Posts tagged science
Articles and news from the latest research reports.
Double-barreled attack on obesity in no way a no-brainer
In the constant cross talk between our brain and our gut, two gut hormones are already known to tell the brain when we have had enough to eat. New research suggests that boosting levels of these hormones simultaneously may be an effective new weapon in the fight against obesity.
Dr Shu Lin, Dr Yan-Chuan Shi and Professor Herbert Herzog, from Sydney’s Garvan Institute of Medical Research, have shown that when mice are injected with PYY3-36 and PP, they eat less, gain less fat, and tend not to develop insulin-resistance, a precursor to diabetes. At the same time, the researchers have shown that the hormones stimulate different nerve pathways, ultimately, however, affecting complementary brain regions. Their findings are now published online in the journal Obesity.
While the double-barreled approach may seem like a no-brainer, the strongly enhanced effect seen was by no means inevitable. In the complex world of neuroscience, two plus two does not always make four.
Drug companies are in the process of conducting pre-clinical trials to examine the separate effects of boosting the hormones PYY3-36 and PP. Until now, there is no research to indicate the detailed molecular interactions that might occur when they are boosted in tandem.
When used together, the hormones independently, yet with combined force, reduce the amount of neuropeptide Y (NPY) produced by the brain, a powerful neurotransmitter that affects a variety of things including appetite, mood, heart rate, temperature and energy levels.
Each hormone also communicates with a different part of the arcuate nucleus in the hypothalamus, a region of the brain where signals can cross the normally impermeable blood / brain barrier. The stimulated regions then produce other neuronal signals deep within the hypothalamus, bringing about a powerful combined effect.
“There are many factors that influence appetite control – and we now realise that there won’t be a single molecular target, or a single drug, that will be effective,” said Dr Yan-Chuan Shi.
“It will be important for drug companies to try different combinations of targets, to see which combinations are most potent, and at the same time have no side effects, or at least minimal side effects.”
“At the moment, the only effective tool against obesity is surgery. Drug companies have so far failed to produce an effective drug without unacceptable side effects, such as mood disorders, nausea or cardiovascular problems.”
(Source: garvan.org.au)
Newly Identified Bone Marrow Stem Cells Reveal Markers for ALS
Amyotrophic Lateral Sclerosis (ALS) is a devastating motor neuron disease that rapidly atrophies the muscles, leading to complete paralysis. Despite its high profile — established when it afflicted the New York Yankees’ Lou Gehrig — ALS remains a disease that scientists are unable to predict, prevent, or cure.
Although several genetic ALS mutations have been identified, they only apply to a small number of cases. The ongoing challenge is to identify the mechanisms behind the non-genetic form of the disease and draw useful comparisons with the genetic forms.
Now, using samples of stem cells derived from the bone marrow of non-genetic ALS patients, Prof. Miguel Weil of Tel Aviv University’s Laboratory for Neurodegenerative Diseases and Personalized Medicine in the Department of Cell Research and Immunology and his team of researchers have uncovered four different biomarkers that characterize the non-genetic form of the disease. Each sample shows similar biological abnormalities to four specific genes, and further research could reveal additional commonalities. “Because these genes and their functions are already known, they give us a specific direction for research into non-genetic ALS diagnostics and therapeutics,” Prof. Weil says. His initial findings were reported in the journal Disease Markers.
Giving in to stress
To hunt for these biomarkers, Prof. Weil and his colleagues turned to samples of bone marrow collected from ALS patients. Though more difficult to collect than blood, bone marrow’s stem cells are easy to isolate and grow in a consistent manner. In the lab, he used these cells as cellular models for the disease. He ultimately discovered that cells from different ALS patients shared the same abnormal characteristics of four different genes that may act as biomarkers of the disease. And because the characteristics appear in tissues that are related to ALS — including in muscle, brain, and spinal cord tissues in mouse models of genetic ALS — they may well be connected to the degenerative process of the disease in humans, he believes.
Searching for the biological significance of these abnormalities, Prof. Weil put the cells under stress, applying toxins to induce the cells’ defense mechanisms. Healthy cells will try to fight off threats and often prove quite resilient, but ALS cells were found to be overwhelmingly sensitive to stress, with the vast majority choosing to die rather than fight. Because this is such an ingrained response, it can be used as a feature for drug screening for the disease, he adds.
The hunt for therapeutics
Whether these biomarkers are a cause or consequence of ALS is still unknown. However, this finding remains an important step towards uncovering the mechanisms of the disease. Because these genes have already been identified, it gives scientists a clear direction for future research. In addition, these biomarkers could lead to earlier and more accurate diagnostics.
Next, Prof. Weil plans to use his lab’s high-throughput screening facility — which can test thousands of compounds’ effects on diseased cells every day — to search for drug candidates with the potential to affect the abnormal expression of these genes or the stress response of ALS cells. A compound that has an impact on these indicators of ALS could be meaningful for treating the disease, he says.
Prof. Weil is the director of the new Cell Screening Facility for Personalized Medicine at TAU. The facility is dedicated to finding potential drugs for rare and Jewish hereditary diseases.
(Source: aftau.org)
Irregular bed times curb young kids’ brain power
Given the importance of early childhood development on subsequent health, there may be knock-on effects across the life course, suggest the authors.
The authors looked at whether bedtimes in early childhood were related to brain power in more than 11,000 seven year olds, all of whom were part of the UK Millennium Cohort Study (MCS).
MCS is a nationally representative long term study of UK children born between September 2000 and January 2002, and the research drew on regular surveys and home visits made when the children were 3, 5, and 7, to find out about family routines, including bedtimes.
The authors wanted to know whether the time a child went to bed, and the consistency of bed-times, had any impact on intellectual performance, measured by validated test scores for reading, maths, and spatial awareness.
And they wanted to know if the effects were cumulative and/or whether any particular periods during early childhood were more critical than others.
Irregular bedtimes were most common at the age of 3, when around one in five children went to bed at varying times. By the age of 7, more than half the children went to bed regularly between 7.30 and 8.30 pm.
Children whose bedtimes were irregular or who went to bed after 9 pm came from more socially disadvantaged backgrounds, the findings showed.
When they were 7, girls who had irregular bedtimes had lower scores on all three aspects of intellect assessed, after taking account of other potentially influential factors, than children with regular bedtimes. But this was not the case in 7 year old boys.
Irregular bedtimes by the age of 5 were not associated with poorer brain power in girls or boys at the age of 7. But irregular bedtimes at 3 years of age were associated with lower scores in reading, maths, and spatial awareness in both boys and girls, suggesting that around the age of 3 could be a sensitive period for cognitive development.
The impact of irregular bedtimes seemed to be cumulative.
Girls who had never had regular bedtimes at ages 3, 5, and 7 had significantly lower reading, maths and spatial awareness scores than girls who had had consistent bedtimes. The impact was the same in boys, but for any two of the three time points.
The authors point out that irregular bedtimes could disrupt natural body rhythms and cause sleep deprivation, so undermining the plasticity of the brain and the ability to acquire and retain information.
"Sleep is the price we pay for plasticity on the prior day and the investment needed to allow learning fresh the next day," they write. And they add: "Early child development has profound influences on health and wellbeing across the life course. Therefore, reduced or disrupted sleep, especially if it occurs at key times in development, could have important impacts on health throughout life."
Study identifies brain circuits involved in learning and decision making
Finding has implications for alcoholism and other patterns of addictive behavior
Research from the National Institutes of Health has identified neural circuits in mice that are involved in the ability to learn and alter behaviors. The findings help to explain the brain processes that govern choice and the ability to adapt behavior based on the end results.
Researchers think this might provide insight into patterns of compulsive behavior such as alcoholism and other addictions.
“Much remains to be understood about exactly how the brain strikes the balance between learning a behavioral response that is consistently rewarded, versus retaining the flexibility to switch to a new, better response,” said Kenneth R. Warren, Ph.D., acting director of the National Institute on Alcohol Abuse and Alcoholism. “These findings give new insight into the process and how it can go awry.”
The study, published online in Nature Neuroscience, indicates that specific circuits in the forebrain play a critical role in choice and adaptive learning.
Like other addictions, alcoholism is a disease in which voluntary control of behavior progressively diminishes and unwanted actions eventually become compulsive. It is thought that the normal brain processes involved in completing everyday activities become redirected toward finding and abusing alcohol.
The research, conducted by investigators from NIAAA, with support from the National Institute of Mental Health and the University of Cambridge, England, used a variety of approaches to study choice.
Researchers used a simple choice task in which mice viewed images on a computer touchscreen and learned to touch a specific image with their nose to get a food reward. Using various techniques to visualize and record neural activity, researchers found that as the mice learned to consistently make a choice, the brain’s dorsal striatum was activated. The dorsal striatum is thought to play an important role in motivation, decision-making, and reward.
Conversely, when the mice later had to shift to a new choice to receive a reward, the dorsal striatum quieted while regions in the prefrontal cortex, an area involved in decision-making and complex cognitive processes, became active.
Building upon these findings, the authors next deleted or pharmacologically blocked a component of nerve cells which normally binds the neurochemical glutamate (specifically, the GluN2B subunit of the NMDA receptor) within two different areas of the brain, the striatum and the frontal cortex. Previous studies have shown that GluN2B plays a role in memory, spatial reference, and attention. Researchers found that making dorsal striatal GluN2B inactive markedly slowed learning, while shutting down GluN2B in the prefrontal cortex made the mice less able to relearn the touchscreen reward task after the reward image was changed.
“These data add to what we understand about the neural control of behavioral flexibility and striatal learning by identifying GluN2B as a critical molecular substrate to both processes,” said the study’s senior author, Andrew Holmes, Ph.D., Laboratory Chief and Principal Investigator of the NIAAA Laboratory of Behavioral and Genomic Neuroscience.
“This is particularly intriguing for future studies because NMDA receptors are a major target for alcohol and contribute to important features of alcoholism, such as withdrawal. These new findings suggest that GluN2B in corticostriatal circuits may also play a key role in driving the transition from controlled drinking to compulsive abuse that characterizes alcoholism.”
(Source: niaaa.nih.gov)
Suspicions confirmed: Common cause for brain tumors in children
An overactive signaling pathway is a common cause in cases of pilocytic astrocytoma, the most frequent type of brain cancer in children. This was discovered by a network of scientists coordinated by the German Cancer Research Center (as part of the International Cancer Genome Consortium, ICGC). In all 96 cases studied, the researchers found defects in genes involved in a particular pathway. Hence, drugs can be used to help affected children by blocking components of the signaling cascade. The project is funded by the German Cancer Aid (Deutsche Krebshilfe) and the Federal Ministry of Education and Research (BMBF). The findings are published in the latest issue of the journal “Nature Genetics”.
Brain cancer is the primary cause of cancer mortality in children. Even in cases when the cancer is cured, young patients suffer from the stress of a treatment that can be harmful to the developing brain. In a search for new target structures that would create more gentle treatments, cancer researchers are systematically analyzing all alterations in the genetic material of these tumors. This is the mission of the PedBrain consortium, which was launched in 2010. Led by Professor Stefan Pfister from the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ), the PedBrain researchers have now published the results of the first 96 genome analyses of pilocytic astrocytomas.
Pilocytic astrocytomas are the most common childhood brain tumors. These tumors usually grow very slowly. However, they are often difficult to access by surgery and cannot be completely removed, which means that they can recur. The disease may thus become chronic and have debilitating effects for affected children.
In previous work, teams of researchers led by Professor Dr. Stefan Pfister and Dr. David Jones had already discovered characteristic mutations in a major proportion of pilocytic astrocytomas. All of the changes involved a key cellular signaling pathway known as the MAPK signaling cascade. MAPK is an abbreviation for “mitogen-activated protein kinase.” This signaling pathway comprises a cascade of phosphate group additions (phosphorylation) from one protein to the next – a universal method used by cells to transfer messages to the nucleus. MAPK signaling regulates numerous basic biological processes such as embryonic development and differentiation and the growth and death of cells.
“A couple of years ago, we had already hypothesized that pilocytic astrocytomas generally arise from a defective activation of MAPK signaling,” says David Jones, first author of the publication. “However, in about one fifth of the cases we had not initially discovered these mutations. In a whole-genome analysis of 96 tumors we have now discovered activating defects in three other genes involved in the MAPK signaling pathway that have not previously been described in astrocytoma.”
“Aside from MAPK mutations, we do not find any other frequent mutations that could promote cancer growth in the tumors. This is a very clear indication that overactive MAPK signals are necessary for a pilocytic astrocytoma to develop,” says study director Stefan Pfister. The disease thus is a prototype for rare cancers that are based on defects in a single biological signaling process.
In total, the genomes of pilocytic astrocytomas contain far fewer mutations than are found, for example, in medulloblastomas, a much more malignant pediatric brain tumor. This finding is in accordance with the more benign growth behavior of astrocytomas. The number of mutations increases with the age of the affected individuals.
About one half of pilocytic astrocytomas develop in the cerebellum, the other 50 percent in various other brain regions. Cerebellar astrocytomas are genetically even more homogenous than other cases of the disease: In 48 out of 49 cases that were studied, the researchers found fusions between the BRAF gene, a central component of the MAPK signaling pathway, and various other fusion partners.
“The most important conclusion from our results,” says study director Stefan Pfister, “is that targeted agents for all pilocytic astrocytomas are potentially available to block an overactive MAPK signaling cascade at various points. We might thus in the future be able to also help children whose tumors are difficult to access by surgery.”
Breakthrough Study Reveals Biological Basis for Sensory Processing Disorders in Kids
Sensory processing disorders (SPD) are more prevalent in children than autism and as common as attention deficit hyperactivity disorder, yet it receives far less attention partly because it’s never been recognized as a distinct disease.
In a groundbreaking new study from UC San Francisco, researchers have found that children affected with SPD have quantifiable differences in brain structure, for the first time showing a biological basis for the disease that sets it apart from other neurodevelopmental disorders.
One of the reasons SPD has been overlooked until now is that it often occurs in children who also have ADHD or autism, and the disorders have not been listed in the Diagnostic and Statistical Manual used by psychiatrists and psychologists.
“Until now, SPD hasn’t had a known biological underpinning,” said senior author Pratik Mukherjee, MD, PhD, a professor of radiology and biomedical imaging and bioengineering at UCSF. “Our findings point the way to establishing a biological basis for the disease that can be easily measured and used as a diagnostic tool,” Mukherjee said.
The work is published in the open access online journal NeuroImage:Clinical.
‘Out of Sync’ Kids
Sensory processing disorders affect 5 to 16 percent of school-aged children.
Children with SPD struggle with how to process stimulation, which can cause a wide range of symptoms including hypersensitivity to sound, sight and touch, poor fine motor skills and easy distractibility. Some SPD children cannot tolerate the sound of a vacuum, while others can’t hold a pencil or struggle with social interaction. Furthermore, a sound that one day is an irritant can the next day be sought out. The disease can be baffling for parents and has been a source of much controversy for clinicians, according to the researchers.
“Most people don’t know how to support these kids because they don’t fall into a traditional clinical group,” said Elysa Marco, MD, who led the study along with postdoctoral fellow Julia Owen, PhD. Marco is a cognitive and behavioral child neurologist at UCSF Benioff Children’s Hospital, ranked among the nation’s best and one of California’s top-ranked centers for neurology and other specialties, according to the 2013-2014 U.S. News & World Report Best Children’s Hospitals survey.
“Sometimes they are called the ‘out of sync’ kids. Their language is good, but they seem to have trouble with just about everything else, especially emotional regulation and distraction. In the real world, they’re just less able to process information efficiently, and they get left out and bullied,” said Marco, who treats affected children in her cognitive and behavioral neurology clinic.
“If we can better understand these kids who are falling through the cracks, we will not only help a whole lot of families, but we will better understand sensory processing in general. This work is laying the foundation for expanding our research and clinical evaluation of children with a wide range of neurodevelopmental challenges – stretching beyond autism and ADHD,” she said.
Imaging the Brain’s White Matter
In the study, researchers used an advanced form of MRI called diffusion tensor imaging (DTI), which measures the microscopic movement of water molecules within the brain in order to give information about the brain’s white matter tracts. DTI shows the direction of the white matter fibers and the integrity of the white matter. The brain’s white matter is essential for perceiving, thinking and learning.
The study examined 16 boys, between the ages of eight and 11, with SPD but without a diagnosis of autism or prematurity, and compared the results with 24 typically developing boys who were matched for age, gender, right- or left-handedness and IQ. The patients’ and control subjects’ behaviors were first characterized using a parent report measure of sensory behavior called the Sensory Profile.
The imaging detected abnormal white matter tracts in the SPD subjects, primarily involving areas in the back of the brain, that serve as connections for the auditory, visual and somatosensory (tactile) systems involved in sensory processing, including their connections between the left and right halves of the brain.
“These are tracts that are emblematic of someone with problems with sensory processing,” said Mukherjee. “More frontal anterior white matter tracts are typically involved in children with only ADHD or autistic spectrum disorders. The abnormalities we found are focused in a different region of the brain, indicating SPD may be neuroanatomically distinct.”
The researchers found a strong correlation between the micro-structural abnormalities in the white matter of the posterior cerebral tracts focused on sensory processing and the auditory, multisensory and inattention scores reported by parents in the Sensory Profile. The strongest correlation was for auditory processing, with other correlations observed for multi-sensory integration, vision, tactile and inattention.
The abnormal microstructure of sensory white matter tracts shown by DTI in kids with SPD likely alters the timing of sensory transmission so that processing of sensory stimuli and integrating information across multiple senses becomes difficult or impossible.
“We are just at the beginning, because people didn’t believe this existed,” said Marco. “This is absolutely the first structural imaging comparison of kids with research diagnosed sensory processing disorder and typically developing kids. It shows it is a brain-based disorder and gives us a way to evaluate them in clinic.”
Future studies need to be done, she said, to research the many children affected by sensory processing differences who have a known genetic disorder or brain injury related to prematurity.
New Research Points to Biomarker that Could Track Huntington’s Disease Progression
A hallmark of neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Huntington’s is that by the time symptoms appear, significant brain damage has already occurred—and currently there are no treatments that can reverse it. A team of SRI International researchers has demonstrated that measurements of electrical activity in the brains of mouse models of Huntington’s disease could indicate the presence of disease before the onset of major symptoms. The findings, “Longitudinal Analysis of the Electroencephalogram and Sleep Phenotype in the R6/2 Mouse Model of Huntington’s Disease,” are published in the July 2013 issue of the neurology journal Brain, published by Oxford University Press.
SRI researchers led by Stephen Morairty, Ph.D., a director in the Center for Neuroscience in SRI Biosciences, and Simon Fisher, Ph.D., a postdoctoral fellow at SRI, used electroencephalography (EEG), a noninvasive method commonly used in humans, to measure changes in neuronal electrical activity in a mouse model of Huntington’s disease. Identification of significant changes in the EEG prior to the onset of symptoms would add to evidence that the EEG can be used to identify biomarkers to screen for the presence of a neurodegenerative disease. Further research on such potential biomarkers might one day enable the tracking of disease progression in clinical trials and could facilitate drug development.
“EEG signals are composed of different frequency bands such as delta, theta and gamma, much as light is composed of different frequencies that result in the colors we call red, green and blue,” explained Thomas Kilduff, Ph.D., senior director, Center for Neuroscience, SRI Biosciences. “Our research identified abnormalities in all three of these bands in Huntington’s disease mice. Importantly, the activity in the theta and gamma bands slowed as the disease progressed, indicating that we may be tracking the underlying disease process.”
EEG has shown promise as an indicator of underlying brain dysfunction in neurodegenerative diseases, which otherwise occurs surreptitiously until symptoms appear. Until now, most investigations of EEG in patients with neurodegenerative diseases and in animal models of neurodegenerative diseases have shown significant changes in EEG patterns only after disease symptoms occurred.
“Our breakthrough is that we have found an EEG signature that appears to be a biomarker for the presence of disease in this mouse model of Huntington’s disease that can identify early changes in the brain prior to the onset of behavioral symptoms,” said Morairty, the paper’s senior author. “While the current study focused on Huntington’s disease, many neurodegenerative diseases produce changes in the EEG that are associated with the degenerative process. This is the first step in being able to use the EEG to predict both the presence and progression of neurodegenerative diseases.”
Although previous studies have shown there are distinct and extensive changes in EEG patterns in Alzheimer’s and Huntington’s disease patients, researchers are looking for changes that may occur decades before disease onset.
Huntington’s disease is an inherited disorder that causes certain nerve cells in the brain to die, resulting in motor dysfunction, cognitive decline and psychiatric symptoms. It is the only major neurodegenerative disease where the cause is known with certainty: a genetic mutation that produces a change in a protein that is toxic to neurons.
(Source: sri.com)
Brain and eye combined monitoring breakthrough could lead to fewer road accidents
Latest advances in capturing data on brain activity and eye movement are being combined to open up a host of ‘mindreading’ possibilities for the future. These include the potential development of a system that can detect when drivers are in danger of falling asleep at the wheel.
The research has been undertaken at the University of Leicester with funding from the Engineering and Physical Sciences Research Council (EPSRC), and in collaboration with the University of Buenos Aires in Argentina.
The breakthrough involves bringing two recent developments in the world of technology together: high-speed eye tracking that records eye movements in unprecedented detail using cutting-edge infra-red cameras*; and high-density electroencephalograph** (EEG) technology that measures electrical brain activity with millisecond precision through electrodes placed on the scalp.
The research has overcome previous technological challenges which made it difficult to monitor eye movement and brain activity simultaneously. The team has done this by developing novel signal processing techniques.
This could be the first step towards a system that combines brain and eye monitoring to automatically alert drivers who are showing signs of drowsiness. The system would be built into the vehicle and connected unobtrusively to the driver, with the EEG looking out for brain signals that only occur in the early stages of sleepiness. The eye tracker would reinforce this by looking for erratic gaze patterns symptomatic of someone starting to feel drowsy and different from those characteristic of someone driving who is constantly looking out for hazards. Fatigue has been estimated to account for around 20 per cent of traffic accidents on the UK’s motorways.***
The breakthrough achieved by the University of Leicester could also ultimately be built on to deliver many other everyday applications in the years ahead. For example:
- Computer games of the future could dispense with the need for the player to physically interact with any type of console, mouse or other hand-operated system. Instead, eye movement and brain activity data would be collected and processed to indicate what action the player wants to take. By distinguishing the tiny differences in various types of brain activity, the EEG would identify the precise action the player desires (e.g. run, jump or throw), while the eye movement data would show exactly where on the screen the player was looking when they had this thought. This information could be combined to enable the correct action to occur. An unobtrusive headset would be all that would be required to capture the necessary data.
- People who have no arm functionality could move their wheelchairs simply through their eye movements. These movements could be tracked and the corresponding brain activity analysed to identify when these indicate a desire to move in a certain direction. This would then automatically activate a steering and propulsion mechanism that would drive the wheelchair to that place.
- The breakthrough could also provide the basis for improved tests to diagnose dyslexia and other reading disorders. Current tests revolve around a rapid succession of single words flashed onto a computer screen, with the resulting brain activity monitored by EEG. The new technique could enable the person being tested to move their eyes and read longer passages of text in a natural way, making the tests much more realistic and revealing.
- With the basic concept now demonstrated successfully, the team aim to continue their work and eventually develop software that, in real time, automatically monitors both eye movement and brain activity.
- Dr Matias Ison, who has led the research, says: “Historically, eye-tracking and EEG have evolved as independent fields. We have managed to overcome the challenges that were standing in the way of integrating these technologies. This is already leading to a much better understanding of how the brain responds when the eyes are moving. Monitoring the alertness of drivers is just one of many potential applications for this work. Building on the foundation provided by our EPSRC-funded project, we hope to see the first of these starting to become feasible within the next three to five years.”
(Source: epsrc.ac.uk)
How well can you see with your ears? Device offers new alternative to blind people
A device that trains the brain to turn sounds into images could be used as an alternative to invasive treatment for blind and partially-sighted people, researchers at the University of Bath have found.
The vOICe sensory substitution device is a revolutionary tool that helps blind people to use sounds to build an image in their minds of the things around them.
A research team, led by Dr Michael Proulx, from the University’s Department of Psychology, looked at how blindfolded sighted participants responded to an eye test using the device.
They were asked to perform a standard eye chart test called the Snellen Tumbling E test, which asked participants to view the letter E turned in four different directions and in various sizes. Normal, best-corrected visual acuity is considered 20/20, calculated in terms of the distance (in feet) and the size of the E on the eye chart.
The participants, even without any training in the use of the device, were able to perform the best performance possible, nearly 20/400. This limit appears to be the highest resolution currently possible with the ever-improving technology.
Dr Michael Proulx said: “This level of visual performance exceeds that of the current invasive techniques for vision restoration, such as stem cell implants and retinal prostheses after extensive training.
"A recent study found successful vision at a level of 20/800 after the use of stem cells. Although this might improve with time and provide the literal sensation of sight, the affordable and non-invasive nature of The vOICe provides another option.
"Sensory substitution devices are not only an alternative, but might also be best employed in combination with such invasive techniques to train the brain to see again or for the first time."
New tissue engineering breakthrough encourages nerve repair
A new combination of tissue engineering techniques could reduce the need for nerve grafts, according to new research by The Open University. Regeneration of nerves is challenging when the damaged area is extensive, and surgeons currently have to take a nerve graft from elsewhere in the body, leaving a second site of damage. Nerve grafts contain aligned tissue structures and Schwann cells that support and guide neuron growth through the damaged area, encouraging function to be restored. The research, published in Biomaterials, reported a way to manufacture artificial nerve tissue with the potential to be used as an alternative to nerve grafts.
Pieces of Engineered Neural Tissue (EngNT) are formed by controlling natural Schwann cell behaviour in a three-dimensional collagen gel so that the cells elongate and align, then a stabilisation process removes excess fluid to leave robust artificial tissues. These living biomaterials contain aligned Schwann cells in an aligned collagen environment, recreating key features of normal nerve tissue.
Incorrect orientation of regenerating nerve cells can lead to delays in repair, scarring and poor restoration of nerve function. Much research has taken place into how support cells (Schwann cells) can be combined with materials to guide nerve regeneration. The new technology from The Open University avoids the use of synthetic materials by building neural tissue from collagen, a protein that is abundant in normal nerve tissue. Building the artificial tissue from natural proteins and directing the cellular alignment using normal cell-material interactions means the EngNT can integrate effectively at the repair site.
Dr James Phillips, Lecturer in Health Sciences at The Open University, said: “We previously reported how self-alignment of Schwann cells could be achieved by using a tethered collagen hydrogel, which exploited cells’ natural ability to orientate in the appropriate direction by using their internal contraction forces. Our current research shows that cell-alignment in the hydrogel can be stabilised using plastic compression. The compression removes fluid from the gels, leaving a strong and stable aligned structure that has many features in common with nerve tissue.”
The team incorporated Schwann cells within the aligned material to form artificial neural tissue that could potentially be used in peripheral nerve repair. The technique could be applied to other regenerative medicine scenarios, where a stable artificial tissue containing aligned cellular architecture would be of benefit.
(Source: www3.open.ac.uk)