Posts tagged neuroscience

Posts tagged neuroscience

Why Facial Disfigurements Creep Us Out
Whether we realize it or not, most of us have a knee-jerk reaction when we see someone with a facial disfigurement, such as psoriasis, a cleft lip, or a birthmark. We may sit away from them on the bus, hesitate to shake their hand, or even give a barely masked look of revulsion. A new study suggests these disgust reactions stem from an ancient disease-avoidance system that normally prevents us from catching illnesses. Essentially, we treat facial disfigurements like infectious diseases.

Video games can be good for your health
Dr. Penelope McNulty, a neurophysiologist at Neuroscience Research Australia, will present new data that shows the Wii is an effective rehabilitation tool at an international conference of the Society of Electrophysiology and Kinesiology in Brisbane on 20 July.
Dr. McNulty’s data shows that an intensive, two-week training program based on the Wii can result in significant improvements in the way stroke patients are able to use their limbs, even for people that had a stroke many years ago.
“It was previously thought that the movement and function stroke patients had at the time they left hospital was the only recovery they would make,” says Dr. McNulty.
“But we have worked with people who have had strokes one month to 21 years ago, and excitingly, they all improve,” she added.
There are over 60,000 strokes in Australia each year and there is a crucial need to improve rehabilitation methods because this is the only method known to restore movement in stroke-affected limbs.
“The Wii is inexpensive, easy to use and, very importantly, fun. This type of rehabilitation motivates participants to actually complete their therapy, which is essential for maximum recovery,” Dr. McNulty says.
“Everyone notices improvements not just using the Wii, but in activities they do every day, such as opening a door or using a fork,” Dr. McNulty concluded.
ScienceDaily (July 20, 2012) — Conditions such as Parkinson’s disease are a result of pathogenic changes to proteins. In the neurodegenerative condition of Parkinson’s disease, which is currently incurable, the alpha-synuclein protein changes and becomes pathological. Until now, there have not been any antibodies that could help to demonstrate the change in alpha-synuclein associated with the disease. An international team of experts led by Gabor G. Kovacs from the Clinical Institute of Neurology at the MedUni Vienna has now discovered a new antibody that actually possesses this ability.
"It opens up new possibilities for the development of a diagnostic test for Parkinsonism," says Kovacs, highlighting the importance of this discovery. "This new antibody will enable us to find the pathological conformation in bodily fluids such as blood or CSF." A clinical study involving around 200 patients is already underway, and the first definitive results are expected at the end of 2012. The tests being carried out in collaboration with the University Department of Neurology, led by Walter Pirker, are designed to determine the extent to which the new antibody can be used as an early diagnostic tool in order to understand the condition better and be able to treat it more effectively.
A step towards a blood test for Parkinson’s With Parkinsonism, the diseased form of alpha-synuclein, which has the same primary structure as the healthy form, undergoes an “abnormal fold.” Says Kovacs: “Until now, however, it was not possible to distinguish between the two.” The previous immunodiagnostic techniques only allowed the general presence of alpha-synuclein to be confirmed. The new, monoclonal antibody, however, which the researchers at the MedUni Vienna have developed in collaboration with the German biotech firm Roboscreen, is now able to detect a strategic part of the protein responsible for the structural changes. The results of the study have now been published in the journal Acta Neuropathologica.
Says Kovacs: “It is still not possible to say whether or not we will be able to diagnose Parkinson’s from a blood test, but this discovery certainly represents a major step in that direction.” Theoretically, it should be possible to diagnose Parkinson’s disease five to eight years before it develops.
In Austria, there are between 15,000 and 16,000 people living with Parkinson’s syndrome. Its frequency increases with age. As society becomes older, Parkinson’s disease, a degenerative condition of the brain, will become an increasingly widespread problem.
Source: Science Daily
ScienceDaily (July 20, 2012) — Scientists at the University of Manchester have uncovered how the internal mechanisms in nerve cells wire the brain. The findings open up new avenues in the investigation of neurodegenerative diseases by analysing the cellular processes underlying these conditions.

Illustration of spectraplakins in axonal growth organising microtubules. (Credit: Image courtesy of University of Manchester)
Dr Andreas Prokop and his team at the Faculty of Life Sciences have been studying the growth of axons, the thin cable-like extensions of nerve cells that wire the brain. If axons don’t develop properly this can lead to birth disorders, mental and physical impairments and the gradual decay of brain capacity during aging.
Axon growth is directed by the hand shaped growth cone which sits in the tip of the axon. It is well documented how growth cones perceive signals from the outside to follow pathways to specific targets, but very little is known about the internal machinery that dictates their behaviour.
Dr Prokop has been studying the key driver of growth cone movements, the cytoskeleton. The cytoskeleton helps to maintain a cell’s shape and is made up of the protein filaments, actin and microtubules. Microtubules are the key driving force of axon growth whilst actin helps to regulate the direction the axon grows.
Dr Prokop and his team used fruit flies to analyse how actin and microtubule proteins combine in the cytoskeleton to coordinate axon growth. They focussed on the multifunctional proteins called spectraplakins which are essential for axonal growth and have known roles in neurodegeneration and wound healing of the skin.
What the team demonstrate in this recent paper is that spectraplakins link microtubules to actin to help them extend in the direction the axon is growing. If this link is missing then microtubule networks show disorganised criss-crossed arrangements instead of parallel bundles and axon growth is hampered.
By understanding the molecular detail of these interactions the team made a second important finding. Spectraplakins collect not only at the tip of microtubules but also along the shaft, which helps to stabilise them and ensure they act as a stable structure within the axon.
This additional function of spectraplakins relates them to a class of microtubule-binding proteins including Tau. Tau is an important player in neurodegenerative diseases, such as Alzheimer’s, which is still little understood. In support of the author’s findings, another publication has just shown that the human spectraplakin, Dystonin, causes neurodegeneration when affected in its linkage to microtubules.
Talking about his research Dr Prokop said: “Understanding cytoskeletal machinery at the cell level is a holy grail of current cell research that will have powerful clinical applications. Thus, cytoskeleton is crucially involved in virtually all aspects of a cell’s life, including cell shape changes, cell division, cell movement, contacts and signalling between cells, and dynamic transport events within cells. Accordingly, the cytoskeleton lies at the root of many brain disorders. Therefore, deciphering the principles of cytoskeletal machinery during the fundamental process of axon growth will essentially help research into the causes of a broad spectrum of diseases. Spectraplakins like at the heart of this machinery and our research opens up new avenues for its investigation”
What Dr Prokop’s paper in the Journal of Neuroscience also demonstrates is the successful research technique using the fruit fly Drosophila. The team was able to replicate its findings regarding axon growth in mice which in turn means the findings can be translated to humans.
Dr Prokop points out fruit flies provide ideal means to make sense of these findings and essentially help to unravel the many mysteries of neurodegeneration.
Dr Prokop continues: “Understanding how spectraplakins perform their cellular functions has important implications for basic as well as biomedical research. Thus, besides their roles during axon growth, spectraplakins of mice and humans are clinically important for a number of conditions and processes including skin blistering, neuro-degeneration, wound healing, synapse formation and neuron migration during brain development. Understanding spectraplakins in one biological process will instruct research on the other clinically relevant roles of these proteins.”
Source: Science Daily

Music has big brain benefits compared to other leisure pursuits
Music rocks. Musical activity was found to preserve cognition, including memory, as you age, when comparing variability in cognitive outcomes of older adults active in musical instrumental and other leisure activities.
You won’t lose it if you don’t use it. A range of cognitive benefits including memory were sustained for musicians between the ages of 60-80 if they played for at least 10 years throughout their life, confirming the maintenance of advantages is not reliant on continued activity.
Start young. Timing of musical instrumental acquisition, before age nine, is important in optimizing cognitive benefits and was associated with enhanced verbal working memory functions.
It’s never too late, so keep at it. Sustained musical activity over the age of 60 was associated with other nonverbal cognitive benefits, and appeared to compensate for low educational attainment, which is possibly the greatest protection against age-related cognitive declines. This suggests that musical training should be considered an alternative form of education.
ScienceDaily (July 19, 2012) — While clinical trial results are being released regarding drugs intended to decrease amyloid production — thought to contribute to decline in Alzheimer’s disease — clinical trials of drugs targeting other disease proteins, such as tau, are in their initial phases.
Penn Medicine research presented July 19 at the 2012 Alzheimer’s Association International Conference (AAIC) shows that an anti-tau treatment called epithilone D (EpoD) was effective in preventing and intervening the progress of Alzheimer’s disease in animal models, improving neuron function and cognition, as well as decreasing tau pathology.
By targeting tau, the drug aims to stabilize microtubules, which help support and transport of essential nutrients and information between cells. When tau malfunctions, microtubules break and tau accumulates into tangles.
"This drug effectively hits a tau target by correcting tau loss of function, thereby stabilizing microtubules and offsetting the loss of tau due to its formation into neurofibrillary tangles in animal models, which suggests that this could be an important option to mediate tau function in Alzheimer’s and other tau-based neurodegenerative diseases," said John Trojanowski, MD, PhD, professor of Pathology and Laboratory Medicine in the Perelman School of Medicine at the University of Pennsylvania. "In addition to drugs targeting amyloid, which may not work in advanced Alzheimer’s disease, our hope is that this and other anti-tau drugs can be tested in people with Alzheimer’s disease to determine whether stabilizing microtubules damaged by malfunctioning tau protein may improve clinical and pathological outcomes."
The drug, identified through Penn’s Center for Neurodegenerative Disease Research (CNDR) Drug Discovery Program, was previously shown to prevent further neurological damage and improve cognitive performance in animal models*. The Penn research team includes senior investigator Bin Zhang, MD, and Kurt Brunden, PhD, director of Drug Discovery at CNDR.
Bristol-Myers Squibb, who developed and owns the rights to the drug, has started enrolling patients into a phase I clinical trial in people with mild Alzheimer’s disease.
Source: Science Daily
July 19, 2012
Korean scientists have used tiny stars, squares and triangles as a toolkit to create live neural circuits in a dish.
They hope the shapes can be used to create a reproducible neural circuit model that could be used for learning and memory studies as well as drug screening applications; the shapes could also be integrated into the latest neural tissue scaffolds to aid the regeneration of neurons at injured sites in the body, such as the spinal cord.
Published today in the Journal of Neural Engineering, the study, by researchers at the Korea Advanced Institute of Science and Technology (KAIST), found that triangles were the most effective shape for helping to facilitate the growth of axons and guide them onto specific paths to form a complete circuit.
Co-author of the study, Professor Yoonkey Nam, said: “Eventually, we want to know if we can design a neural tissue model that biologically mimics some neural circuits in our brain.”
A neuron is an electrically excitable cell that processes and transmits information around the body. The neuron is composed of three main parts: a cell body, or soma, dendrites and an axon, which extends from the soma and links to other cells, creating a network.
When axons grow they are usually guided by proteins. Many researchers have been trying to re-create this key process in a dish by manipulating nerve cells from rat brains.
As nerve cells are usually just a few tens of micrometres in size, the challenge associated with creating a live neural network is firstly positioning cells in desired locations and, secondly, making connections between these cells by guiding the axons in designated directions.
The researchers investigated whether two star shapes, five regular shapes (square, circle, triangle, pentagon and hexagon) and three different sizes of isosceles triangles could guide axons in designated directions. Each shape was the size of a single cell and was replicated to form an array which was printed onto a glass surface.
Each of the arrays had an overall size of 1cm-by-1cm with a gap of 10 micrometres between each shape. Hippocampal neurons were taken from rats and plated onto the patterned surfaces. The neurons were fluorescently labelled with dyes so that images could be taken of their growth.
The researchers found that triangles were the most efficient shape to encourage the growth and guidance of an axon. The key to this was the angles at the points where two of the triangle’s lines meet, also known as the vertices. It was shown that the smaller the vertices, the higher chance the triangle had of inducing growth.
"Based on our results, we are suggesting a new design principle for guiding axons in a dish. We can control the axonal growth in a certain direction by putting a sharp triangle pointing to a certain direction. Then, a neuron that adhered to the triangle will have an axon in the sharp vertex direction.
"Overall, we integrated microtechnology with neurobiology to find a new engineering solution" continued Professor Nam.
Provided by Institute of Physics
Source: medicalxpress.com

Synapses are modified through learning. Up until now, scientists believed that a particular form of synaptic plasticity in the brain’s hippocampus was responsible for learning spatial relations. This was based on a receptor type for the neurotransmitter glutamate: the NMDA receptor. Researchers at the Max Planck Institute for Medical Research in Heidelberg and Oxford University have now observed that mice develop a spatial memory, even when the NMDA receptor-transmitted plasticity is switched off in parts of their hippocampus. However, if these mice have to resolve a conflict while getting their bearings, they are not successful in resolving it; the hippocampal NMDA receptors are clearly needed to detect or resolve the conflict. This has led the researchers involved in this experiment to refute a central tenet of neuroscience regarding the function of hippocampal NMDA receptor-transmitted plasticity in spatial learning.
ScienceDaily (July 19, 2012) — A joint study carried out by The University of Nottingham and the multinational food company Unilever has found for the first time that fat in food can reduce activity in several areas of the brain which are responsible for processing taste, aroma and reward.
The research, now available in the Springer journal Chemosensory Perception, provides the food industry with better understanding of how in the future it might be able to make healthier, less fatty food products without negatively affecting their overall taste and enjoyment. Unveiled in 2010, Unilever’s Sustainable Living Plan sets out its ambition to help hundreds of millions of people improve their diet around the world within a decade.
This fascinating three-year study investigated how the brains of a group of participants in their 20s would respond to changes in the fat content of four different fruit emulsions they tasted while under an MRI scanner. All four samples were of the same thickness and sweetness, but one contained flavour with no fat, while the other three contained fat with different flavour release properties.
The research found that the areas of the participants’ brains which are responsible for the perception of flavour — such as the somatosensory cortices and the anterior, mid & posterior insula — were significantly more activated when the non-fatty sample was tested compared to the fatty emulsions despite having the same flavour perception. It is important to note that increased activation in these brain areas does not necessarily result in increased perception of flavour or reward.
Dr Joanne Hort, Associate Professor in Sensory Science at The University of Nottingham said: “This is the first brain study to assess the effect of fat on the processing of flavour perception and it raises questions as to why fat emulsions suppress the cortical response in brain areas linked to the processing of flavour and reward. It also remains to be determined what the implications of this suppressive effect are on feelings of hunger, satiety and reward.”
Unilever food scientist Johanneke Busch, based at the company’s Research & Development laboratories in Vlaardingen, Netherlands added: “There is more to people’s enjoyment of food than the product’s flavour — like its mouthfeel, its texture and whether it satisfies hunger, so this is a very important building block for us to better understand how to innovate and manufacture healthier food products which people want to buy.”
Source: Science Daily
July 19, 2012 By Emily Martinez
(Medical Xpress) — UT Dallas researchers recently demonstrated how nerve stimulation paired with specific experiences, such as movements or sounds, can reorganize the brain. This technology could lead to new treatments for stroke, tinnitus, autism and other disorders.

Dr. Michael Kilgard helped lead a team that paired vagus nerve stimulation with physical movement to improve brain function.
In a related paper, UT Dallas neuroscientists showed that they could alter the speed at which the brain works in laboratory animals by pairing stimulation of the vagus nerve with fast or slow sounds.
A team led by Dr. Robert Rennaker and Dr. Michael Kilgard looked at whether repeatedly pairing vagus nerve stimulation with a specific movement would change neural activity within the laboratory rats’ primary motor cortex. To test the hypothesis, they paired the vagus nerve stimulation with movements of the forelimb in two groups of rats. The results were published in a recent issue of Cerebral Cortex.
After five days of stimulation and movement pairing, the researchers examined the brain activity in response to the stimulation. The rats who received the training along with the stimulation displayed large changes in the organization of the brain’s movement control system. The animals receiving identical motor training without stimulation pairing did not exhibit any brain changes, or plasticity.
People who suffer strokes or brain trauma often undergo rehabilitation that includes repeated movement of the affected limb in an effort to regain motor skills. It is believed that repeated use of the affected limb causes reorganization of the brain essential to recovery. The recent study suggests that pairing vagus nerve stimulation with standard therapy may result in more rapid and extensive reorganization of the brain, offering the potential for speeding and improving recovery following stroke, said Rennaker, associate professor in The University of Texas at Dallas’ School of Behavioral and Brain Sciences.
“Our goal is to use the brain’s natural neuromodulatory systems to enhance the effectiveness of standard therapies,” Rennaker said. “Our studies in sensory and motor cortex suggest that the technique has the potential to enhance treatments for neurological conditions ranging from chronic pain to motor disorders. Future studies will investigate its effectiveness in treating cognitive impairments.”