Posts tagged brain

ScienceDaily (July 24, 2012) — Neuroscientists from Wayne State University and the Massachusetts Institute of Technology (MIT) are taking a deeper look into how the brain mechanisms for memory retrieval differ between adults and children. While the memory systems are the same in many ways, the researchers have learned that crucial functions with relevance to learning and education differ.

The team’s findings were published on July 17, 2012, in the Journal of Neuroscience.

According to lead author Noa Ofen, Ph.D., assistant professor in WSU’s Institute of Gerontology and Department of Pediatrics, cognitive ability, including the ability to learn and remember new information, dramatically changes between childhood and adulthood. This ability parallels with dramatic changes that occur in the structure and function of the brain during these periods.

In the study, “The Development of Brain Systems Associated with Successful Memory Retrieval of Scenes,” Ofen and her collaborative team tested the development of neural underpinnings of memory from childhood to young adulthood. The team of researchers exposed participants to pictures of scenes and then showed them the same scenes mixed with new ones and asked them to judge whether each picture was presented earlier. Participants made retrieval judgments while researchers collected images of their brains with magnetic resonance imaging (MRI).

Using this method, the researchers were able to see how the brain remembers. “Our results suggest that cortical regions related to attentional or strategic control show the greatest developmental changes for memory retrieval,” said Ofen.

The researchers said that older participants used the cortical regions more than younger participants when correctly retrieving past experiences.

"We were interested to see whether there are changes in the connectivity of regions in the brain that support memory retrieval," Ofen added. "We found changes in connectivity of memory-related regions. In particular, the developmental change in connectivity between regions was profound even without a developmental change in the recruitment of those regions, suggesting that functional brain connectivity is an important aspect of developmental changes in the brain."

This study marks the first time that the development of connectivity within memory systems in the brain has been tested, and the results suggest that the brain continues to rearrange connections to achieve adult-like performance during development.

Ofen and her research team plan to continue research in this area, focused on modeling brain network connectivity, and applying these methods to study abnormal brain development.

Source: Science Daily

July 23, 2012

Mice appear to have a specialized system for detecting and at least initially processing instinctually important smells such as those that denote predators. The finding raises a question about whether their response to those smells is hardwired.

A separate subsystem for the smell of fear. Experiments in mice suggest neurons that detect odors associated with an instinctive response — like fleeing when an approaching predator is detected — are configured differently than other olfactory neurons. Further research could determine whether this system automatically triggers flight or other primal behaviors.Credit: Mike Cohea/Brown University

PROVIDENCE, R.I. [Brown University] — A new study finds that mice have a distinct neural subsystem that links the nose to the brain and is associated with instinctually important smells such as those emitted by predators. That insight, published online this week in Proceedings of the National Academy of Sciences, prompts the question whether mice and other mammals have specially hardwired neural circuitry to trigger instinctive behavior in response to certain smells.

In the series of experiments and observations described in the paper, the authors found that nerve cells in the nose that express members of the gene family of trace amine-associated receptors (TAAR) have several key biological differences from the much more common and diverse neurons that express members of the olfactory receptor gene family. Those other nerve cells detect a much broader range of smells, said corresponding author Gilad Barnea, the Robert and Nancy Carney Assistant Professor of Neuroscience at Brown University.

The differences between TAAR neurons and olfactory receptor neurons led Barnea and his co-authors to conclude that they form an independent subsystem for certain smells.

“Our observations suggest that the TAAR-expressing sensory neurons constitute a distinct olfactory subsystem that extracts specific environmental cues that then elicit innate responses,” Barnea said.

Read more …

ScienceDaily (July 23, 2012) — Stroboscopic training, performing a physical activity while using eyewear that simulates a strobe-like experience, has been found to increase visual short-term memory retention, and the effects lasted 24 hours.

(Credit: Image courtesy of Duke University)

Participants completed a memory test that required them to note the identity of eight letters of the alphabet that were briefly displayed on a computer screen. After a variable delay, participants were asked to recall one of the eight letters. On easy-level trials, the recall prompt came immediately after the letters disappeared, but on more difficult trials, the prompt came as late as 2.5 seconds following the display. Because participants did not know which letter they would be asked to recall, they had to retain all of the items in memory.

"Humans have a memory buffer in their brain that keeps information alive for a certain short-lived period," said Greg Appelbaum, assistant professor of psychiatry at Duke University and first author of the study. "Wearing the strobe eyewear during the physical training seemed to boost the ability to retain information in this buffer."

The strobe eyewear disrupts vision by only allowing the user to see glimpses of the world. The user must adjust their visual processing in order to perform normally, and this adjustment produces a lingering benefit; once participants removed the strobe eyewear, there was an observed boost in their visual memory retention, which was found to last 24 hours.

Earlier work by Appelbaum and the project’s senior researcher, Stephen Mitroff, had shown that stroboscopic training improves visual perception, including the ability to detect subtle motion cues and the processing of briefly presented visual information. Yet the earlier study had not determined how long the benefits might last.

"Our earlier work on stroboscopic training showed that it can improve perceptual abilities, but we don’t know exactly how," says Mitroff, associate professor of psychology & neuroscience and member of the Duke Institute for Brain Sciences. "This project takes a big step by showing that these improved perceptual abilities are driven, at least in part, by improvements in visual memory."

"Improving human cognition is an important goal with so many benefits," said Appelbaum, also a member of the Duke Institute for Brain Sciences. "Interestingly, our findings demonstrate one way in which visual experience has the capacity to improve cognition."

Source: Science Daily

ScienceDaily (July 23, 2012) — Snack consumption and BMI are linked to both brain activity and self-control, new research has found.

Snack consumption and BMI are linked to both brain activity and self-control, new research has found. (Credit: © farbkombinat / Fotolia)

The research, carried out by academics from the Universities of Exeter, Cardiff, Bristol, and Bangor, discovered that an individual’s brain ‘reward centre’ response to pictures of food predicted how much they subsequently ate. This had a greater effect on the amount they ate than their conscious feelings of hunger or how much they wanted the food,

A strong brain response was also associated with increased weight (BMI), but only in individuals reporting low levels of self-control on a questionnaire. For those reporting high levels of self-control a stronger brain response to food was actually related to a lower BMI.

This study, which is now published in the journal NeuroImage, adds to mounting evidence that overeating and increased weight are linked, in part, to a region of the brain associated with motivation and reward, called the nucleus accumbens. Responses in this brain region have been shown to predict weight gain in healthy weight and obese individuals, but only now have academics discovered that this is independent of conscious feelings of hunger, and that self-control also plays a key role.

Following these results, academics at the University of Exeter and Cardiff have begun testing ‘brain training’ techniques designed to reduce the influence of food cues on individuals who report low levels of self-control. Similar tests are being used to assist those with gambling or alcohol addiction.

Dr Natalia Lawrence of Psychology at the University of Exeter, lead researcher in both the original research and the new studies, said: “Our research suggests why some individuals are more likely to overeat and put on weight than others when confronted with frequent images of snacks and treats. Food images, such as those used in advertising, cause direct increases in activity in brain ‘reward areas’ in some individuals but not in others. If those sensitive individuals also struggle with self-control, which may be partly innate, they are more likely to be overweight. We are now developing computer programs that we hope will counteract the effects of this high sensitivity to food cues by training the brain to respond less positively to these cues.”

Twenty-five young, healthy females with BMIs ranging from 17-30 were involved in the study. Female participants were chosen because research shows females typically exhibit stronger responses to food-related cues. The hormonal changes during the menstrual cycle affect this reaction, so all participants were taking the monophasic combined oral contraceptive pill. Participants had not eaten for at least six hours to ensure they were hungry at the time of the scan and were given a bowl containing 150 g (four and a half packets) of potato chips to eat at the end of the study; they were informed that potato chip intake had been measured afterwards.

Researchers used MRI scanning to detect the participants’ brain activity while they were shown images of household objects, and food that varied in desirability and calorific content. After scanning, participants rated the food images for desirability and rated their levels of hunger and food craving. Results showed that participants’ brain responses to food (relative to objects) in the nucleus accumbens predicted how many potato chips they ate after the scan. However, participants’ own ratings of hunger and how much they liked and wanted the foods, including potato chips, were unrelated to their potato chip intake.

This study was funded by the Wales Institute of Cognitive Neuroscience.

What this study shows:

• Brain responses to food images vary considerably between individuals.
• Brain responses to food images but not conscious feelings of hunger or desire to eat predict subsequent potato chip consumption.
• Individuals’ reported levels of self-control influence whether this brain response is associated with a higher or lower BMI.

What this study does NOT show:

• Brain responses to food cues cause overeating.
• The associations reported here are true in everyone — only healthy young women were included.
• Whether our brain response and levels of self-control are learned or innate.

Source: Science Daily

JUL 23, 2012

A new and powerful class of antioxidants could one day be a potent treatment for Parkinson’s disease, researchers report.

Dr. Bobby Thomas

A class of antioxidants called synthetic triterpenoids blocked development of Parkinson’s in an animal model that develops the disease in a handful of days, said Dr. Bobby Thomas, neuroscientist at the Medical College of Georgia at Georgia Health Sciences University and corresponding author of the study in the journal Antioxidants & Redox Signaling.

Thomas and his colleagues were able to block the death of dopamine-producing brain cells that occurs in Parkinson’s by using the drugs to bolster Nrf2, a natural antioxidant and inflammation fighter.

Stressors from head trauma to insecticide exposure to simple aging increase oxidative stress and the body responds with inflammation, part of its natural repair process. “This creates an environment in your brain that is not conducive for normal function,” Thomas said. “You can see the signs of oxidative damage in the brain long before the neurons actually degenerate in Parkinson’s.”

Nrf2, the master regulator of oxidative stress and inflammation, is – inexplicably – significantly decreased early in Parkinson’s. In fact, Nrf2 activity declines normally with age.

“In Parkinson’s patients you can clearly see a significant overload of oxidative stress, which is why we chose this target,” Thomas said. “We used drugs to selectively activate Nrf2.”

They parsed a number of antioxidants already under study for a wide range of diseases from kidney failure to heart disease and diabetes, and found triterpenoids the most effective on Nrf2. Co-author Dr. Michael Sporn, Professor of Pharmacology, Toxicology and Medicine at Dartmouth Medical School, chemically modified the agents so they could permeate the protective blood-brain barrier.

Both in human neuroblastoma and mouse brain cells they were able to document an increase in Nrf2 in response to the synthetic triterpenoids. Human dopaminergic cells are not available for research so the scientists used the human neuroblastoma cells, which are actually cancer cells that have some properties similar to neurons.

Their preliminary evidence indicates the synthetic triterpenoids also increase Nrf2 activity in astrocytes, a brain cell type which nourishes neurons and hauls off some of their garbage. The drugs didn’t protect brain cells in an animal where the Nrf2 gene was deleted, more proof that that Nrf2 is the drugs’ target.

The researchers used the powerful neurotoxin MPTP to mimic Parkinson’s-like brain cell damage in a matter of days. They are now looking at the impact of synthetic triterpenoids in an animal model genetically programmed to acquire the disease more slowly, as humans do. Collaborators at Johns Hopkins School of Medicine also will be providing induced pluripotent stem cells, adult stem cells that can be coaxed into forming dopaminergic neurons, for additional drug testing.

Other collaborators include scientists at Weill Medical College of Cornell University, Johns Hopkins School of Public Health, Moscow State University, Tohoku University and the University of Pittsburgh.

Source: EarthSky

ScienceDaily (July 23, 2012) — New research conducted by neuroscientists from the Royal College of Surgeons in Ireland (RCSI) published in Nature Medicine has identified a new gene involved in epilepsy and could potentially provide a new treatment option for patients with epilepsy.

The research focussed on a new class of gene called a ‘microRNA’ which controls protein production inside cells. The research looked in detail at one particular microRNA called ‘microRNA-134’ and found that levels of microRNA-134 are much higher in the part of the brain that causes seizures in patients with epilepsy.

By using a new type of drug-like molecule called an antagomir which locks onto the ‘microRNA-134’ and removes it from the brain cell, the researchers found they could prevent epileptic seizures from occurring.

Professor David Henshall, Department of Physiology & Medical Physics, RCSI and senior author on the paper said ‘We have been looking to find what goes wrong inside brain cells to trigger epilepsy. Our research has discovered a completely new gene linked to epilepsy and it shows how we can target this gene using drug-like molecules to reduce the brain’s susceptibility to seizures and the frequency in which they occur.”

Dr Eva Jimenez-Mateos, Department of Physiology & Medical Physics, RCSI and first author on the paper said “Our research found that the antagomir drug protects the brain cells from toxic effects of prolonged seizures and the effects of the treatment can last up to one month.”

Epilepsy affects 37,000 in Ireland alone. For every two out of three people with epilepsy their seizures are controlled by medication, but one in three patients continues to have seizures despite being prescribed medication. This study could potentially offer new treatment methods for patients.

The research was supported by a grant from Science Foundation Ireland (SFI). Researchers in the Department of Physiology & Medical Physics and Molecular & Cellular Therapeutics, RCSI, clinicians at Beaumont Hospital and experts in brain structure from the Cajal Institute in Madrid were involved in the study.

Source: Science Daily

23 JUILLET 2012

Children with trisomy 13 or 18, who are for the most part severely disabled and have a very short life expectancy, and their families lead a life that is happy and rewarding overall, contrary to the usually gloomy predictions made by the medical community at the time of diagnosis, according to a study of parents who are members of support groups published today inPediatrics. The study was conducted by Dr. Annie Janvier of the Sainte-Justine University Hospital Center and the University of Montreal with the special collaboration of the mother of a child who died from trisomy 13, Barbara Farlow, Eng, MSc as the second author.

Source : Wikimedia Commons

The study interviewed 332 parents who live or have lived with 272 children with trisomy 13 or 18. It turns out that their experience diverges substantially from what healthcare providers said it would be, according to which their child would have been “incompatible with life” (87 %), would have been “a vegetable” (50 %), would have led “a life of suffering” (57 %) or would have “ruin their family or life as a couple” (23 %).

It should be noted that trisomies 13 and 18 are rare chromosome disorders that are most often diagnosed before birth and sometimes after. Children who have received these diagnoses generally do not survive beyond their first year of life, while some who do have severe disabilities and a short life. When trisomy 13 or 18 is diagnosed before birth, many parents decide to interrupt the pregnancy, whereas others choose to carry it to term and in such cases miscarriages are common.

As children with trisomies 13 or 18 generally receive palliative care at birth, some parents who opt to continue the pregnancy or desire life-prolonging interventions for their child encounter the prejudices of the medical system. In this regard, the parents interviewed in the study consider that caregivers often view their child in terms of a diagnosis (“a T13”, “a lethal trisomy”) rather than a unique baby.

“Our study points out that physicians and parents can have different views of what constitutes quality of life,” states Dr. Annie Janvier, a neonatologist and co-founder of the Master’s program in Pediatric Clinical Ethics at the University of Montreal. In fact, over 97% of the parents interviewed considered that their child was happy and its presence enriched the life of their family and their life as a couple regardless of longevity. “In the medical literature on all handicaps, disabled patients – or their families – rated their quality of life as being higher than caregivers did,” adds Dr. Annie Janvier.

Parents who receive a new diagnosis of trisomy 13 and 18 and join a parental support group often acquire a more positive image of these diagnoses than the predictions made by the medical profession. In fact, according to the parents interviewed, belonging to a support group helped them view their experience positively. “Our research reveals that some parents who chose a path to accept and to love a disabled child with a short life expectancy have experienced happiness and enrichment. My hope is that this knowledge improves the ability of physicians to understand, communicate and make decisions with these parents,” concludes Barbara Farlow.

Given the rarity of trisomy 13 or 18 cases (one case out of approximately every 10,500 births), the parents were recruited through online support groups that parents often join after receiving the physicians’ diagnosis. Dr. Annie Janvier and Barbara Farlow sometimes give joint talks on the subject of trisomies 13 and 18.

Source: Université de Montréal

July 23, 2012

Neural precursor cells (NPC) in the young brain suppress certain brain tumors such as high-grade gliomas, especially glioblastoma (GBM), which are among the most common and most aggressive tumors. Now researchers of the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch and Charité – Universitätsmedizin Berlin have deciphered the underlying mechanism of action with which neural precursor cells protect the young brain against these tumors. They found that the NPC release substances that activate TRPV1 ion channels in the tumor cells and subsequently induce the tumor cells to undergo stress-induced cell-death. (Nature Medicine http://dx.doi.org/10.1038/nm.2827)*.

Despite surgery, radiation or chemotherapy or even a combination of all three treatment options, there is currently no cure for glioblastoma. In an earlier study the research group led by Professor Helmut Kettenmann (MDC) showed that neural precursor cells migrate to the glioblastoma cells and attack them. The neural precursor cells release a protein belonging to the family of BMP proteins (bone morphogenetic protein) that directly attacks the tumor stem cells. The current consensus of researchers is that tumor stem cells are the actual cause for continuous tumor self-renewal.

Kristin Stock, Jitender Kumar, Professor Kettenmann (all MDC), Dr. Michael Synowitz (MDC and Charité), Professor Rainer Glass (Munich University Hospitals, formerly MDC) and Professor Vincenzo Di Marzo (Istituto di Chimica Biomolecolare Pozzuoli, Naples, Italy) now report a new mechanism of action of NPC in astrocytomas. Like glioblastomas, astrocytomas are brain tumors that belong to the family of gliomas. Gliomas are most common in older people and are almost invariably fatal.

As the MDC researchers showed, the NPC also migrate to the astrocytomas. There they do not secrete proteins, but rather release fatty-acid substances (endovanilloids) which are harmful to the cancer cells. However, in order to exert their lethal effect, the endovanilloids need the aid of a specific ion channel, the TRPV1 channel (transient receptor potential vanilloid type 1), also called the vanilloid receptor 1. TRPV1 is already known to researchers as a transducer of painful stimuli. It has, among other things, a binding site for capsaicin, the irritant of hot chili peppers, and is responsible for the hot sensation after eating them. Clinical trials are currently underway to develop new pain treatments by blocking or desensitizing this ion channel.

MDC researchers describe an additional role of the TRPV1 ion channel

In contrast to its use in pain management, this ion channel, which is located on the surface of glioblastoma cells and is much more abundant there than on normal glial cells, must be activated to trigger cell death in gliomas. The activated ion channel mediates stress-induced cell-death in tumor cells. If however TRPV1 is downregulated or blocked, the glioma cells are not destroyed. The MDC researchers are thus the first to identify neural precursor cells as the source of fatty acids that induce tumor cell death and to describe the role of the TRPV1 ion channel in the fight against gliomas.

However, the activity of neural precursor cells in the brain and thus of the body’s own protective mechanism against gliomas diminishes with increasing age. This could explain why these tumors usually develop in older adults and not in children and young people. How can the natural protection of neural precursor cells be harnessed for older brains? According to the researchers, neural precursor cell therapy is not a solution. The benefit this obviously brings in the treatment of young people can have the opposite effect in older adults and may trigger brain tumors.

One possible treatment would be to use drugs to activate the TRPV1 channels. In mice, the group showed that a synthetic substance (arvanil), which is similar to capsaicin, reduced tumor growth. However, this substance has not yet been approved as a drug because the adverse side effects for humans are too severe. It is only used in basic research on mice, which tolerate the substance well. “In principle, however,” the researchers suggest, “synthetic vanilloid compounds may have clinical potential for brain tumor treatment.”

Source: Science Codex

ScienceDaily (July 23, 2012) — A team of University of Alberta researchers has identified a new class of compounds that inhibit the spread of prions, misfolded proteins in the brain that trigger lethal neurodegenerative diseases in humans and animals.

U of A chemistry researcher Frederick West and his team have developed compounds that clear prions from infected cells derived from the brain.

"When these designer molecules were put into infected cells in our lab experiments, the numbers of misfolded proteins diminished — and in some cases we couldn’t detect any remaining misfolded prions," said West.

West and his collaborators at the U of A’s Centre for Prions and Protein Folding Diseases say this research is not yet a cure, but does open a doorway for developing treatments.

"We’re not ready to inject these compounds in prion-infected cattle," said David Westaway, director of the prion centre. "These initial compounds weren’t created for that end-run scenario but they have passed initial tests in a most promising manner."

West notes that the most promising experimental compounds at this stage are simply too big to be used therapeutically in humans or animals.

Human exposure to prion-triggered brain disorder is limited to rare cases of Creutzfeldt-Jakob or mad cow disease. The researchers say the human form of mad cow disease shows up in one in a million people in industrialized nations, but investigating the disease is nonetheless well worth the time and expense.

"There is a strong likelihood that prion diseases operate in a similar way to neurodegenerative diseases such as Alzheimer’s, which are distressingly common around the world," said West.

Source: Science Daily