Posts tagged neuroscience
Articles and news from the latest research reports.
New research investigates how the common ‘cat parasite’ gets into the brain
The Toxoplasma gondii parasite causes toxoplasmosis. The parasite is common and infects between 30 and 50 per cent of the global population. It also infects animals, especially domestic cats. Human infection is contracted by eating poorly cooked (infected) meat and handling cat feces. Toxoplasmosis first appears with mild flu-like symptoms in adults and otherwise healthy people before entering a chronic and dormant phase, which has previously been regarded as symptom-free. But when the immune system is weakened toxoplasmosis in the brain can be fatal. The fetus can be infected through the mother and because of this risk, pregnant women are recommended to avoid contact with cat litter boxes. Surprisingly, several studies in humans and mice have suggested that even in the dormant phase, the parasite can influence increasing risk taking and infected people show higher incidence of schizophrenia, anxiety and depression, which are broader public health concerns.
In their recent study Fuks et al. showed for the first time how the parasite enters the brain and increases the release of a neurotransmitter called GABA (gaba-Aminobutyric acid), that, amongst other effects, inhibits the sensation of fear and anxiety. In one laboratory experiment, human dendritic cells were infected with toxoplasma. After infection, the cells, which are a key component of the immune defense, began actively releasing GABA), In another experiment on live mice, the team was able to trace the movement of infected dendritic cells in the body after introducing the parasite into the brain, from where it spread and continued to affect the GABA system.
"For toxoplasma to make cells in the immune defense secrete GABA was as surprising as it was unexpected, and is very clever of the parasite," says Antonio Barragan, researcher at the Center for Infectious Medicine at Karolinska Institute and the Swedish Institute for Communicable Disease Control. "It would now be worth studying the links that exist between toxoplasmosis, the GABA systems and major public health threats."
(Image: Maria Sbytova/Shutterstock)
Discovery of pathway leading to depression reveals new drug targets
Scientists have identified the key molecular pathway leading to depression, revealing potential new targets for drug discovery, according to research led by King’s College London’s Institute of Psychiatry. The study, published in Neuropsychopharmacology, reveals for the first time that the ‘Hedgehog pathway’ regulates how stress hormones, usually elevated during depression, reduce the number of brain cells.
Depression affects approximately 1 in 5 people in the UK at some point in their lives. The severity of symptoms can range from feelings of sadness and hopelessness to, in the most severe cases, self-harm or suicide. Treatment for depression involves either medication or talking treatment, or usually a combination of the two.
Recent studies have demonstrated that depression is associated with a reduction in a brain process called ‘neurogenesis’- the ability of the brain to produce new brain cells. However, the pathway responsible for this process has, until now, remained unknown.
In this study, Dr Christoph Anacker from the Centre for the Cellular Basis of Behaviour (CCBB) at King’s Institute of Psychiatry and his team studied human stem cells, which are the source of new cells in the human brain, to investigate the effect of stress hormones on brain cell development. The study was funded by the National Institute for Health Research Biomedical Research Centre for Mental Health at the South London and Maudsley NHS Foundation Trust and King’s College London and the Medical Research Council UK.
Stress hormones, such as cortisol, are generally elevated in stress and depression. The team studied stem cells in a laboratory and found that high concentrations of cortisol damaged these stem cells and reduced the number of newborn brain cells. They discovered that a specific signalling mechanism in the cell, the ‘Hedgehog pathway’, is responsible for this process. Then, using an animal model, the team confirmed that exposure to stress inhibited this pathway in the brain.
Finally, in order to test the findings, the researchers used a compound called purmorphamine, which is known to stimulate the Hedgehog pathway. They found that by using this drug, they were able to reverse the damaging effects of stress hormones, and normalise the production of new brain cells.
Mu-rhythm in the brain: The neural mechanism of speech as an audio-vocal perception-action system
Speech production is one of the most important components in human communication. However, the cortical mechanisms governing speech are not well understood because it is extremely challenging to measure the activity of the brain in action, that is, during speech production.
Now, Takeshi Tamura and Michiteru Kitazaki at Toyohashi University of Technology, Atsuko Gunji and her colleagues at National Institute of Mental Health, Hiroshige Takeichi at RIKEN, and Hiroaki Shigemasu at Kochi University of Technology have found modulation of mu-rhythms in the cortex related to speech production.
The researchers measured EEG (electroencephalogram) with pre-amplified electrodes during simulated vocalization, simulated vocalization with delayed auditory feedback, simulated vocalization under loud noise, and silent reading. The authors define ‘mu-rhythm’ as a decrease of power in 8-16Hz EEG during the task period.
The mu-rhythm at the sensory-motor cortical area was not only observed under all simulated vocalization conditions, but was also found to be boosted by the delayed feedback and attenuated by loud noises. Since these auditory interferences influence speech production, it supports the premise that audio-vocal monitoring systems play an important role in speech production. The motor-related mu-rhythm is a critical index to clarify neural mechanisms of speech production as an audio-vocal perception-action system.
In the future, a neurofeedback method based on monitoring mu-rhythm at the sensory-motor cortex may facilitate rehabilitation of speech-related deficits.
Pokemon provides rare opening for IU study of face-recognition processes
At a Bloomington, Ind., toy store, kids ages 8 to 12 gather weekly to trade Pokemon cards and share their mutual absorption in the intrigue and adventure of Pokemon.
This may seem an unlikely source of material to test theories in cognitive neuroscience. But that is where Indiana University brain scientists Karin Harman James and Tom James were when an idea took hold.
"We were down at the club with our son, watching the way the kids talked about the cards, and noticed it was bigger than just a trading game," Tom James said.
Pokemon has since provided a rich testing ground for a theory of facial cognition that until now has been difficult to support. With the use of cutting-edge neuroimaging, the study challenges the prevailing theory of face recognition by offering new evidence for a theory that face recognition depends on a generalized system for recognizing objects, rather than a special area of the brain just for this function.
'Smart' genes put us at risk of mental illness
Humans may be endowed with the ability to perform complex forms of learning, attention and function but the evolutionary process that led to this has put us at risk of mental illness.
Data from new research, published today in the journal Nature Neuroscience, was analysed by Dr Richard Emes, a bioinformatics expert from the School of Veterinary Medicine and Science at The University of Nottingham. The results showed that disease-causing mutations occur in the genes that evolved to make us smarter than our fellow animals.
Dr Emes, Director of The University of Nottingham’s Advanced Data Analysis Centre, conducted an analysis of the evolutionary history of the Discs Large homolog (Dlg) family of genes which make some of the essential building blocks of the synapse — the connection between nerve cells in the brain. He said: “This study highlights the importance of the synapse proteome — the proteins involved in the brains signalling processes — in the understanding of cognition and the power of comparative studies to investigate human disease.”
The study involved scientists from The University of Edinburgh, The Wellcome Trust Sanger Institute, the University of Aberdeen, The University of Nottingham and the University of Cambridge.
This cross-disciplinary team of experts carried out what they believe to be the first genetic dissection of the vertebrate’s ability to perform complex forms of learning, attention and function. They focussed on Dlg — a family of genes that humans shared with the ancestor of all backboned animals some 550 million years ago. Gene families like the Dlgs arose by duplication of DNA, changed by mutation over millions of years and now contribute to the complex cognitive processes we have today. However, this redundancy and subsequent accumulation of changes in the DNA may have led to increased susceptibility to some diseases.
Components of the human cognitive repertoire are routinely assessed by using computerised touch-screen methods. By using the same technique with mice researchers were able to probe the cognitive mechanisms conserved since humans and mice shared a common ancestor — around 100 million years ago. By comparing the effect of DNA changes on behavioural test outcomes this research showed a common cause of mutation and effect of learning changes in both mice and humans.
Dr Emes said: “This research shows the importance of discerning information from data and how the power of computational research combined with behavioural and cognitive studies can provide such novel insight into the basis of clinical disorders. This research provides continued support that discovery occurs at the boundary of disciplines by the integration of data.”
(Source: nottingham.ac.uk)
Experimental prosthetic leg lets amputees ‘feel’ each step
Human prosthetics have come a long way in recent decades. We’ve gone from simple plastic molds that vaguely resemble the original limb, to high-tech articulating devices that return most of a person’s mobility. Through all this progress, one nagging issue has continued to plague doctors — there’s still no way for a patient to feel a prosthetic. A new project out of UCLA might be on the path to changing that.
Having something that acts like a leg turns out to be only part of the puzzle, says UCLA grad student Zachary McKinney. When you take a step with your flesh-and-blood leg, the limb is constantly sending sensory signals back to the brain that inform you when it touches the ground, how much weight is on it, and how that weight is distributed among other things. Lacking that kind of feedback in a prosthetic causes long-term problems like uneven gait or strain on the remaining limb.
The UCLA project is not seeking to exactly replicate the sensation of having a real leg, but to provide a system that can relay the same information. The system currently consists of four sensors in the shoe of the prosthetic leg. As the subject takes a step, the system register how much pressure is on each sensor and sends that data to a small computer strapped to the user’s midsection.
The computer will analyze the data, and control the inflation of a series of small balloons on the thigh cuff. These 12 dime-sized silicon balloons are split into four sets of three, each one corresponding to one of the shoe sensors. The more pressure detected, the larger the balloons inflate. Current lag time is roughly 0.1 seconds, which is only a little slower than nerve impulses. For the patient, it is functionally instantaneous.
Results have been encouraging in initial testing. Nine subjects who had lost a leg were asked to walk across a 30-foot wide space with a normal prosthetic. After being given time to acclimate to the pressure-sensitive system, the test was run again. According to the researchers, seven distinct measurements of gait improved with the test rig.
The many maps of the brain
Your brain has at least four different senses of location – and perhaps as many as 10. And each is different, according to new research from the Kavli Institute for Systems Neuroscience, at the Norwegian University of Science and Technology.
The findings, published in the 6 December 2012 issue of Nature, show that rather than just a single sense of location, the brain has a number of “modules” dedicated to self-location. Each module contains its own internal GPS-like mapping system that keeps track of movement, and has other characteristics that also distinguishes one from another.
"We have at least four senses of location," says Edvard Moser, director of the Kavli Institute. "Each has its own scale for representing the external environment, ranging from very fine to very coarse. The different modules react differently to changes in the environment. Some may scale the brain’s inner map to the surroundings, others do not. And they operate independently of each other in several ways."
This is also the first time that researchers have been able to show that a part of the brain that does not directly respond to sensory input, called the association cortex, is organized into modules. The research was conducted using rats.
See-through ‘MitoFish’ opens a new window on brain diseases
Scientists have demonstrated a new way to investigate mechanisms at work in Alzheimer’s and other neurodegenerative diseases, which also could prove useful in the search for effective drugs. For new insights, they turned to the zebrafish, which is transparent in the early stages of its life. The researchers developed a transgenic variety, the “MitoFish,” that enables them to see – within individual neurons of living animals – how brain diseases disturb the transport of mitochondria, the power plants of the cell.
Neurodegenerative diseases such as Alzheimer’s, Parkinson’s, ALS (amyotrophic lateral sclerosis), and MS (multiple sclerosis) are quite different in their effects on patients’ cognitive and motor functions, behavior, and prognosis. Yet on the level of individual neurons, common mechanisms can be observed that either cause or accompany nerve degeneration in a number of different diseases. One of these is a disturbance in the transport of mitochondria, organelles that play several vital roles in the life of a cell — above all, delivering energy where it is needed. And in a neuron, an extremely power-hungry cell, that means moving mitochondria all the way down its longest extension, the axon. Studying mitochondria transport in other animal models of neurodegenerative disease, particularly in mice, has been revealing. But the MitoFish model opens up new possibilities.
The new model was jointly developed in the labs of Prof. Thomas Misgeld of the Technische Universität München (TUM) and Dr. Bettina Schmid, a senior scientist of the German Center for Neurodegenerative Diseases (DZNE) based at the institute of LMU Prof. Christian Haass. “This collaboration has provided a system,” Misgeld says, “with which we can try to understand the traffic rules or the life cycle of a given organelle, in this case mitochondria, in the context of a nerve cell that’s existing in its physiological environment, where it is developing and changing. Most of these things we don’t understand well enough to model them in another setting, so we have the organism do it for us.”
The MitoFish is both readily manipulated, enabling researchers to pose specific questions, and literally transparent — allowing non-invasive in vivo observation of changes relevant to disease processes. It is possible to image a whole, living neuron over time and to follow the movements of mitochondria within it. “The zebrafish is an established genetic model,” Schmid explains, “which means you can bring foreign genes or certain proteins into a fish to test hypotheses about basic biology, disease mechanisms, or potential therapies. And because the early embryo is transparent, you can label specific nerve cells with a fluorescent protein and then look at them in an intact, living animal.”
New technique to deliver stem cell therapy may help damaged eyes regain their sight
Engineers at the University of Sheffield have developed a new technique for delivering stem cell therapy to the eye which they hope will help the natural repair of eyes damaged by accident or disease. This could help millions of people across the world retain – or even regain - their sight.
In research published in the journal Acta Biomaterialia, the team describe a new method for producing membranes to help in the grafting of stem cells onto the eye, mimicking structural features of the eye itself. The technology has been designed to treat damage to the cornea, the transparent layer on the front of the eye, which is one of the major causes of blindness in the world.
Using a combination of techniques known as microstereolithography and electrospinning, the researchers are able to make a disc of biodegradable material which can be fixed over the cornea. The disc is loaded with stem cells which then multiply, allowing the body to heal the eye naturally.
“The disc has an outer ring containing pockets into which stem cells taken from the patient’s healthy eye can be placed,” explains EPSRC Fellow, Dr Ílida Ortega Asencio, from Sheffield’s Faculty of Engineering. “The material across the centre of the disc is thinner than the ring, so it will biodegrade more quickly allowing the stem cells to proliferate across the surface of the eye to repair the cornea.”
A key feature of the disc is that it contains niches or pockets to house and protect the stem cells, mirroring niches found around the rim of a healthy cornea. Standard treatments for corneal blindness are corneal transplants or grafting stem cells onto the eye using donor human amniotic membrane as a temporary carrier to deliver these cells to the eye. For some patients, the treatment can fail after a few years as the repaired eyes do not retain these stem cells, which are required to carry out on-going repair of the cornea. Without this constant repair, thick white scar tissue forms across the cornea causing partial or complete sight loss. The researchers have designed the small pockets they have built into the membrane to help cells to group together and act as a useful reservoir of daughter cells so that a healthy population of stem cells can be retained in the eye.
Research identifies a way to block memories associated with PTSD or drug addiction
New research from Western University could lead to better treatments for Post-Traumatic Stress Disorder (PTSD) and drug addiction by effectively blocking memories. The research performed by Nicole Lauzon, a PhD candidate in the laboratory of Steven Laviolette at Western’s Schulich School of Medicine & Dentistry has revealed a common mechanism in a region of the brain called the pre-limbic cortex, can control the recall of memories linked to both aversive, traumatic experiences associated with PTSD and rewarding memories linked to drug addiction. More importantly, the researchers have discovered a way to actively suppress the spontaneous recall of both types of memories, without permanently altering memories. The findings are published online in the journal Neuropharmacology.
“These findings are very important in disorders like PTSD or drug addiction. One of the common problems associated with these disorders is the obtrusive recall of memories that are associated with the fearful, emotional experiences in PTSD patients. And people suffering with addiction are often exposed to environmental cues that remind them of the rewarding effects of the drug. This can lead to drug relapse, one of the major problems with persistent addictions to drugs such as opiates,” explains Laviolette, an associate professor in the Departments of Anatomy and Cell Biology, and Psychiatry. “So what we’ve found is a common mechanism in the brain that can control recall of both aversive memories and memories associated with rewarding experience in the case of drug addiction.”
In their experiments using a rat model, the neuroscientists discovered that stimulating a sub-type of dopamine receptor called the “D1” receptor in a specific area of the brain, could completely prevent the recall of both aversive and reward-related memories. “The precise mechanisms in the brain that control how these memories are recalled are poorly understood, and there are presently no effective treatments for patients suffering from obtrusive memories associated with either PTSD or addiction,” says Lauzon. “If we are able to block the recall of those memories, then potentially we have a target for drugs to treat these disorders.”