Posts tagged brain

ScienceDaily (June 13, 2012) — Wake up, America, and lose some weight — it’s keeping you tired and prone to accidents. Three studies being presented June 13 at sleep 2012 conclude that obesity and depression are the two main culprits making us excessively sleepy while awake.

Researchers at Penn State examined a random population sample of 1,741 adults and determined that obesity and emotional stress are the main causes of the current “epidemic” of sleepiness and fatigue plaguing the country. Insufficient sleep and obstructive sleep apnea also play a role; both have been linked to high blood pressure, heart disease, stroke, depression, diabetes, obesity and accidents.

"The ‘epidemic’ of sleepiness parallels an ‘epidemic’ of obesity and psychosocial stress," said Alexandros Vgontzas, MD, the principal investigator for the three studies. "Weight loss, depression and sleep disorders should be our priorities in terms of preventing the medical complications and public safety hazards associated with this excessive sleepiness."

In the Penn State cohort study, 222 adults reporting excessive daytime sleepiness (EDS) were followed up 7½ years later. For those whose EDS persisted, weight gain was the strongest predicting factor. “In fact, our results showed that in individuals who lost weight, excessive sleepiness improved,” Vgontzas said.

Adults from that same cohort who developed EDS within the 7½-year span also were studied. The results show for the first time that depression and obesity are the strongest risk factors for new-onset excessive sleepiness. The third study, of a group of 103 research volunteers, determined once again that depression and obesity were the best predictors for EDS.

"The primary finding connecting our three studies are that depression and obesity are the main risk factors for both new-onset and persistent excessive sleepiness," Vgontzas said.

In the Penn State cohort study, the rate of new-onset excessive sleepiness was 8 percent, and the rate of persistent daytime sleepiness was 38 percent. Like insufficient sleep and obstructive sleep apnea, EDS also is associated with significant health risks and on-the-job accidents.

Source: Science Daily

ScienceDaily (June 13, 2012) — Older people who take omega-3 fish oil supplements are probably not reducing their chances of losing cognitive function, according to a new Cochrane systematic review. Based on the available data from studies lasting up to 3.5 years, the researchers concluded that the supplements offered no benefits for cognitive health over placebo capsules or margarines, but that longer term effects are worth investigating.

Omega-3 fatty acids are fats responsible for many important jobs in the body. We get these fats through our daily diets and the three major omega-3 fats are: alpha linolenic acid (ALA) from sources such as nuts and seeds and eicosapentoic acid (EPA) and docosahexaenoic acid (DHA) from sources including oily fish such as salmon and mackerel. A number of studies have hinted that omega-3 fatty acids and DHA in particular may be involved in keeping nerve cells in the brain healthy into old age. However, there is limited evidence for the role of these fats in preventing cognitive decline and dementia.

The researchers, led by Emma Sydenham at the London School of Hygiene & Tropical Medicine (LSHTM), London, UK, gathered together evidence from three high quality trials comparing the effects of omega-3 fatty acids taken in capsules or margarine spread to those of sunflower oil, olive oil or regular margarine. A total of 3,536 people over the age of 60 took part in the trials, which lasted between six and 40 months. None of the participants had any signs of poor cognitive health or dementia at the start of the trials.

The researchers found no benefit of taking the omega-3 capsules or spread over placebo capsules or spread. Participants given omega-3 did not score better in standard mental state examinations or in memory and verbal fluency tests than those given placebo.

"From these studies, there doesn’t appear to be any benefit for cognitive health for older people of taking omega-3 supplements," said Alan Dangour, a nutritionist at LSHTM and co-author of the report. "However, these were relatively short-term studies, so we saw very little deterioration in cognitive function in either the intervention groups or the control groups. It may take much longer to see any effect of these supplements."

The researchers conclude that the longer term effects of omega-3 fatty acids on cognitive decline and dementia need to be explored in further studies, particularly in people with low intakes of omega-3 fatty acids in their diet. In the meantime, they stress other potential health benefits. “Fish is an important part of a healthy diet and we would still support the recommendation to eat two portions a week, including one portion of oily fish,” said Dangour.

Source: Science Daily

ScienceDaily (June 13, 2012) — Research into alcohol’s effect on juvenile rats shows they have an ability to build up a physical, but not cognitive, tolerance over the short term — a finding that could have implications for adolescent humans, according to Baylor University psychologists.

The research findings are significant because they indicate that blood alcohol concentration levels alone may not fully account for impaired orientation and navigation ability, said Jim Diaz-Granados, Ph.D., professor and chair of psychology and neuroscience at Baylor. He co-authored the study, published in the journal Brain Research.  “There’s been a lot of supposition about the reaction to blood alcohol levels,” Diaz-Granados said. “We use the blood alcohol level to decide if someone is going to get arrested, because we think that a high level means impairment. But here we see a model where we can separate that out. You may have a tolerance in metabolism, but just because your blood alcohol concentration is less than the legal limit doesn’t mean your behavior isn’t impaired.”

"More research is needed to fully understand how adolescents react to alcohol, but this contributes a piece to the puzzle," said study co-author Douglas Matthews, Ph.D., a research scientist at Baylor and an associate professor in Psychology at Nanyang Technological University in Singapore.

The study was conducted in the Baylor Addiction Research Center of Baylor’s Department of Psychology and Neuroscience in Baylor’s College of Arts & Sciences.

More than half of under-age alcohol use is due to binge drinking, according to the Substance Abuse and Mental Health Services Administration, and “when initial alcohol use occurs during adolescence, it increases the chance of developing alcoholism later in life,” said lead study author Candice E. Van Skike, a doctoral candidate in psychology at Baylor. Researchers have long been interested in whether adolescents react differently to alcohol than adults and how alcohol use affects their brains when they reach adulthood, but Baylor researchers also wanted to test the short-term effect of alcohol on adolescents’ brains in terms of memory about space and dimension.

In the study, 96 rats were trained to navigate a water maze to an escape platform. Half were exposed to alcohol vapor in chambers for 16 hours a day over four days (a method to approximate binge-like alcohol intake), while others were exposed only to air. After a 28-hour break, some were injected with alcohol, then both groups tested again in the maze. A comparison found that those who had undergone the chronic intermittent ethanol exposure built up a metabolic tolerance. They were better able to eliminate alcohol from their systems than ones who had been exposed only to air, based on a comparison of the blood ethanol concentrations of the two groups after they had been injected with alcohol later. While the alcohol-injected rats swam as hard and as fast as the others, their ability to find the escape platform was impaired.

Previous research at Baylor led by Matthews showed that adolescents are less sensitive than adults to motor impairment during alcohol intake because a particular neuron fires more slowly in adults who are drinking. The lack of sensitivity may be part of the reason adolescents do not realize they have had too much to drink.

"It’s difficult to compare metabolic and cognitive tolerance in adults with those of juveniles, because many studies that have looked at the cognitive aspect of chronic ethanol exposure didn’t measure blood alcohol concentration levels," Van Skike said. "It would be an interesting comparison to make, and it is an avenue for future research."

Other research has shown that high levels of alcohol consumption during human adolescence are mirrored in animals. Adolescent rats consume two to three times more ethanol than adults relative to body weight, suggesting that adolescents are who drink are pre-disposed to do so in binges.

Source: Science Daily

ScienceDaily (June 13, 2012) — Normally, male California mice are surprisingly doting fathers, but new research published in the journal Physiological and Biochemical Zoology suggests that high anxiety can turn these good dads bad.

Unlike most rodents, male and female California mice pair up for life with males providing extensive parental care, helping deliver the pups, lick them clean, and keep them warm during their first few weeks of life. Experienced fathers are so paternal that they’ll even take care of pups that aren’t theirs. “If we place a male California mouse in a test cage and present it with an unknown pup, experienced fathers will quickly start to lick and huddle with it,” said Trynke de Jong, a post-doctoral researcher at University of California, Riverside.

Inexperienced males, on the other hand, aren’t always so loving. “Virgin males show more variability,” de Jong explained. “They may behave paternally, or they may ignore the pup, or even attack it. We want to understand what triggers these three behavioral responses in virgin males.”

De Jong and her colleagues thought this variability might have something to do with social status. In other species — including another rodent, Mongolian gerbils — dominant virgin males are more likely than subordinate ones to kill pups. Perhaps social status influences parenting in California mice as well.

To test this, de Jong and her colleagues paired up 12 virgin males in six enclosures, and performed several tests to see which was dominant. First was a food competition. “If a cornflake is dropped in the cage, the more dominant male will manage to eat most of it,” de Jong said. The researchers also observed each mouse’s urine marking. “Dominant males will make more, smaller, and more widespread marks than subordinate males,” said de Jong

After determining the mightier mouse in each pair, the team tested parental behavior by introducing a pup. Contrary to the hypothesis, scores on the dominance tests did not predict whether a male licked or huddled up to the pup. However, the research did turn up signs that anxiety, not status, plays a role in paternal behavior.

Males who shied away from urinating the middle of a new enclosure — a behavioral signal that a mouse is anxious — were slower to approach a pup. Further tests showed that less paternal males had higher levels of the vasopressin in their brains. Vasopressin is a hormone that is strongly associated with stress and anxiety.

"Our findings support the theory that vasopressin may alter the expression of paternal behavior depending on the emotional state of the animal," de Jong said. She believes these results could shed light on the role of stress in paternal care in other mammals — including humans.

Source: Science Daily

June 13, 2012

Researchers from Boston University School of Medicine (BUSM) have identified a novel group of proteins that accumulate in the brains of patients with Alzheimer’s disease. These findings, which appear online in the Journal of Neuroscience, may open up novel approaches to diagnose and stage the progression likelihood of the disease in Alzheimer patients.

Alzheimer’s disease is presumed to be caused by the accumulation of β-amyloid, which then induces aggregation of a neuronal protein, called tau, and neurodegeneration ensues. The diagnosis of Alzheimer’s disease focuses on β-amyloid and tau protein, with much attention focusing on radiolabeled markers that bind to β-amyloid (such as the compound PiB). However, imaging β-amyloid is problematic because many cognitively normal elderly have large amounts of β-amyloid in their brain, and appear as “positives” in the imaging tests.

Therapeutic approaches for Alzheimer’s disease generally have focused on β-amyloid because the process of producing a neurofibrillary tangle composed on tau protein has been poorly understood. Hence, few tau therapies have been developed. According to the researchers, this study makes important advances on both of these fronts.

The BUSM researchers identified a new group of proteins, termed RNA-binding proteins, which accumulate in the brains of patients with Alzheimer’s disease, and are present at much lower levels in subjects who are cognitively intact. The group found two different proteins, both of which show striking patterns of accumulation. “Proteins such as TIA-1 and TTP, accumulate in neurons that accumulate tau protein, and co-localize with neurofibrillary tangles. These proteins also bind to tau, and so might participate in the disease process,” explained senior author Benjamin Wolozin, MD, PhD, a professor in the departments of pharmacology and neurology at BUSM. “A different RNA binding protein, G3BP, accumulates primarily in neurons that do not accumulate pathological tau protein. This observation is striking because it shows that neurons lacking tau aggregates (and neurofibrillary tangles) are also affected by the disease process,” he added.

The researchers believe this work opens up novel approaches to diagnose and stage the likelihood of progression by quantifying the levels of these RNA-binding protein biomarkers that accumulate in the brains of Alzheimer patients.

Wolozin’s group also pursued the observation that some of the RNA binding proteins bind to tau protein, and tested whether one of these proteins, TIA-1, might contribute to the disease process. Previously, scientists have demonstrated that TIA-1 spontaneously aggregates in response to stress as a normal part of the stress response. Wolozin and his colleagues hypothesize that since TIA-1 binds tau, it might stimulate tau aggregation during the stress response. They introduced TIA-1 into neurons with tau protein, and subjected the neurons to stress. Consistent with their hypothesis, tau spontaneously aggregated in the presence of TIA-1, but not in the absence. Thus, the group has potentially identified an entirely novel mechanism to induce tau aggregates de novo. In future work, the group hopes to use this novel finding to understand how neurofibrillary tangles for in Alzheimer’s disease and to screen for novel compounds that might inhibit the progression of Alzheimer’s disease.

Provided by Boston University Medical Center

Source: medicalxpress.com

June 13, 2012

(Medical Xpress) — Consciousness is a selective process that allows only a part of the sensory input to reach awareness. But up to today it has yet to be clarified which areas of the brain are responsible for the content of conscious perception. Theofanis Panagiotaropoulos and his colleagues - researchers at the Max Planck Institute for Biological Cybernetics in Tübingen and University Pompeu Fabra in Barcelona - have now discovered that the content of consciousness is not localized in a unique cortical area, but is most likely an emergent property of global networks of neuronal populations.

Neurons in the lateral prefrontal cortex represent the content of consciousness. The red trace depicts neural activity (neuronal discharges) in the lateral prefrontal cortex when a stimulus is consciously perceived for 1 second while the green trace depicts neural activity when the same stimulus is suppressed from awareness. Credit: MPI for Biological Cybernetics

The question which parts of the brain are responsible for the things that reach our awareness is one of the main puzzles in neurobiology today. Previous research on the brains of primates has shown that neurons in primary and secondary cortices provide poor representation of visual consciousness. In contrast, the neurons in the temporal lobe seem to reliably reflect the actual conscious perception of a visual stimulus. These findings indicated that not all parts of the brain are responsible for the content of conscious awareness. Nevertheless, the question whether only one of the brain’s areas is responsible for the content of perception or whether more regions are involved in the process has so far remained unanswered.

The Max Planck scientists in Tübingen led by Nikos Logothetis have now addressed this issue using electrophysiological methods to monitor the neural activity in the lateral prefrontal cortex of macaque monkeys during ambiguous visual stimulation. The visual stimuli used allow for multiple perceptual interpretations, even though the actual input remained the same. In doing so, Panagiotaropoulos and his team were able to show that the electrical activity monitored in the lateral prefrontal cortex correlates with what the macaque monkeys actually perceive.

They thus concluded that visual awareness is not only reliably reflected in the temporal lobe, but also in the lateral prefrontal cortex of primates. The results depict that the neuronal correlates of consciousness are embedded in this area, which has a direct connection to premotor and motor areas of the brain, and is therefore able to directly affect motor output. These findings support the “frontal lobe hypothesis” of conscious visual perception established in 1995 by the researchers Crick (the co-discoverer of the structure of the DNA molecule) and Koch that awareness is related to neural activity with direct access to the planning stages of the brain.

The results support this theory in so far as they show that the lateral prefrontal cortex is involved in the process of visual awareness. However, the fact that neural activity in two different cortical areas reflects conscious perception shows that the decision which sensory input reaches our awareness is most likely not made in a unique cortical area but, rather, that a global network of neurons from different areas of the brain is responsible for it. “Our results therefore broaden the hypothesis and create new questions regarding the cortical mechanisms of visual awareness”, Panagiotaropoulos explains. In the near future the group is going to record the electrical activity in both regions simultaneously.

By this they will try to find out which of the two areas is activated first and draw conclusions on how the two areas interact with each other during conscious perception. This may lead to a better understanding of why only certain things reach our awareness and others remain suppressed.

Provided by Max Planck Society

Source: medicalxpress.com

ScienceDaily (June 12, 2012) — As science rushes to develop safe weight loss drugs, a new research report approaches this problem from an entirely new angle: What if there were a pill that would make you want to exercise harder? It may sound strange, but a new research report appearing online in The FASEB Journal suggests that it might be possible. That’s because a team of Swiss researchers found that when a hormone in the brain, erythropoietin (Epo), was elevated in mice, they were more motivated to exercise.

In addition, the form of erythropoietin used in these experiments did not elevate red blood cell counts. Such a treatment has obvious benefits for a wide range of health problems ranging from Alzheimer’s to obesity, including mental health disorders for which increased physical activity is known to improve symptoms.

"Here we show that Epo increases the motivation to exercise," said Max Gassmann, D.V.M., a researcher involved in the work from the Institute of Veterinary Physiology, Vetsuisse-Faculty and Zurich Center for Integrative Human Physiology at the University of Zurich in Switzerland. "Most probably, Epo has a general effect on a person’s mood and might be used in patients suffering from depression and related diseases."

To make this discovery, Gassmann and colleagues used three types of mice: those that received no treatment, those that were injected with human Epo, and those that were genetically modified to produce human Epo in the brain. Compared to the mice that did not have any increase in Epo, both mouse groups harboring human Epo in the brain showed significantly higher running performance without increases in red blood cells.

"If you can’t put exercise in a pill, then maybe you can put the motivation to exercise in a pill instead," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “As more and more people become overweight and obese, we must attack the problem from all angles. Maybe the day will come when gyms are as easily found as fast food restaurants.”

Source: Science Daily

ScienceDaily (June 12, 2012) — A team led by investigators at the Stanford University School of Medicine has found that the most common genetic risk factor for Alzheimer’s disease disrupts brain function in healthy, older women but has little impact on brain function in healthy, older men. Women harboring the gene variant, known to be a potent risk factor for Alzheimer’s disease, show brain changes characteristic of the neurodegenerative disorder that can be observed before any outward symptoms manifest.

Both men and women who inherit two copies (one from each parent) of this gene variant, known as ApoE4, are at extremely high risk for Alzheimer’s. But the double-barreled ApoE4 combination is uncommon, affecting only about 2 percent of the population, whereas about 15 percent of people carry a single copy of this version of the gene.

The Stanford researchers demonstrated for the first time the existence of a gender distinction among outwardly healthy, older people who carry the ApoE4 variant. In this group, women but not men exhibit two telltale characteristics that have been linked to Alzheimer’s disease: a signature change in their brain activity, and elevated levels of a protein called tau in their cerebrospinal fluid.

One implication of the study, published June 13 in the Journal of Neuroscience, is that men revealed by genetic tests to carry a single copy of ApoE4 shouldn’t be assumed to be at elevated risk for Alzheimer’s, a syndrome afflicting about 5 million people in the United States and nearly 30 million worldwide. The new findings also may help explain why more women than men develop this disease, said Michael Greicius, MD, assistant professor of neurology and neurological sciences and medical director of the Stanford Center for Memory Disorders. Most critically, identifying the prominent interaction between ApoE4 and gender opens a host of new experimental avenues that will allow Greicius’ team and the field generally to better understandhow ApoE4 increases risk for Alzheimer’s disease.

For every three women with Alzheimer’s disease, only about two men have the neurodegenerative disorder, said Greicius, the study’s senior author. (The first author is Jessica Damoiseaux, PhD, a postdoctoral scholar in Greicius’ laboratory. They collaborated with colleagues at the University of California-San Francisco and UCLA.) True, women live longer than men do, on average, and old age is by far the greatest risk factor for Alzheimer’s, Greicius said. “But the disparity in Alzheimer’s risk persists even if you correct for the difference in longevity,” he said. “This disparate impact of ApoE4 status on women versus men might account for a big part of the skewed gender ratio.”

Besides age, another well-studied major risk factor is genetic: possession of a particular version of the gene known as ApoE. This gene is a recipe for a protein involved in transporting cholesterol into cells — an important job, as cholesterol is a crucial constituent of all cell membranes including those of nerve cells. And nerve cells are constantly responding to experience by developing or enhancing small, bulblike electrochemical contacts to other nerve cells, or diminishing or abolishing them. For all these processes, efficient cholesterol transport is critical.

The ApoE protein comes in three versions, each the product of a slightly differing version of the ApoE gene: E2, E3 or E4. Most people have two copies of the E3 version of ApoE. A small percentage carries one copy of E3 and one of E2, and even fewer two copies of E2. The protein specified by the E4 gene version seems to be somewhat defective in comparison to the one encoded by either E2 or the much more common E3. Thus, while only about 10-15 percent of the population carries one copy of E4 (or, much less commonly, two), more than 50 percent of people who develop Alzheimer’s are E4 carriers.

But, as it turns out, the heightened risk E4 imposes may be largely restricted to women.

To demonstrate this, the scientists first obtained functional MRI scans of 131 healthy people, with a median age of 70, to examine connections in the brain’s memory network. They used sophisticated brain-imaging analysis to show that in older women carrying the E4 variant, this network of interconnected brain regions, which normally share a synchronized pattern of activity, exhibit a loss of that synchrony — a pattern typically seen in Alzheimer’s patients. In healthy, older women (but not men) with at least one E4 allele, activity in a brain area called the precuneus appeared be out of synch with other regions whose firing patterns generally are closely coordinated.

The brain-imaging technique Greicius and his colleagues used is known as functional-connectivity magnetic resonance imaging, or fcMRI. Performed on “resting” subjects, who remain in the scanner awake but not focusing on any particular task, fcMRI can discern on the order of 20 different brain networks, each consisting of a set of dispersed brain regions that are physically connected by nerve tracts and whose pulses of activity are synchronized, or in phase. Greicius, Damoiseaux and their associates have previously shown that the synchronous firing pattern of one network in particular, critical to memory function and known as the “default mode network,” is specifically targeted by Alzheimer’s and deteriorates as the disease progresses.

To independently confirm their imaging-based observations, the scientists assessed records from a large public database compiled from the Alzheimer’s Disease Neuroimaging Initiative, a multi-site study of healthy aging and Alzheimer’s disease. The Stanford study focused on the healthy 55- to 90-year-old volunteers who had agreed to undergo a spinal tap and have their cerebrospinal fluid analyzed.

From this database the Greicius team extracted the records of 91 subjects, with an average age of 75, and divided them into four groups representing women with or without a copy of the E4 variant, and men with or without a copy. For each group, they checked recorded concentrations of a protein named tau in these subjects’ cerebrospinal fluid. Elevated tau levels in cerebrospinal fluid are a key biomarker of Alzheimer’s disease. The results — the CSF of women, but not men, who carried at least one E4 allele was substantially enriched in tau — confirmed the brain-imaging findings.

The tau findings constitute another first. “It was only possible to see these differences in tau levels when we separated the patients by gender,” Greicius said.

Notably, all the men and women participating in the Journal of Neuroscience study were screened for cognitive status. Only those whose ability to think and remember appeared normal for their age were admitted. Thus, the observed changes in brain activity and CSF composition were occurring well before the onset of classic Alzheimer’s symptoms such as memory loss, disorientation and dementia. It may someday be practical to substitute fcMRI, which is noninvasive, for a spinal tap as a diagnostic tool, Greicius said.

Source: Science Daily

June 12, 2012

One of the brain’s jobs is to help us figure out what’s important enough to be remembered. Scientists at Yerkes National Primate Research Center, Emory University have achieved some insight into how fleeting experiences become memories in the brain.

Their experimental system could be a way to test or refine treatments aimed at enhancing learning and memory, or interfering with troubling memories. The results were published recently in the Journal of Neuroscience.

The researchers set up a system where rats were exposed to a light followed by a mild shock. A single light-shock event isn’t enough to make the rat afraid of the light, but a repeat of the pairing of the light and shock is, even a few days later.

"I describe this effect as ‘priming’," says the first author of the paper, postdoctoral fellow Ryan Parsons. "The animal experiences all sorts of things, and has to sort out what’s important. If something happens just once, it doesn’t register. But twice, and the animal remembers."

Parsons was working with Michael Davis, PhD, Robert W. Woodruff professor of psychiatry and behavioral sciences at Emory University School of Medicine, who has been studying the molecular basis for fear memory for several years.

Even though a robust fear memory was not formed after the first priming event, at that point Parsons could already detect chemical changes in the amygdala, part of the brain critical for fear responses. Long term memory formation could be blocked by infusing a drug into the amygdala. The drug inhibits protein kinase A, which is involved in the chemical changes Parsons observed.

It is possible to train rats to become afraid of something like a sound or a smell after one event, Parsons says. However, rats are less sensitive to light compared with sounds or smells, and a relatively mild shock was used.

Fear memories only formed when shocks were paired with light, instead of noise or nothing at all, for both the priming and the confirmation event. Parsons measured how afraid the rats were by gauging their “acoustic startle response” (how jittery they were in response to a loud noise) in the presence of the light, compared to before training began.

Scientists have been able to study the chemical changes connected with the priming process extensively in neurons in culture dishes, but not as much in live animals. The process is referred to as “metaplasticity,” or how the history of the brain’s experiences affects its readiness to change and learn.

"This could be a good model for dissecting the mechanisms involved in learning and memory,” Parsons says. “We’re going to be able to look at what’s going on in that first priming event, as well as when the long-term memory is triggered.”

"We believe our findings might help explain how events are selected out for long-term storage from what is essentially a torrent of information encountered during conscious experience," Parsons and Davis write in their paper.

Provided by Emory University

Source: medicalxpress.com

ScienceDaily (June 12, 2012) — UCC scientists have shown that brain levels of serotonin, the ‘happy hormone’ are regulated by the amount of bacteria in the gut during early life. Their research is being published June 12 in the international psychiatry journal, Molecular Psychiatry.

Happy children. UCC scientists have shown that brain levels of serotonin, the ‘happy hormone’ are regulated by the amount of bacteria in the gut during early life. (Credit: © Marzanna Syncerz / Fotolia)

This research shows that normal adult brain function depends on the presence of gut microbes during development. Serotonin, the major chemical involved in the regulation of mood and emotion, is altered in times of stress, anxiety and depression and most clinically effective antidepressant drugs work by targeting this neurochemical.

Scientists at the Alimentary Pharmabiotic Centre in UCC used a germ-free mouse model to show that the absence of bacteria during early life significantly affected serotonin concentrations in the brain in adulthood. The research also highlighted that the influence is sex dependent, with more marked effects in male compared with female animals. Finally, when the scientists colonized the animals with bacteria prior to adulthood, they found that many of the central nervous system changes, especially those related to serotonin, could not be reversed indicating a permanent imprinting of the effects of absence of gut flora on brain function.

This builds on earlier work, from the Cork group and others, showing that a microbiome-gut-brain axis exists that is essential for maintaining normal health which can affect brain and behavior. The research was carried out by Dr Gerard Clarke, Professor Fergus Shanahan, Professor Ted Dinan and Professor John F Cryan and colleagues at the Alimentary Pharmabiotic Centre in UCC.

"As a neuroscientist these findings are fascinating as they highlight the important role that gut bacteria play in the bidirectional communication between the gut and the brain, and opens up the intriguing opportunity of developing unique microbial-based strategies for treatment for brain disorders," said Professor John F Cryan, senior author on the publication and Head of the Department of Anatomy & Neuroscience at UCC.

This research has multiple health implications as it shows that manipulations of the microbiota (e.g. by antibiotics, diet, or infection) can have profound knock-on effects on brain function. “We’re really excited by these findings” said lead author Dr Gerard Clarke. “Although we always believed that the microbiota was essential for our general health, our results also highlight how important our tiny friends are for our mental wellbeing.”

Source: Science Daily