Neuroscience

Articles and news from the latest research reports.

177 notes

New Hope for Victims of Traumatic Brain Injury

Researchers from TAU demonstrate hyperbaric oxygen therapy significantly revives brain functions and life quality

image

Every year, nearly two million people in the United States suffer traumatic brain injury (TBI), the leading cause of brain damage and permanent disabilities that include motor dysfunction, psychological disorders, and memory loss. Current rehabilitation programs help patients but often achieve limited success.

Now Dr. Shai Efrati and Prof. Eshel Ben-Jacob of Tel Aviv University’s Sagol School of Neuroscience have proven that it is possible to repair brains and improve the quality of life for TBI victims, even years after the occurrence of the injury.

In an article published in PLoS ONE, Dr. Efrati, Prof. Ben Jacob, and their collaborators present evidence that hyperbaric oxygen therapy (HBOT) should repair chronically impaired brain functions and significantly improve the quality of life of mild TBI patients. The new findings challenge the often-dismissive stand of the US Food and Drug Administration, Centers for Disease Control and Prevention, and the medical community at large, and offer new hope where there was none.

The research trial

The trial included 56 participants who had suffered mild traumatic brain injury one to five years earlier and were still bothered by headaches, difficulty concentrating, irritability, and other cognitive impairments. The patients’ symptoms were no longer improving prior to the trial.

The participants were randomly divided into two groups. One received two months of HBOT treatment while the other, the control group, was not treated at all. The latter group then received two months of treatment following the first control period. The treatments, administered at the Institute of Hyperbaric Medicine at Assaf Harofeh Medical Center, headed by Dr. Efrati, consisted of 40 one-hour sessions, administered five times a week over two months, in a high pressure chamber, breathing 100% oxygen and experiencing a pressure of 1.5 atmospheres, the pressure experienced when diving under water to a depth of 5 meters. The patients’ brain functions and quality of life were then assessed by computerized evaluations and compared with single photon emission computed tomography (SPECT) scans.

Persuasive confirmation

In both groups, the hyperbaric oxygen therapy sessions led to significant improvements in tests of cognitive function and quality of life. No significant improvements occurred by the end of the period of non-treatment in the control group. Analysis of brain imaging showed significantly increased neuronal activity after a two-month period of HBOT treatment compared to the control periods of non-treatment.

"What makes the results even more persuasive is the remarkable agreement between the cognitive function restoration and the changes in brain functionality as detected by the SPECT scans," explained Prof. Ben-Jacob. "The results demonstrate that neuroplasticity can be activated for months and years after acute brain injury."

"But most important, patients experienced improvements such as memory restoration and renewed use of language," Dr. Efrati said. "These changes can make a world of difference in daily life, helping patients regain their independence, go to work, and integrate back into society."

The regeneration process following brain injury involves complex processes, such as building new blood vessels and rebuilding connections between neurons, and requires much energy.

"This is where HBOT treatment can help," said Dr. Efrati. "The elevated oxygen levels during treatment supply the necessary energy for facilitating the healing process."

The findings offer new hope for millions of traumatic brain injury patients, including thousands of veterans wounded in action in Iraq and Afghanistan. The researchers call for additional larger scale, multi-center clinical studies to further confirm the findings and determine the most effective and personalized treatment protocols. But since the hyperbaric oxygen therapy is the only treatment proven to heal TBI patients, the researchers say that the medical community and the US Armed Forces should permit the victims of TBI benefit from the new hope right now, rather than waiting until additional studies are completed.

(Source: aftau.org)

Filed under TBI brain injury hyperbaric oxygen therapy cognitive function memory neuroscience science

57 notes

Statin Use Not Linked to a Decline in Cognitive Function Based on the largest comprehensive systematic review to date, researchers at the Perelman School of Medicine at the University of Pennsylvania concluded that available evidence does not support an association between statins and memory loss or dementia. The new study, a collaborative effort between faculty in Penn Medicine’s Preventive Cardiovascular Program, the Penn Memory Center, and the Penn Center for Evidence-Based Practice, will be published in Annals of Internal Medicine. “Statins are prescribed to approximately 30 million people in the United States, and these numbers may increase as a result of the national cholesterol guidelines recently released,” said senior study author Emil deGoma, MD, assistant professor of Medicine and medical director of the Preventive Cardiovascular Program at Penn. “A wealth of data supports a benefit of these cholesterol-lowering medications among individuals at risk for cardiovascular disease in terms of a reduction in the risk of heart attack and stroke; however, potential side effects of statins are less well understood. In February 2012, largely based on anecdotal reports, the U.S. Food and Drug Administration (FDA) issued a safety statement warning patients of possible adverse cognitive effects associated with statin use. Many concerned patients have asked if there is a relationship between statins and memory problems. Their concerns, along with the FDA statement, prompted us to pursue a rigorous analysis of all available evidence to better answer the question – are statins associated with changes in cognition?” The research team conducted a systematic review of the published literature and identified 57 statin studies reporting measures of cognitive function. Dr. deGoma and colleagues found no evidence of an increased risk of dementia with statin therapy. In fact, in cohort studies, statin users had a 13 percent lower risk of dementia, a 21 percent lower risk of Alzheimer’s disease, and a 34 percent lower risk of mild cognitive impairment compared to people who did not take statins. Most importantly, cognitive test scores were not adversely affected by statin treatment in randomized controlled trials. In these trials, roughly half of the study participants received statins and the other half received placebo. All study participants underwent formal testing of memory and other cognitive domains through tests such as the ability to recall a set of numbers. The analysis of 155 cognitive tests spanning eight categories of cognitive function, including 26 tests of memory, revealed no differences between study participants treated with statins and those provided placebo. The research team additionally performed an analysis of the FDA post-marketing surveillance databases and found no difference in the frequency of cognitive adverse event reports between statins and two commonly prescribed cardiovascular medications that have not been associated with cognitive impairment, namely, clopidogrel and losartan. “Overall, these findings are quite reassuring. I wouldn’t let concerns about adverse effects on cognition influence the decision to start a statin in patients suffering from atherosclerotic disease or at risk for cardiovascular disease. I also wouldn’t jump to the conclusion that statins are the culprit when an individual who is taking a statin describes forgetfulness. We may be doing more harm than good if we withhold or stop statins – medications proven to reduce the risk of heart attack and stroke – due to fears that statins might possibly cause memory loss,” said Dr. deGoma. The team acknowledges that while their analysis is reassuring, large, high-quality randomized controlled trials are needed to confirm their findings.  “For many of the cognitive outcomes that we examined, the identified studies were small, were at risk for bias, used varying diagnostic tests to assess cognitive domains, and did not include patients on high-dose statins, which is important given the increasing use of high-dose statins for secondary prevention,” noted study co-author Craig Umscheid, MD, MSCE, assistant professor of Medicine and Epidemiology and director of the Penn Center for Evidence-based Practice. “Thus, additional trials addressing these limitations would strengthen our conclusions. Despite this, the totality of the evidence does reassure us that there’s unlikely to be a significant link between statins and cognitive impairment.”

Statin Use Not Linked to a Decline in Cognitive Function

Based on the largest comprehensive systematic review to date, researchers at the Perelman School of Medicine at the University of Pennsylvania concluded that available evidence does not support an association between statins and memory loss or dementia. The new study, a collaborative effort between faculty in Penn Medicine’s Preventive Cardiovascular Program, the Penn Memory Center, and the Penn Center for Evidence-Based Practice, will be published in Annals of Internal Medicine.

“Statins are prescribed to approximately 30 million people in the United States, and these numbers may increase as a result of the national cholesterol guidelines recently released,” said senior study author Emil deGoma, MD, assistant professor of Medicine and medical director of the Preventive Cardiovascular Program at Penn. “A wealth of data supports a benefit of these cholesterol-lowering medications among individuals at risk for cardiovascular disease in terms of a reduction in the risk of heart attack and stroke; however, potential side effects of statins are less well understood. In February 2012, largely based on anecdotal reports, the U.S. Food and Drug Administration (FDA) issued a safety statement warning patients of possible adverse cognitive effects associated with statin use. Many concerned patients have asked if there is a relationship between statins and memory problems. Their concerns, along with the FDA statement, prompted us to pursue a rigorous analysis of all available evidence to better answer the question – are statins associated with changes in cognition?”

The research team conducted a systematic review of the published literature and identified 57 statin studies reporting measures of cognitive function. Dr. deGoma and colleagues found no evidence of an increased risk of dementia with statin therapy. In fact, in cohort studies, statin users had a 13 percent lower risk of dementia, a 21 percent lower risk of Alzheimer’s disease, and a 34 percent lower risk of mild cognitive impairment compared to people who did not take statins.

Most importantly, cognitive test scores were not adversely affected by statin treatment in randomized controlled trials. In these trials, roughly half of the study participants received statins and the other half received placebo. All study participants underwent formal testing of memory and other cognitive domains through tests such as the ability to recall a set of numbers. The analysis of 155 cognitive tests spanning eight categories of cognitive function, including 26 tests of memory, revealed no differences between study participants treated with statins and those provided placebo.

The research team additionally performed an analysis of the FDA post-marketing surveillance databases and found no difference in the frequency of cognitive adverse event reports between statins and two commonly prescribed cardiovascular medications that have not been associated with cognitive impairment, namely, clopidogrel and losartan.

“Overall, these findings are quite reassuring. I wouldn’t let concerns about adverse effects on cognition influence the decision to start a statin in patients suffering from atherosclerotic disease or at risk for cardiovascular disease. I also wouldn’t jump to the conclusion that statins are the culprit when an individual who is taking a statin describes forgetfulness. We may be doing more harm than good if we withhold or stop statins – medications proven to reduce the risk of heart attack and stroke – due to fears that statins might possibly cause memory loss,” said Dr. deGoma.

The team acknowledges that while their analysis is reassuring, large, high-quality randomized controlled trials are needed to confirm their findings. 

“For many of the cognitive outcomes that we examined, the identified studies were small, were at risk for bias, used varying diagnostic tests to assess cognitive domains, and did not include patients on high-dose statins, which is important given the increasing use of high-dose statins for secondary prevention,” noted study co-author Craig Umscheid, MD, MSCE, assistant professor of Medicine and Epidemiology and director of the Penn Center for Evidence-based Practice. “Thus, additional trials addressing these limitations would strengthen our conclusions. Despite this, the totality of the evidence does reassure us that there’s unlikely to be a significant link between statins and cognitive impairment.”

Filed under cognitive decline statins cardiovascular disease memory neurodegenerative diseases medicine neuroscience science

199 notes

Caffeine Consumption Within Six Hours Of Bedtime May Disrupt Sleep Consumption of caffeine, even six hours before bedtime, can have significant, disruptive effects on sleep. The study, from the American Academy of Sleep Medicine, was published in the Journal of Clinical Sleep Medicine. “Sleep specialists have always suspected that caffeine can disrupt sleep long after it is consumed,” said American Academy of Sleep Medicine President M. Safwan Badr, MD. “This study provides objective evidence supporting the general recommendation that avoiding caffeine in the late afternoon and at night is beneficial for sleep.” The researchers found that 400 mg of caffeine (about 2-3 cups of coffee) taken at bedtime, or three to six hours before bedtime, significantly impacts sleep. Objectively measured total sleep time was reduced by more than an hour even when the caffeine was consumed six hours before going to bed. Subjective reports, however, suggest that the study participants were unaware of this sleep disturbance. “Drinking a big cup of coffee on the way home from work can lead to negative effects on sleep just as if someone were to consume caffeine closer to bedtime,” said Christopher Drake, PhD, investigator at the Henry Ford Sleep Disorders and Research Center and associate professor of psychiatry and behavioral neurosciences at Wayne State University. People tend to be less likely to detect the disruptive effects of caffeine on sleep when taken in the afternoon,” noted Drake, who is also on the board of directors of the Sleep Research Society. The researchers recruited 12 healthy normal sleepers, as determined by a physical examination and clinical interview. Subjects were instructed to maintain their normal sleep schedule, but were given three pills a day for four days to be taken at six, three and zero hours before scheduled bedtime. Two of the pills were placebos, and one was 400 mg of caffeine. On one of the four days, all three of the participants’ pills were a placebo. The researchers measured sleep disturbance subjectively using a standard sleep diary and objectively using an in-home sleep monitor. This is the first study to investigate the effects of a given dose of caffeine taken at different times before sleep. The findings suggest that, in order to allow healthy sleep, individuals should avoid caffeine after 5pm.

Caffeine Consumption Within Six Hours Of Bedtime May Disrupt Sleep

Consumption of caffeine, even six hours before bedtime, can have significant, disruptive effects on sleep. The study, from the American Academy of Sleep Medicine, was published in the Journal of Clinical Sleep Medicine.

“Sleep specialists have always suspected that caffeine can disrupt sleep long after it is consumed,” said American Academy of Sleep Medicine President M. Safwan Badr, MD. “This study provides objective evidence supporting the general recommendation that avoiding caffeine in the late afternoon and at night is beneficial for sleep.”

The researchers found that 400 mg of caffeine (about 2-3 cups of coffee) taken at bedtime, or three to six hours before bedtime, significantly impacts sleep. Objectively measured total sleep time was reduced by more than an hour even when the caffeine was consumed six hours before going to bed. Subjective reports, however, suggest that the study participants were unaware of this sleep disturbance.

“Drinking a big cup of coffee on the way home from work can lead to negative effects on sleep just as if someone were to consume caffeine closer to bedtime,” said Christopher Drake, PhD, investigator at the Henry Ford Sleep Disorders and Research Center and associate professor of psychiatry and behavioral neurosciences at Wayne State University.

People tend to be less likely to detect the disruptive effects of caffeine on sleep when taken in the afternoon,” noted Drake, who is also on the board of directors of the Sleep Research Society.

The researchers recruited 12 healthy normal sleepers, as determined by a physical examination and clinical interview. Subjects were instructed to maintain their normal sleep schedule, but were given three pills a day for four days to be taken at six, three and zero hours before scheduled bedtime. Two of the pills were placebos, and one was 400 mg of caffeine. On one of the four days, all three of the participants’ pills were a placebo. The researchers measured sleep disturbance subjectively using a standard sleep diary and objectively using an in-home sleep monitor.

This is the first study to investigate the effects of a given dose of caffeine taken at different times before sleep. The findings suggest that, in order to allow healthy sleep, individuals should avoid caffeine after 5pm.

Filed under caffeine caffeine consumption sleep circadian rhythms psychology neuroscience science

122 notes

Image: Mice lacking autophagy and with high levels of Aβ (right) have degenerated brain structures compared with normal mice (left). The benefits of a spotless mind Alzheimer’s disease is an age-related memory disorder characterized by the accumulation of clumps of the toxic amyloid-β (Aβ) protein fragment in the extracellular space around neurons in the brain. Drugs that help to ‘clean up’ cells by inducing autophagy—the degradation of unnecessary cellular components—are known to lower Aβ levels within cells and have been shown to rescue memory deficits in mice. A team of researchers including Per Nilsson and Takaomi Saido from the RIKEN Brain Science Institute have now found that autophagy also plays an important role in secreting Aβ from the cell into the extracellular space. The researchers set out to investigate what would happen to extracellular Aβ aggregates, called plaques, when genetic methods were used to eliminate the autophagy process. They started with transgenic mice commonly used as a model for Alzheimer’s disease. These mice have high levels of Aβ and Aβ plaque accumulation in their brains, and display learning and memory deficits. Surprisingly, in genetically engineered variants of these mice lacking autophagy-related gene 7 (Atg7), which is required for normal autophagy, the researchers found fewer extracellular Aβ plaques in the brain; instead, the Aβ seemed to accumulate inside the neurons. Conversely, increasing the expression of the Atg7 protein in neurons grown in cell culture resulted in an increase in the release of Aβ from the cells into the tissue culture medium. The findings suggest that autophagy is required for the secretion of Aβ from neurons into the extracellular environment. Mice with an elevated expression of Aβ but defective autophagy seemed to have degenerated brain structures, as well as sicker neurons—as defined by their expression of markers of cell death—and worse learning and memory functions than mice with high Aβ expression but normal autophagy. This result indicates that autophagy is important for maintaining normal neuronal function and cognition in Alzheimer’s disease. Moreover, because autophagy lowers Aβ levels within the cell, the researchers deduced that intracellular Aβ may be more toxic than extracellular Aβ with respect to inducing neuronal dysfunction and memory impairment. The findings suggest that the effectiveness of therapeutic strategies for Alzheimer’s disease may be improved by targeting the elimination of intracellular Aβ deposits rather than extracellular plaques. “Intraneuronal Aβ accumulation is seen in early Alzheimer’s disease in humans, similar to what we found upon autophagy deletion in mice,” explains Nilsson. “Targeting this pool of Aβ may therefore offer a potential treatment for Alzheimer’s disease,” he says.

Image: Mice lacking autophagy and with high levels of Aβ (right) have degenerated brain structures compared with normal mice (left).

The benefits of a spotless mind

Alzheimer’s disease is an age-related memory disorder characterized by the accumulation of clumps of the toxic amyloid-β (Aβ) protein fragment in the extracellular space around neurons in the brain. Drugs that help to ‘clean up’ cells by inducing autophagy—the degradation of unnecessary cellular components—are known to lower Aβ levels within cells and have been shown to rescue memory deficits in mice. A team of researchers including Per Nilsson and Takaomi Saido from the RIKEN Brain Science Institute have now found that autophagy also plays an important role in secreting Aβ from the cell into the extracellular space.

The researchers set out to investigate what would happen to extracellular Aβ aggregates, called plaques, when genetic methods were used to eliminate the autophagy process. They started with transgenic mice commonly used as a model for Alzheimer’s disease. These mice have high levels of Aβ and Aβ plaque accumulation in their brains, and display learning and memory deficits. Surprisingly, in genetically engineered variants of these mice lacking autophagy-related gene 7 (Atg7), which is required for normal autophagy, the researchers found fewer extracellular Aβ plaques in the brain; instead, the Aβ seemed to accumulate inside the neurons. Conversely, increasing the expression of the Atg7 protein in neurons grown in cell culture resulted in an increase in the release of Aβ from the cells into the tissue culture medium. The findings suggest that autophagy is required for the secretion of Aβ from neurons into the extracellular environment.

Mice with an elevated expression of Aβ but defective autophagy seemed to have degenerated brain structures, as well as sicker neurons—as defined by their expression of markers of cell death—and worse learning and memory functions than mice with high Aβ expression but normal autophagy. This result indicates that autophagy is important for maintaining normal neuronal function and cognition in Alzheimer’s disease. Moreover, because autophagy lowers Aβ levels within the cell, the researchers deduced that intracellular Aβ may be more toxic than extracellular Aβ with respect to inducing neuronal dysfunction and memory impairment.

The findings suggest that the effectiveness of therapeutic strategies for Alzheimer’s disease may be improved by targeting the elimination of intracellular Aβ deposits rather than extracellular plaques. “Intraneuronal Aβ accumulation is seen in early Alzheimer’s disease in humans, similar to what we found upon autophagy deletion in mice,” explains Nilsson. “Targeting this pool of Aβ may therefore offer a potential treatment for Alzheimer’s disease,” he says.

Filed under alzheimer's disease beta amyloid autophagy degeneration neuroscience science

57 notes

Drug Shows Early Promise in Treating Liver Failure-Related Seizures

A study out today in the journal Nature Medicine suggests a potential new treatment for the seizures that often plague children with genetic metabolic disorders and individuals undergoing liver failure. The discovery hinges on a new understanding of the complex molecular chain reaction that occurs when the brain is exposed to too much ammonia. 

image

The study shows that elevated levels of ammonia in the blood overwhelm the brain’s defenses, ultimately causing nerve cells to become overexcited. The researchers have also discovered that bumetanide – a diuretic drug used to treat high blood pressure – can restore normal electrical activity in the brains of mice with the condition and prevent seizures. 

 “Ammonia is a ubiquitous waste product of regular protein metabolism, but it can accumulate in toxic levels in individuals with metabolic disorders,” said Maiken Nedergaard, M.D., D.M.Sc., co-director of the University of Rochester Medical Center (URMC) Center for Translational Neuromedicine and lead author of the article. “It appears that the key to preventing the debilitating neurological effects of ammonia toxicity is to correct a molecular malfunction which causes nerve cells in the brain to become chemically unbalanced.”

In healthy people, ammonia is processed in the liver, converted to urea, and expelled from the body in urine. Because it is a gas, ammonia can slip through the blood-brain-barrier and make its way into brain tissue. Under normal circumstances, the brain’s housekeeping cells – called astrocytes – sweep up this unwanted ammonia and convert it into a compound called glutamine which can be more easily expelled from the brain. 

However, individuals with certain genetic metabolic disorders and people with impaired liver function because of chronic hepatitis, alcoholism, acetaminophen overdose, and other toxic liver conditions cannot remove ammonia from their bodies quickly enough. The result is a larger than normal concentration of ammonia in the blood, a condition called hyperammonemia. 

When too much ammonia makes its way into the central nervous system, it can lead to tremors, seizures and, in extreme cases, can cause comas and even lead to death. In children with metabolic disorders the frequent seizures can lead to long-term neurological impairment. 

While ammonia has long been assumed to be the culprit behind the neurological problems associated with inherited metabolic disorders and liver failure, the precise mechanisms by which it triggers seizures and comas have not been fully understood. The new study reveals that ammonia causes a chain of events that alters the chemistry and electrical activity of the brain’s nerve cells, causing them to fire in uncontrolled bursts.

One of the keys to unraveling the effects of ammonia on the brain has been new imagining technologies such as two-photon microscopy which allow researchers to watch this phenomenon in real time in the living brains of mice. As suspected, they observed that when high levels of ammonia enter the brain, astrocytes become quickly overwhelmed and cannot remove it fast enough. 

The abundant ammonia in the brain mimics the function of potassium, an important player in neurotransmission, and tricks neurons into becoming depolarized. This makes it more likely that electrical activity in the brain will exceed the threshold necessary to trigger seizures.

Furthermore, the researchers observed that one of the neuron’s key molecular gatekeepers – a transporter known as NKCC1 – was also fooled into thinking that the ammonia was potassium. As a result, it went into overdrive, loading neurons with too much chloride. This in turn prevents the cells from stabilizing itself after spikes in activity, keeping the cells in a heightened level of electrical “excitability.” 

The team found that the drug bumetanide, a known NKCC1 inhibitor, blocked this process and prevented the cells from overloading with chloride. By knocking down this “secondary” cellular effect of ammonia, the researchers were able to control the seizures in the mice and prolong their survival.

“The neurologic impact of hyperammonemia is a tremendous clinical problem without an effective medical solution,” said Nedergaard.   “The fact that bumetanide is already approved for use gives us a tremendous head start in terms of developing a potential treatment for this condition. This study provides a framework to further explore the therapeutic potential of this and other NKCC1 inhibitors.”

(Source: urmc.rochester.edu)

Filed under liver failure ammonia seizures nerve cells bumetanide astrocytes metabolic disorders neuroscience science

1,589 notes

Researcher advances retinal implant that could restore sight for the blind

People who went blind as a result of certain diseases or injuries may have renewed hope of seeing again thanks to a retinal implant developed with the help of Florida International University’s W. Kinzy Jones, a professor and researcher in the College of Engineering and Computing.

A tiny video camera mounted on special glasses captures the scene in the patient’s environment, and a pocket controller relays the captured video signal to the implant. Inspired by cochlear implants that can restore hearing to some deaf people, the retinal implant works by electrically stimulating nerve cells that normally carry visual input from the retina to the brain, and bypassing the lost retinal cells.

The Boston Retinal Implant Project, a highly-specialized, academically-based team of 30 researchers including Jones, was responsible for bringing the implant to light. The group is comprised of biologists and engineers from Harvard, Cornell, Massachusetts Institute of Technology (MIT) and others who are developing new technologies for the blind.

“Jones’ work was one the most important technological developments needed to make the device possible,” said Douglas Shire, engineering manager for the Boston Retinal Implant Project. “As a result, users of the retinal implant will be able to adjust the implant according to their needs.”

Jones has been working for years to advance the airtight sealed titanium housing and feed-through component that transfers the signals from the implanted microchip to the electrodes. His improvements in the density of that feed-through will greatly improve the quality of the image the person wearing the device will see.

The retinal implant was designed for people who lost vision due to injury to the eyes; progressive vision loss caused by eye disorders (also known as retinitis pigmentosa); or age-related macular degeneration, when the center of the retina that is responsible for central vision deteriorates. According to the National Institutes of Health, age-related macular degeneration is a leading cause of vision loss in Americans 60 years old and older.

“The impact of this technology, which increases the available pixels that can be stimulated, will bring enhanced visual acuity to people with debilitating eye loss,” Jones said. “My mother had macular degeneration and I saw the quality of her life degrade as the disease progressed. Hopefully, when these devices are available for FDA approved use, total loss of eye sight from macular degeneration or retinitis pigmentosa will be a thing of the past within 10 to 15 years.”

Recently, a similar device that features 60 electrodes was approved for use in patients and has proven successful in allowing people who were blind to read words on a screen.

Shire explained that the device that the Boston Group is building with Jones’ help has more than 256 electrodes and therefore allows for images with a larger number of pixels, which is expected to give patients a meaningful visual experience.

Filed under retinal implant retinitis pigmentosa macular degeneration blindness vision loss neuroscience science

199 notes

Pregnant mother’s stress affects baby’s gut and brain

Pregnant women may pass on the effects of stress to their fetus by way of bacterial changes in their vagina, suggests a study in mice. It may affect how well their baby’s brain is equipped to deal with stress in adulthood.

image

The bacteria in our body outnumber our own cells by about 10 to 1, with most of them found in our gut. Over the last few years, it has become clear that the bacterial ecosystem in our body – our microbiome – is essential for developing and maintaining a healthy immune system.

Our gut bugs also help to prevent germs from invading our bodies, and help to absorb nutrients from food.

A baby gets its first major dose of bacteria in life as it passes through its mother’s birth canal. En route, the baby ingests the mother’s vaginal microbes, which begin to colonise the newborn’s gut.

Chris Howerton, then at the University of Pennsylvania in Philadelphia, and his colleagues wanted to know if this initial population of bacteria is important in shaping a baby’s neurological development, and whether that population is influenced by stress during pregnancy.

Stressful pregnancy

The first step was to figure out what features of the mother’s vaginal microbiome might be altered by stress, and then see if any of those changes were transmitted to the offspring’s gut.

To do this, the team exposed 10 pregnant mice to a different psychologically stressful experience, such as exposing them to fox odour, keeping their cages lit at night, or temporarily restraining them every day for what would be the equivalent of the first trimester of their pregnancy. Another 10 pregnant mice were housed normally during the same time.

The team took samples of their vaginal bacteria throughout the pregnancy and again just after the mice had given birth. These samples were genetically sequenced to see what types of bacteria were present.

The microbiomes of the stressed mice were remarkably different to those of the unstressed mice after they had each given birth. There were more types of bacteria present, and the proportion of one common gut bacteria, Lactobacillus, was significantly reduced.

Like mother, like pup

To see whether these changes had been passed on to the pups, a few days after birth the pups’ nascent gut bacteria was removed from their colon and sequenced. Sure enough, the same bacterial patterns were seen in the pups of stressed mothers.

By analysing tissue from the pups’ hypothalamus – a brain area involved in hormone control, behaviour and sleep, among other things – the team was able to infer which genes were affected by the stress-induced changes in each mother’s microbiome.

They found that the expression of 20 genes was affected by the decrease in Lactobacillus, including genes related to the production of new neurons and the growth of synaptic connections in the brain.

These genetic outcomes in the brain are probably a result of a different suite of nutrients and metabolites circulating in the “stressed” pup’s blood, thanks to the altered gut flora they inherited. Indeed, when the team analysed the blood of the pups of the stressed mothers, they found that there were fewer molecules present necessary for the formation of essential neurotransmitters – chemicals that transmit signals to the brain. Furthermore, there were lower levels of a molecule thought to protect the brain from harmful oxidative stress.

"These changes are significant and are likely to be important for determining how the brain initially develops and how it will respond in the future to things like stress or changes in the environment," says Tracy Bale, Howerton’s supervisor during the research and director of the University of Pennsylvania lab.

As well as changing the nutrients available, the microbiome could also affect the brain via the immune system or by innervating the nerves in the gut that connect to it. “These three mechanisms aren’t mutually exclusive. It’s likely that they all play a role,” says Howerton.

Human angle

If the same effects are seen in humans, there may be a straightforward solution. “We can easily manipulate the bacteria we have inside of us,” says Howerton. For example, if a certain cocktail of bacteria is found to be beneficial to the newborns of stressed mothers, we could give it to them right after birth, he suggests. This approach could also benefit babies born via C-section, who do not pass through their mother’s birth canal, or those born to mothers whose gut bacteria has been disrupted as a result of antibiotic use during pregnancy.

Bale is now investigating the link between bacteria and brain development in pregnant women who have been through several traumatic experiences to analyse the effects on their babies’ gut bacteria. She also intends to follow their children’s behaviour as they grow up.

Resource rationale

"This is a remarkable trans-disciplinary study in how it bridged multiple organ systems to illuminate a complex question," says Catherine Hagan from the University of Missouri in Columbia. She says that more work needs to be done to show a causal link. "Mice are not tiny people – people are not big mice – more data is needed to understand how stress in mothers affects brain development in children," she says. "That said, mice and people have enough in common that this study provides a rationale for allocating resources to address such a concern."

"At the end of the day, most of what makes you ‘you’, and what drives your quality of life, comes down to the brain," says Bale. "It’s this very important, vulnerable tissue that is susceptible to many perturbations. If the microbiome is proven to be one of these driving forces, then it’s essential we know just how factors in our environment can change it and can reprogram the brain."

(Source: newscientist.com)

Filed under pregnancy stress microbiome animal model brain development Neuroscience 2013 neuroscience science

197 notes

Brain Stimulation May Treat Bulimia A mild electrical stimulation to a specific brain area could be an effective treatment for some patients with eating disorders such as bulimia, who suffer from episodes of severe binge eating and purging behaviors, researchers say. After one 42-year-old woman received the electrical stimulation, called transcranial magnetic stimulation (TMS), as a treatment for her depression, and showed an unexpected recovery from her 20-year battle against bulimia nervosa, her doctors conducted a pilot study to see whether the treatment would also work for other patients with eating disorders, said Dr. Jonathan Downar, of the University of Toronto. Downar described the study Tuesday (Nov. 12) here at the annual meeting of the Society for Neuroscience. In the study, Downar and his colleagues recruited 20 patients with bulimia and stimulated a part of their frontal lobes called the dorsomedial prefrontal cortex, which is next to the brain region usually stimulated for treating depression. The patients, who had already tried conventional therapies and medications but had seen no improvement, received 20 sessions of electrical stimulation daily for four weeks. At the end of the treatment, six of the patients saw their binge eating and purging symptoms almost completely disappear. In another four patients, symptoms improved by more than 50 percent. Eight patients saw only little improvement, and two got worse, Downar said. Although larger studies and clinical trials are needed to confirm the results of the pilot study, Downar said he is optimistic about the promise of using TMS for treating certain patients with eating disorders. "There are lots of things you could do to treat disorders like depression, but for these folks [with bulimia], there’s really nothing if they have gone through all of the medications" and therapy options, Downar said. Eating disorders, such as anorexia and bulimia, affect more than 8 million people in North America. These disorders often carry emotional distress, disrupt the person’s normal life and can even lead to life-threatening medical problems. TMS is a relatively new technique, and involves a large electromagnetic coil that is placed over the skull, and changes the activity in a targeted brain region by inducing electric currents. Although the change is temporary and reversible, with repeated stimulation, doctors can create lasting changes in neuronal activity. Repeated TMS has been approved by the U.S. Food and Drug Administration as a treatment for some forms of depression. In the study, the researchers used brain imaging to examine whether differences in brain activity could explain why some patients respond well to TMS treatment while others show little or no improvement. They found that before the treatment, responders had lower connectivity between the frontal lobe and a set of brain areas (such as the striatum) that are linked to rewards and cravings. This low connectivity could be a sign of impulsiveness, and stimulation may have helped to make the missing connection in these patients’ brains, Downar said. In contrast, the brains of the people whose bulimia was not helped by TMS appeared more connected in those areas. In these patients, TMS appears to be ineffective in treating bulimia because the brain stimulation is “giving them something they don’t need, because they already have it,” Downar said. The brain imaging results suggest that doctors may be able to identify which patients will respond to TMS treatment, and spare others from a weeks-long treatment. "By using brain imaging to detect these patterns, we may eventually be able to predict which patients are most likely to benefit," Downar said.

Brain Stimulation May Treat Bulimia

A mild electrical stimulation to a specific brain area could be an effective treatment for some patients with eating disorders such as bulimia, who suffer from episodes of severe binge eating and purging behaviors, researchers say.

After one 42-year-old woman received the electrical stimulation, called transcranial magnetic stimulation (TMS), as a treatment for her depression, and showed an unexpected recovery from her 20-year battle against bulimia nervosa, her doctors conducted a pilot study to see whether the treatment would also work for other patients with eating disorders, said Dr. Jonathan Downar, of the University of Toronto. Downar described the study Tuesday (Nov. 12) here at the annual meeting of the Society for Neuroscience.

In the study, Downar and his colleagues recruited 20 patients with bulimia and stimulated a part of their frontal lobes called the dorsomedial prefrontal cortex, which is next to the brain region usually stimulated for treating depression. The patients, who had already tried conventional therapies and medications but had seen no improvement, received 20 sessions of electrical stimulation daily for four weeks.

At the end of the treatment, six of the patients saw their binge eating and purging symptoms almost completely disappear. In another four patients, symptoms improved by more than 50 percent. Eight patients saw only little improvement, and two got worse, Downar said.

Although larger studies and clinical trials are needed to confirm the results of the pilot study, Downar said he is optimistic about the promise of using TMS for treating certain patients with eating disorders.

"There are lots of things you could do to treat disorders like depression, but for these folks [with bulimia], there’s really nothing if they have gone through all of the medications" and therapy options, Downar said.

Eating disorders, such as anorexia and bulimia, affect more than 8 million people in North America. These disorders often carry emotional distress, disrupt the person’s normal life and can even lead to life-threatening medical problems.

TMS is a relatively new technique, and involves a large electromagnetic coil that is placed over the skull, and changes the activity in a targeted brain region by inducing electric currents. Although the change is temporary and reversible, with repeated stimulation, doctors can create lasting changes in neuronal activity. Repeated TMS has been approved by the U.S. Food and Drug Administration as a treatment for some forms of depression.

In the study, the researchers used brain imaging to examine whether differences in brain activity could explain why some patients respond well to TMS treatment while others show little or no improvement.

They found that before the treatment, responders had lower connectivity between the frontal lobe and a set of brain areas (such as the striatum) that are linked to rewards and cravings. This low connectivity could be a sign of impulsiveness, and stimulation may have helped to make the missing connection in these patients’ brains, Downar said.

In contrast, the brains of the people whose bulimia was not helped by TMS appeared more connected in those areas. In these patients, TMS appears to be ineffective in treating bulimia because the brain stimulation is “giving them something they don’t need, because they already have it,” Downar said.

The brain imaging results suggest that doctors may be able to identify which patients will respond to TMS treatment, and spare others from a weeks-long treatment.

"By using brain imaging to detect these patterns, we may eventually be able to predict which patients are most likely to benefit," Downar said.

Filed under eating disorders bulimia transcranial magnetic stimulation Neuroscience 2013 neuroscience science

97 notes

New hope for heavy smokers after study finds zapping their brains with magnetic pulses made it easier for them to quit Heavy smokers could be helped to kick the habit by having their brains zapped with electromagnetic pulses, new research suggests. Repeated use of a high frequency magnet to stimulate the brain helps some smokers quit for up to six months after treatment, an Israeli study found. The smokers had already tried a range of treatments, from patches to psychotherapy, raising hopes that brain stimulation could be an effective alternative for those who had so far failed to kick the habit. Abraham Zangen of Ben Gurion University told the annual meeting of the Society for Neuroscience in San Diego, California, that more than half the smokers given high-frequency magnetic pulses quit. More than a third were still abstaining six months on. 'Our research shows us that we may actually be able to undo some of the changes to the brain caused by chronic smoking,' said Dr Zangen. 'We know that many smokers want to quit or smoke less and this could help put a dent in the number one cause of preventable deaths.' Dr Zangen’s team recruited 115 heavy smokers aged between 21 and 70 who were interested in quitting but who had failed in doing so on at least two previous attempts. They then split the smokers into three groups, giving them either high frequency repeated Transcranial Magnetic Stimulation (rTMS), low frequency rTMS, or placebo treatment for 13 days. Repeated high frequency Transcranial Magnetic Stimulation (rTMS) is a non-invasive technique that uses magnetic fields to stimulate large areas of neurons in the brain. The researchers focused on stimulating the prefrontal cortex and the insula, which are the two brain areas associated with nicotine addiction. Before each session, Dr Zangen got one of his PhD students to light a cigarette and take a drag in front of half the smokers in each group to awaken their cravings. This was to make sure the smokers’ attention was directed at their addiction and not some other craving, said Dr Zangen. The results were striking. Nearly half - 44 per cent - of the smokers who received the cue before their rTMS session gave up immediately after the 13-day course, with 33 per cent still of the smokes six months later. Overall, participants who received high frequency rTMS smoked less and were more likely to quit, with success rates four times that of the low frequency group and more than six times greater than the placebo group. Dr Zangen’s team are now planning a much larger trial involving smokers in several countries, which is set to start in the next few months. He told The Guardian: ‘It’s quite easy to quit for a few days, or even for a few weeks, but if we can help people quit for more than three months, then they are actually quite unlikely to relapse later on.’ Dr Zanger did reveal that he has a financial interest in the company which provided the Transcranial Magnetic Stimulation equipment used in the study.

New hope for heavy smokers after study finds zapping their brains with magnetic pulses made it easier for them to quit

Heavy smokers could be helped to kick the habit by having their brains zapped with electromagnetic pulses, new research suggests.

Repeated use of a high frequency magnet to stimulate the brain helps some smokers quit for up to six months after treatment, an Israeli study found.

The smokers had already tried a range of treatments, from patches to psychotherapy, raising hopes that brain stimulation could be an effective alternative for those who had so far failed to kick the habit.

Abraham Zangen of Ben Gurion University told the annual meeting of the Society for Neuroscience in San Diego, California, that more than half the smokers given high-frequency magnetic pulses quit.

More than a third were still abstaining six months on.

'Our research shows us that we may actually be able to undo some of the changes to the brain caused by chronic smoking,' said Dr Zangen.

'We know that many smokers want to quit or smoke less and this could help put a dent in the number one cause of preventable deaths.'

Dr Zangen’s team recruited 115 heavy smokers aged between 21 and 70 who were interested in quitting but who had failed in doing so on at least two previous attempts.

They then split the smokers into three groups, giving them either high frequency repeated Transcranial Magnetic Stimulation (rTMS), low frequency rTMS, or placebo treatment for 13 days.

Repeated high frequency Transcranial Magnetic Stimulation (rTMS) is a non-invasive technique that uses magnetic fields to stimulate large areas of neurons in the brain.

The researchers focused on stimulating the prefrontal cortex and the insula, which are the two brain areas associated with nicotine addiction.

Before each session, Dr Zangen got one of his PhD students to light a cigarette and take a drag in front of half the smokers in each group to awaken their cravings.

This was to make sure the smokers’ attention was directed at their addiction and not some other craving, said Dr Zangen.

The results were striking. Nearly half - 44 per cent - of the smokers who received the cue before their rTMS session gave up immediately after the 13-day course, with 33 per cent still of the smokes six months later.

Overall, participants who received high frequency rTMS smoked less and were more likely to quit, with success rates four times that of the low frequency group and more than six times greater than the placebo group.

Dr Zangen’s team are now planning a much larger trial involving smokers in several countries, which is set to start in the next few months.

He told The Guardian: ‘It’s quite easy to quit for a few days, or even for a few weeks, but if we can help people quit for more than three months, then they are actually quite unlikely to relapse later on.’

Dr Zanger did reveal that he has a financial interest in the company which provided the Transcranial Magnetic Stimulation equipment used in the study.

Filed under smoking nicotine addiction prefrontal cortex insula transcranial magnetic stimulation Neuroscience 2013 neuroscience science

408 notes

Synthetic alcohol substitute could eliminate health risks – and hangovers

A drug that mimics some effects of alcohol but lacks its harmful properties would have real benefit for public health, a leading scientist has argued.

image

Professor David Nutt, the Edmond J. Safra Professor of Neuropsychopharmacology at Imperial College London, has identified candidate molecules that reproduce the pleasurable effects of alcohol but are much less toxic. He is looking for investors to help develop the product and bring it to the market.

Alcohol mimics a chemical called GABA which is produced in the brain, but it also acts on receptors for other brain chemicals. The alcohol substitute would be designed to target GABA receptors very selectively, avoiding undesirable side effects such as hangovers and loss of coordination. An antidote could also be made to block the receptor, allowing drinkers to sober up quickly.

Professor Nutt told the Today programme on BBC Radio 4 that he first tested such a compound many years ago, but even better substitutes could be developed.

“There’s no question that you can produce a whole range of effects like alcohol by manipulating this system in the brain,” he said. “In some experiments, the effect is indistinguishable from alcohol.

“What we want to do is get rid of any the unwanted effects of inebriation, like aggression and memory impairment, and we just want to keep the pleasure and the sense of relaxation.

“We think by clever molecular modelling we can get rid of the risk of addiction as well.”

Professor Nutt hopes to make a range of cocktails containing his synthetic alcohol substitute. He has spoken to investors about taking the product to market, but many are wary that the drug might be controlled by legislation.

“I would like the government to make a recommendation that we try to improve on the health of our people by allowing these kind of substitute alcohols to be legal.”

Alcohol is responsible for 2.5 million deaths worldwide each year. Making safer alternatives available could reduce the harms significantly, Professor Nutt argued.

“I think this would be a serious revolution in health benefits, just as the e-cigarette is going to revolutionise the smoking of tobacco. I find it weird that we haven’t been talking about this before because it’s such an obvious target for health improvement.”

(Source: www3.imperial.ac.uk)

Filed under alcohol synthetic alcohol addiction GABA receptors neuroscience science

free counters