim is to keep the level of activity constant, as the long-term overexcitement of neurons can result in damage to the brain.
Too little activity is not good either. “The cells can only re-establish connections with their neighbours when they are ‘awake’, so to speak, that is when they display a minimum level of activity,” explains Mark Hübener, head of the recently published study. The international team of researchers succeeded in demonstrating for the first time that the brain itself compensates for massive changes in neuronal activity within a period of two days, and can return to a similar level of activity to that before the change.
Up to now, the only indication of this astonishing capacity of the brain came from cell cultures. It was also unclear as to how neurons could control their own excitability in relation to the activity of the entire network. Now, the scientists have made significant progress towards finding an answer to this question. In their study, they examined the visual cortex of mice that recently went blind. As expected, but never previously demonstrated, the activity of the neurons in this area of the brain did not fall to zero but to half of the original value. “That alone was an astonishing finding, as it shows the extent to which the visual cortex also processes information from other areas of the brain,” explains Tobias Bonhoeffer, who has been researching processes in the visual cortex at his department in the Max Planck Institute of Neurobiology for many years. “However, things really became exciting when we observed the area further over the following hours and days.”
The scientists were able, under the microscope, to witness “live” how the neurons in the visual cortex became active again. After just a few hours, they could clearly observe how the points of contact between the affected cells and neighbouring cells increased in size. When synapses get bigger, they also become stronger and signals are transmitted faster and more effectively. As a result of this intensification of the contact between the neurons, the activity of the affected network returned to its starting value after a period of between 24 and 48 hours. “To put it simply, due to the absence of visual input, the cells had less to say – but when they did say something, they said it with particular emphasis,” explains Mark Hübener.
Due to the simultaneous strengthening of all of the synapses of the affected neurons, major reductions in the neuronal activity can be normalised again with surprising speed. The relatively stable activity level thereby achieved is an essential prerequisite for maintaining a healthy, adaptable brain.
Glowing Neurons Reveal Networked Link Between Brain, Whiskers
Research in mouse whiskers reveals signal pathway from touch neuron to brain
Human fingertips have several types of sensory neurons that are responsible for relaying touch signals to the central nervous system. Scientists have long believed these neurons followed a linear path to the brain with a “labeled-lines” structure.
But new research on mouse whiskers from Duke University reveals a surprise — at the fine scale, the sensory system’s wiring diagram doesn’t have a set pattern. And it’s probably the case that no two people’s touch sensory systems are wired exactly the same at the detailed level, according to Fan Wang, Ph.D., an associate professor of neurobiology in the Duke Medical School.
The results, which appear online in Cell Reports, highlight a “one-to-many, many-to-one” nerve connectivity strategy. Single neurons send signals to multiple potential secondary neurons, just as signals from many neurons can converge onto a secondary neuron. Many such connections are likely formed by chance, Wang said. This connectivity scheme allows the touch system to have many possible combinations to encode a large repertoire of textures and forms.
"We take our sense of touch for granted," Wang said. "When you speak, you are not aware of the constant tactile feedback from your tongue and teeth. Without such feedback, you won’t be able to say the words correctly. When you write with a pen, you’re mostly unaware of the sensors telling you how to move it."
It’s not feasible to visualize the touch pathways in the human brain at high resolutions. So, Wang and her collaborators from the University of Tsukuba in Japan and the Friedrich Miescher Institute for Biomedical Research in Switzerland used the whiskers of laboratory mice to map how distinct sensor neurons, presumably detecting different mechanical stimuli, are connected to signal the brain. When the sensory neurons are activated, they send the signal along an axon — a long, slender nerve fiber than conducts electric impulses to the brain. The researchers traced signals running the long path from the mouse’s whiskers to the brain.
Wang’s group used a combination of genetic engineering and fluorescent tags delivered by viruses to color-code four different kinds of neurons and map their connections.
Earlier work by Wang and others had found that all of the 100 to 200 sensors associated with a single whisker project their axons to a large structure representing that whisker in the brain. Each whisker has its own neural representation structure.
"People have thought that within the large whisker-representing structure, there will be finer-scale, labeled lines," Wang said. "In other words, different touch sensors would send information through separate parallel pathways, into that large structure. But surprisingly, we did not find such organized pathways. Instead, we found a completely unorganized mosaic pattern of connections within the large structure. Information from different sensors is intermixed already at the first relay station inside the brain."
Wang said the next step will be to stimulate the labeled circuits in different ways to see how impulses travel the network.
"We want to figure out the exact functions and signals transmitted by different sensors during natural tactile behaviors and determine their exact roles on the perception of textures," she said.
(Source: today.duke.edu)
Schizophrenia linked to abnormal brain waves
Neuroscientists discover neurological hyperactivity that produces disordered thinking
Schizophrenia patients usually suffer from a breakdown of organized thought, often accompanied by delusions or hallucinations. For the first time, MIT neuroscientists have observed the neural activity that appears to produce this disordered thinking.
The researchers found that mice lacking the brain protein calcineurin have hyperactive brain-wave oscillations in the hippocampus while resting, and are unable to mentally replay a route they have just run, as normal mice do.
Mutations in the gene for calcineurin have previously been found in some schizophrenia patients. Ten years ago, MIT researchers led by Susumu Tonegawa, the Picower Professor of Biology and Neuroscience, created mice lacking the gene for calcineurin in the forebrain; these mice displayed several behavioral symptoms of schizophrenia, including impaired short-term memory, attention deficits, and abnormal social behavior.
In the new study, which appears in the Oct. 16 issue of the journal Neuron, Tonegawa and colleagues at the RIKEN-MIT Center for Neural Circuit Genetics at MIT’s Picower Institute for Learning and Memory recorded the electrical activity of individual neurons in the hippocampus of these knockout mice as they ran along a track.
Previous studies have shown that in normal mice, “place cells” in the hippocampus, which are linked to specific locations along the track, fire in sequence when the mice take breaks from running the course. This mental replay also occurs when the mice are sleeping. These replays occur in association with very high frequency brain-wave oscillations known as ripple events.
In mice lacking calcineurin, the researchers found that brain activity was normal as the mice ran the course, but when they paused, their ripple events were much stronger and more frequent. Furthermore, the firing of the place cells was abnormally augmented and in no particular order, indicating that the mice were not replaying the route they had just run.
This pattern helps to explain some of the symptoms seen in schizophrenia, the researchers say.
“We think that in this mouse model, we may have some kind of indication that there’s a disorganized thinking process going on,” says Junghyup Suh, a research scientist at the Picower Institute and one of the paper’s lead authors. “During ripple events in normal mice we know there is a sequential replay event. This mutant mouse doesn’t seem to have that kind of replay of a previous experience.”
The paper’s other lead author is David Foster, a former MIT postdoc. Other authors are Heydar Davoudi and Matthew Wilson, the Sherman Fairchild Professor of Neuroscience at MIT and a member of the Picower Institute.
The researchers speculate that in normal mice, the role of calcineurin is to suppress the connections between neurons, known as synapses, in the hippocampus. In mice without calcineurin, a phenomenon known as long-term potentiation (LTP) becomes more prevalent, making synapses stronger. Also, the opposite effect, known as long-term depression (LTD), is suppressed.
“It looks like this abnormally high LTP has an impact on activity of these cells specifically during resting periods, or post exploration periods. That’s a very interesting specificity,” Tonegawa says. “We don’t know why it’s so specific.”
The researchers believe the abnormal hyperactivity they found in the hippocampus may represent a disruption of the brain’s “default mode network” — a communication network that connects the hippocampus, prefrontal cortex (where most thought and planning occurs), and other parts of the cortex.
This network is more active when a person (or mouse) is resting between goal-oriented tasks. When the brain is focusing on a specific goal or activity, the default mode network gets turned down. However, this network is hyperactive in schizophrenic patients before and during tasks that require the brain to focus, and patients do not perform well in these tasks.
Further studies of these mice could help reveal more about the role of the default mode network in schizophrenia, Tonegawa says.
"Smart glasses" can improve gait of Parkinson’s patients
A new app for intelligent glasses, such as Google Glass, will soon make it possible to improve the gait of patients suffering from Parkinson’s disease and to decrease their risk of falling. Researchers at the University of Twente’s MIRA Institute have received a grant from the NutsOhra fund for the development of the app.
The gait of Parkinson’s patients is often disturbed: sometimes this presents as a shuffling movement with the patient taking small steps, or it may result in the patient constantly looking for additional support. Gait disturbance also increases the chance of a fall, despite the progress made in terms of medication. Researchers have established that the gait of patients improves when they regularly see or hear a pattern. Examples might include stripes on the floor, or the regular ticking of a metronome.
The researchers, working under the leadership of Prof. Richard van Wezel, who is professor of Neurophysiology at the UT and is also attached to the Donders Institute in Nijmegen, are now looking at exploring the possibility of using the intelligent glasses, such as Google Glass, that are now coming on to the consumer market.
Intelligent glasses would be able to provide patients with the regular visual or audible patterns required. These patterns may take the form of moving stripes or shapes which the patient sees through the glasses, flashing shapes, or music with varying tempos. The latest intelligent glasses already have inbuilt cameras and accelerometers. By using these, it will be possible to determine which approach works best for each individual patient.
The MIRA Institute for Biomedical Technology and Technical Medicine is working on the project together with the Donders Institute for Brain, Cognition and Behaviour (Nijmegen), the Medisch Spectrum Twente hospital and the VUmc University Medical Centre in Amsterdam.
"Fonds NutsOhra", a fund that provides financial support for healthcare projects, has granted the sum of € 94,000 to the project.
Teachers More Likely to Have Progressive Speech and Language Disorders
Mayo Clinic researchers have found a surprising occupational hazard for teachers: progressive speech and language disorders. The research, recently published in the American Journal of Alzheimer’s Disease & Other Dementias, found that people with speech and language disorders are about 3.5 times more likely to be teachers than patients with Alzheimer’s dementia.
Speech and language disorders are typically characterized by people losing their ability to communicate — they can’t find words to use in sentences, or they’ll speak around a word. They may also have trouble producing the correct sounds and articulating properly. Speech and language disorders are not the same as Alzheimer’s dementia, which is characterized by the loss of memory. Progressive speech and language disorders are degenerative and ultimately lead to death anywhere from 8-10 years after diagnosis.
In the study, researchers looked at a group of about 100 patients with speech and language disorders and noticed many of them were teachers. For a control, they compared them to a group of more than 400 Alzheimer’s patients from the Mayo Clinic Study on Aging. Teachers were about 3.5 times more likely to develop a speech and language disorder than Alzheimer’s disease. For other occupations, there was no difference between the speech and language disorders group and the Alzheimer’s group.
When compared to the 2008 U.S. census, the speech and language cohort had a higher proportion of teachers, but it was consistent with the differences observed with the Alzheimer’s dementia group.
This study has important implications for early detection of progressive speech and language disorders, says Mayo Clinic neurologist, Keith Josephs, M.D., who is the senior author of the study. A large cohort study focusing on teachers may improve power to identify the risk factors for these disorders.
"Teachers are in daily communication," says Dr. Josephs. "It’s a demanding occupation, and teachers may be more sensitive to the development of speech and language impairments."
(Image: Corbis)
Individuals Genetically Predisposed to Anxiousness May Be Less Likely to Volunteer and Help Others
Scientists increasingly are uncovering answers for human behavior through genetic research. Now, a University of Missouri researcher has found that prosocial behavior, such as volunteering and helping others, is related to the same gene that predisposes individuals to anxiety disorders. Helping such individuals cope with their anxiety may increase their prosocial behavior, the researcher said.
“Prosocial behavior is linked closely to strong social skills and is considered a marker of individuals’ health and well-being,” said Gustavo Carlo, Millsap Professor of Diversity in MU’s College of Human Environmental Sciences. “Social people are more likely to be healthier, excel academically, experience career success and develop deeper interpersonal relationships that may help alleviate stress.”
Carlo and his colleagues found that, on average, those individuals who carried the genotype associated with higher social anxiety were less likely to engage in prosocial behavior.
“Previous research has shown that the brain’s serotonin neurotransmitter system plays an important role in regulating emotions,” said study co-author Scott Stoltenberg, an associate professor at the University of Nebraska-Lincoln. “Our findings suggest that individual differences in social anxiety levels are influenced by this serotonin system gene and that these differences help to partially explain why some people are more likely than others to behave prosocially. Studies like this one show that biological factors are critical influences on how people interact with one another.”
Because prosocial behavior is linked to genetically based anxiety, Carlo suggests that helping nervous individuals cope with their social anxiety through targeted efforts, such as encouragement, support, counseling and medication, could help them engage in more prosocial behavior.
“Some forms of anxieties can be very debilitating for individuals,” Carlo said. “When people have severe levels of social anxiety, such as agoraphobia, which is the fear of public places and large crowds, they will avoid social situations altogether and miss the prosocial opportunities.”
Carlo said that it is difficult to distinguish how much of prosocial behavior is based on learned environmental behavior and how much is biologically based.
“The nature-versus-nurture debate is always interesting,” Carlo said. “However, I think that in our contemporary models of human behavior, we are beginning to understand the interplay between biology and the environment.”
Much of Carlo’s previous study on prosocial development has focused on how environmental influences, such as family relationships, influence prosocial behavior. This study brings researchers closer to understanding the effect that individuals’ biological makeup has on their behaviors, Carlo said.