Posts tagged science

May 24, 2012

Despite a long-held scientific belief that much of the wiring of the brain is fixed by the time of adolescence, a new study shows that changes in sensory experience can cause massive rewiring of the brain, even as one ages. In addition, the study found that this rewiring involves fibers that supply the primary input to the cerebral cortex, the part of the brain that is responsible for sensory perception, motor control and cognition. These findings promise to open new avenues of research on brain remodeling and aging.

Published in the May 24, 2012 issue of Neuron, the study was conducted by researchers at the Max Planck Florida Institute (MPFI) and at Columbia University in New York.

"This study overturns decades-old beliefs that most of the brain is hard-wired before a critical period that ends when one is a young adult," said MPFI neuroscientist Marcel Oberlaender, PhD, first author on the paper. "By changing the nature of sensory experience, we were able to demonstrate that the brain can rewire, even at an advanced age. This may suggest that if one stops learning and experiencing new things as one ages, a substantial amount of connections within the brain may be lost."

The researchers conducted their study by examining the brains of older rats, focusing on an area of the brain known as the thalamus, which processes and delivers information obtained from sensory organs to the cerebral cortex. Connections between the thalamus and the cortex have been thought to stop changing by early adulthood, but this was not found to be the case in the rodents studied.

Being nocturnal animals, rats mainly rely on their whiskers as active sensory organs to explore and navigate their environment. For this reason, the whisker system is an ideal model for studying whether the brain can be remodeled by changing sensory experience. By simply trimming the whiskers, and preventing the rats from receiving this important and frequent form of sensory input, the scientists sought to determine whether extensive rewiring of the connections between the thalamus and cortex would occur.

On examination, they found that the animals with trimmed whiskers had altered axons, nerve fibers along which information is conveyed from one neuron (nerve cell) to many others; those whose whiskers were not trimmed had no axonal changes. Their findings were particularly striking as the rats were considered relatively old – meaning that this rewiring can still take place at an age not previously thought possible. Also notable was that the rewiring happened rapidly – in as little as a few days.

"We’ve shown that the structure of the rodent brain is in constant flux, and that this rewiring is shaped by sensory experience and interaction with the environment," said Dr. Oberlaender. "These changes seem to be life-long and may pertain to other sensory systems and species, including people. Our findings open the possibility of new avenues of research on development of the aging brain using quantitative anatomical studies combined with noninvasive imaging technologies suitable for humans, such as functional MRI (fMRI)."

The study was possible due to recent advances in high-resolution imaging and reconstruction techniques, developed in part by Dr. Oberlaender at MPFI. These novel methods enable researchers to automatically and reliably trace the fine and complex branching patterns of individual axons, with typical diameters less than a thousandth of a millimeter, throughout the entire brain.

Provided by Tartaglia Communications

Source: medicalxpress.com

May 24, 2012

The birth of sensory perception on the human cerebral cortex is yet to be fully explained. The different areas on the cortex function in cooperation, and no perception is the outcome of only one area working alone. In his doctoral dissertation for the Department of Biomedical Engineering and Computational Science in Aalto University Jaakko Kauramäki shows that the auditory cortex is not left to its own devices.

Kauramäki’s dissertation in the field of cognitive neuroscience studied neural top-down processes, that is, the ways the brain as a system handles sounds arriving onto the auditory cortex in the frontal lobes.

Moving from parts towards a whole, bottom-up processes analyse a sound by dissecting it in hierarchical chain reactions from small and sophisticated bits towards a concise auditory sensation.

"The operation of the system as a whole can be affected by focusing on a specific task or sound. In my research I focused precisely on how the top-down effects manifest themselves on the auditory cortex," explains Kauramäki his study.

Right kind of noise promotes concentration and reinforces perception?

Kauramäki studied the auditory cortex in two separate tasks: reactions caused by selective attention during sound recognition and by lipreading. Kauramäki recorded the electrical and magnetic activity on the cortex using electroencephalography (EEG) and magnetoencephalography (MEG) respectively.

"40 years ago a so-called ‘gain effect’ was formulated: focusing attention enhances responses on the auditory cortex, which means that attention helps to better perceive audio stimuli," tells Kauramäki.

In the attention tests Kauramäki masked the sounds played for the test subjects with different frequencies of noise – and made a discovery. During periods of selective attention, the enhanced responses on the auditory cortex depended on the type of noise used. The frequency content of the noise affected the prominence of the responses. The responses are not only enhanced, but they are feature and task-specific.

"Similar results have not been obtained earlier because the stimuli used in the experiments have been too simple. The noise mask added a combinatory effect that brought the specificity and selectivity of the responses to the fore."

"Focusing attention may then be easier in a rich sound environment. Complete silence is of course an extreme case, but in total silence the auditory cortex begins to create connections out of thin air, to make up sensory perceptions."

"Then again, the more stimuli there are in the environment, the harder it becomes to focus. In attention disorders such as ADHD, precisely the top-down ability to filter sounds may be lacking," suspects Kauramäki.

In the lipreading tasks Kauramäki did not encounter such a dependency on frequency. Instead, lipreading suppressed the auditory cortex’s ability to react. The reason for this is the neural response of the speech production system.

"The suppressing effect is caused by the adaptation of the areas on the auditory cortex that specialise in speech. Suppressing occurs even when the speech is inaudible – the articulatory gestures of the mouth alone activate parts of the auditory cortex."

For Kauramäki the result suggests that the neural responses of the speech production system can reach the auditory cortex and thus reinforce perception.

"In noisy meetings, for example, it pays off to concentrate on the face of whoever is speaking: lipreading helps in the processing. It may suppress the reaction of the auditory cortex, but the big picture becomes clearer."

Provided by Aalto University

Source: medicalxpress.com

May 24, 2012

(Medical Xpress) — Patients given a clot-busting drug within six hours of a stroke are more likely to make a better recovery than those who do not receive the treatment, new research has found.

The trial was set up in 2000 by the University of Sydney’s Professor Richard Lindley, while he was employed at the University of Edinburgh.

The study of more than 3000 patients is the world’s largest trial of the drug rt-PA and was coordinated at the University of Edinburgh. Since coming to Sydney Medical School in 2003, Professor Lindley has continued as the co-principal investigator of the research.

The findings of the study are published today in The Lancet, alongside an analysis of all other trials of the drug carried out in the past 20 years.

The trial found that following treatment with the drug rt-PA, which is given intravenously to patients who have suffered an acute ischaemic stroke, more patients were able to look after themselves.

"The trial results, together with the updated review, mean that rt-PA can now be offered to a much wider group of patients presenting with stroke", Professor Lindley said.

A patient’s chances of making a complete recovery within six months of a stroke were also increased.

An ischaemic stroke happens when the brain’s blood supply is interrupted by a blood clot. The damage caused can be permanent or fatal.

Researchers now know that for every 1000 patients given rt-PA within three hours of stroke, 80 more will survive and live without help from others than if they had not been given the drug.

The benefits of using rt-PA do come at a price, say researchers. Patients are at risk of death within seven days of treatment because the drug can cause a secondary bleed in the brain. The research team concluded that the benefits were seen in a wide variety of patients, despite the risks.

Stroke experts stress that these mortality figures need to be viewed in the context of deaths from stroke. Without treatment, one third of people who suffer a stroke die, with another third left permanently dependent and disabled.

Researchers say the threat of death and disability means many stroke patients are prepared to take the early risks of being treated with rt-PA to avoid being disabled.

The authors conclude that for those who do not experience bleeding, the drug improves patients’ longer term recovery.

About half of those who took part in the trial were over 80.

"The trial underlines the benefits of treating patients with the drug as soon as possible and provides the first reliable evidence that treatment is effective for those aged 80 and over," Professor Lindley said.

The study also found no reason to restrict use of rt-PA - also known as alteplase - on the basis of how severe a patient’s stroke has been.

Chief investigator Professor Peter Sandercock of the University of Edinburgh’s Centre for Clinical Brain Sciences said: “Our trial shows that it is crucial that treatment is given as fast as possible to all suitable patients.”

Provided by University of Sydney

Source: medicalxpress.com

May 24, 2012

Within the nervous system, a handful of signaling pathways modulate development of a cornucopia of different neuronal subtypes. “Even small alterations in neuron differentiation pathways can disrupt subsequent circuit organization and catalyze the genesis of neurological disorders,” explains Adrian Moore of the RIKEN Brain Science Institute in Wako.

Figure 1: Interplay between Notch signaling and Hamlet activity gives rise to diverse olfactory receptor neurons (ORNs), each with distinct structures and subsets of olfactory receptors (left). The precursor cell (right) divides to yield two daughter cells, one of which undergoes Notch (N)-mediated gene activation. Hamlet (Ham) subsequently resets Notch’s genetic effects, and the absence or subsequent restoration of Notch signaling determines which type of ORN (Naa or Nab) will result from differentiation. Credit: 2012 Adrian Moore, RIKEN Brain Science Institute

Recent work from Moore’s team, which includes Keita Endo of the University of Tokyo, has revealed mechanisms governing this complexity in the fruit fly olfactory system. Within the antennae—the fly equivalent of the nose—it was known that cells called neuronal precursors undergo multiple rounds of ‘asymmetric division’, wherein each resulting daughter cell follows a distinct developmental path, yielding different combinations of olfactory receptor neurons (ORNs). Moore’s team showed specifically that ORN precursors undergo two rounds of division, yielding four different cellular subtypes, three of which will typically mature into ORNs.

Earlier work from Endo showed that the activation or suppression of signaling by the Notch protein helps differentiate these cellular fates, but other factors were clearly involved. Their joint research demonstrated that a second protein, Hamlet, modulates the effects of Notch. 

“This [process] provides an important foundation for all future studies of odorant receptor expression and axon targeting control on the olfactory system,” says Moore. The researchers found that presence or absence of Notch and Hamlet activity plays a central role in establishing the identity of these subtypes, and this in turn determines both the connections formed by the resulting ORNs as well as the subset of olfactory receptor proteins that will be expressed (Fig. 1). 

Moore and Endo’s study also revealed a surprising mode of action for Hamlet. Chromosomal DNA is wrapped around clusters of protein, and chemical changes to those proteins profoundly alter local gene activity—a mechanism called ‘epigenetic regulation’. They found that Hamlet selectively deactivates genes activated by Notch by triggering such changes. This means that immature ORNs produced by division of a Notch-activated cell can essentially be ‘reset’ by Hamlet. The ultimate developmental fate of those cells is then determined, in part, by whether or not they subsequently undergo a new round of Notch activation. 

Moore and colleagues also observed that, beyond simply switching off active Notch genes, Hamlet may define subsets of target genes that can subsequently be reactivated by Notch signaling. “The modifications induced by Hamlet may help establish cell fate by marking gene promoters for use later during differentiation,” says Moore. “This could prove fundamental to understanding the process of neuronal diversification.”

Provided by RIKEN

Source: medicalxpress.com

May 24, 2012

(Medical Xpress) — Research from Karolinska Institutet shows that the human olfactory bulb - a structure in the brain that processes sensory input from the nose - differs from that of other mammals in that no new neurons are formed in this area after birth. The discovery, which is published in the scientific journal Neuron, is based on the age-determination of the cells using the carbon-14 method, and might explain why the human sense of smell is normally much worse than that of other animals.

"I’ve never been so astonished by a scientific discovery," says lead investigator Jonas Frisén, Tobias Foundation Professor of stem cell research at Karolinska Institutet. "What you would normally expect is for humans to be like other animals, particularly apes, in this respect."

It was long thought that all brain neurons were formed up to the time of birth, after which production stopped. A paradigm shift occurred when scientists found that nerve cells were being continually formed from stem cells in the mammalian brain, which changed scientific views on the plasticity of the brain and raised hopes of being able to replace neurons lost during some types of neurological disease.

In the adult mammal, new nerve cells are formed in two regions of the brain: the hippocampus and the olfactory bulb. While the former has an important part to play in memory, the latter is essential to the interpretation of smells. However, owing to the difficulty of studying the formation of new neurons in humans, the extent to which this phenomenon also occurs in the human brain has remained unclear. In this present study, researchers at Karolinska Institutet and their Austrian and French colleagues made use of the sharp rise in atmospheric carbon-14 caused by Cold War nuclear tests to find an answer to this question.

Carbon-14 is incorporated in DNA, making it possible to gauge the age of the cells by measuring how much of the isotope they contain. Doing this, the team found that the olfactory bulb neurons in their adult human subjects had carbon-14 levels that matched those at the atmosphere at the time of their birth. This is a strong indication that there is no significant generation of new neurons in this part of the brain, something that sets humans apart from all other mammals.

"Humans are less dependent on their sense of smell for their survival than many other animals, which may be related to the loss of new cell generation in the olfactory bulb, but this is just speculation,” says Professor Frisén.

Professor Frisén and his team now plan to study the extent of neuron generation in the hippocampus, a part of the brain that is important for higher cerebral functions in humans.

Provided by Karolinska Institutet

Source: medicalxpress.com

ScienceDaily (May 23, 2012) — Blame it on your genes? Researchers from The Miriam Hospital’s Weight Control and Diabetes Research Center say individuals with variations in certain “obesity genes” tend to eat more meals and snacks, consume more calories per day and often choose the same types of high fat, sugary foods.

Blame it on your genes? Researchers say individuals with variations in certain “obesity genes” tend to eat more meals and snacks and consume more calories per day. (Credit: © Gennadiy Poznyakov / Fotolia)

Their study, published online by the American Journal of Clinical Nutrition and appearing in the June issue, reveals certain variations within the FTO and BDNF genes — which have been previously linked to obesity — may play a role in eating habits that can cause obesity.

The findings suggest it may be possible to minimize genetic risk by changing one’s eating patterns and being vigilant about food choices, in addition to adopting other healthy lifestyle habits, like regular physical activity.

"Understanding how our genes influence obesity is critical in trying to understand the current obesity epidemic, yet it’s important to remember that genetic traits alone do not mean obesity is inevitable," said lead author Jeanne M. McCaffery, Ph.D., of The Miriam Hospital’s Weight Control and Diabetes Research Center.

"Our lifestyle choices are critical when it comes to determining how thin or heavy we are, regardless of your genetic traits," she added. "However, uncovering genetic markers can possibly pinpoint future interventions to control obesity in those who are genetically predisposed."

Previous research has shown individuals who carry a variant of the fast mass and obesity-associated gene FTO and BDNF (or brain-derived neurotrophic factor gene) are at increased risk for obesity. The genes have also been linked with overeating in children and this is one of the first studies to extend this finding to adults. Both FTO and BDNF are expressed in the part of the brain that controls eating and appetite, although the mechanisms by which these gene variations influence obesity is still unknown.

As part of the Look AHEAD (Action in Health and Diabetes) trial, more than 2,000 participants completed a questionnaire about their eating habits over the past six months and also underwent geneotyping. Researchers focused on nearly a dozen genes that have been previously associated with obesity. They then examined whether these genetic markers influenced the pattern or content of the participants’ diet.

Variations in the FTO gene specifically were significantly associated with a greater number of meals and snacks per day, greater percentage of energy from fat and more servings of fats, oils and sweets. The findings are largely consistent with previous research in children.

Researchers also discovered that individuals with BDNF variations consumed more servings from the dairy and the meat, eggs, nuts and beans food groups. They also consumed approximately 100 more calories per day, which McCaffery notes could have a substantial influence on one’s weight.

"We show that at least some of the genetic influence on obesity may occur through patterns of dietary intake," she said. "The good news is that eating habits can be modified, so we may be able to reduce one’s genetic risk for obesity by changing these eating patterns."

McCaffery says that while this research greatly expands their knowledge on how genetics may influence obesity, the data must be replicated before the findings can be translated into possible clinical measures.

Source: Science Daily

May 23rd, 2012

Study supports urate protection against Parkinson’s disease, hints at novel mechanism

In vitro study indicates urate protection extends beyond antioxidant effect

Use of the antioxidant urate to protect against the neurodegeneration caused by Parkinson’s disease appears to rely on more than urate’s ability to protect against oxidative damage. In the May issue of the open-access journal PLoS One, researchers from the MassGeneral Institute for Neurodegenerative Diseases (MGH-MIND) describe experiments suggesting the involvement of a novel mechanism in urate’s protection of cultured brain cells against Parkinson’s-like damage.

“Our experiments showed, unexpectedly, that urate’s ability to protect neurons requires the presence of neighboring cells called astrocytes,” says Michael Schwarzschild, MD, PhD, of MGH-MIND, the study’s senior author. “The results suggest there may be multiple ways that raising urate could help protect against neurodegeneration in diseases like Parkinson’s and further support the development of treatments designed to elevate urate in the brain.” Schwarzschild and colleagues in the Parkinson’s Study Group currently are conducting a clinical trial investigating one approach to that strategy.

Characterized by tremors, rigidity, difficulty walking and other symptoms, Parkinson’s disease is caused by destruction of brain cells that produce the neurotransmitter dopamine. Several epidemiological studies suggested that healthy people with elevated levels of urate, a normal component of the blood, may have a reduced risk of developing Parkinson’s disease, and investigations by Schwarzschild’s team found that Parkinson’s patients with higher naturally occuring urate levels had slower progression of their symptoms.

The current study was designed to investigate whether both added urate and urate already present within the cells protect cultured dopamine-producing neurons against Parkinson-like degeneration. In addition, since previous studies suggested that urate’s protective effects depended on the presence of astrocytes,  star-shaped cells of the central nervous system that provide both structural and metabolic support to neurons,  the MGH-MIND team explored how the presence of astrocytes affects the ability of urate to protect against damage induced by MPP+, a toxic molecule that produces the same kind of neurodegeneration seen in Parkinson’s and is widely used in research studies.

Raising urate levels could help to protect against neurodegenerative diseases like Parkinsons. Image adapted from Flickr user Niels_Olson.

The experiments showed that, while added urate reduced MPP+-induced cell death by about 50 percent in cultured dopamine-producing mouse neurons, urate treatment virtually eliminated neuronal death in cultures containing both neurons and astrocytes. They also showed that reducing intracellular urate levels by induced expression of the enzyme that breaks it down increased neuronal vulnerability to MPP+ toxicity significantly in cultures that included astrocytes but only slightly in neuron-rich cultures. The fact that the presence of astrocytes greatly increases the protection of both externally applied urate and urate produced within cells indicates that the effect depends on more than urate’s ability to directly protect neurons against oxidative stress.

“A valuable next step will be determining whether endogenous urate is protective in live animal models of Parkinson’s disease,” says Schwarzschild. “It also will be important to determine whether we can selectively increase urate levels in brain cells by targeting urate transporter molecules. The approach now in early clinical trials examines whether treatment with the urate precursor inosine, which increases urate levels throughout the body, can slow the progression of the disease. If we could raise urate levels in brain cells without changing them in the rest of the body, we could avoid the risks of of excessive urate, which when accumulated in joints can cause gout.”

Source: Neuroscience News

May 23, 2012

Researchers have shown in mice how immune cells in the brain target and remove unused connections between brain cells during normal development. This research, supported by the National Institutes of Health, sheds light on how brain activity influences brain development, and highlights the newly found importance of the immune system in how the brain is wired, as well as how the brain forms new connections throughout life in response to change.

Disease-fighting cells in the brain, known as microglia, can prune the billions of tiny connections (or synapses) between neurons, the brain cells that transmit information through electric and chemical signals. This new research demonstrates that microglia respond to neuronal activity to select synapses to prune, and shows how this pruning relies on an immune response pathway – the complement system – to eliminate synapses in the way that bacterial cells or other pathogenic debris are eliminated. The study was led by Beth Stevens, Ph.D., assistant professor of neurology at Boston Children’s Hospital and Harvard Medical School.

The brain is created with many more synapses than it retains into adulthood. As the brain develops, it goes through dynamic changes to refine its circuitry, trimming away the synaptic connections that do not have a lot of activity, and preserving the stronger, more active synapses. This period, known as synaptic pruning, is a key part of normal brain development.

Scientists do not have a clear understanding of how these synapses are selected, targeted and then pruned. However, precise elimination of unused synapses and strengthening those that are most needed is essential for normal brain function. Many childhood disorders, such as amblyopia (a loss of vision in one eye that can occur when the eyes are misaligned), various forms of mental retardation, epilepsy and autism are thought to be due to abnormal brain development.

Microglia originate in the bone marrow and transform into an activated state to defend the body against infections. Activated microglia are also found in other disease states, ranging from stroke to Alzheimer’s disease. It is not always clear, however, if these cells cause degeneration of brain cells, or if they are part of the brain’s recovery process. In more recent years, several research groups reported that activated microglia are also present in the normal brain. Additionally, during the most robust synaptic pruning periods there is an increased number of activated microglia present and clustered around synapses.

As reported in the May 24 issue of Neuron, scientists in Dr. Stevens’s lab used the visual system in mice to study synaptic pruning, a model that undergoes robust change and remodeling during development and which has circuitry that is well-defined and easy to manipulate. Researchers labeled neurons that project from the eye into an area of the brain called the lateral geniculate nucleus, or LGN, and found that reactive microglia contained portions of the synapses from the labeled neurons. They also saw that these labeled pieces of synaptic material were specifically found inside the microglia’s lysosomes – compartments responsible for digesting foreign particles.

The researchers then investigated if the amount of neuronal activity at a synapse determines whether microglia target it for removal. They used a drug to increase activity in the neurons projecting from one eye and saw less pruning of synapses in the corresponding brain region, as compared to the untreated eye. When they used a drug to reduce activity, this resulted in more pruning compared to the untreated eye. The researchers think microglia select a synapse for removal based on the synapse’s level of activity. This may be directly relevant to amblyopia, a loss of vision in one eye that can occur when the eyes are misaligned. Children with amblyopia will preferentially use one eye and vision in the less used eye deteriorates due loss of synapses and cells in the LGN.

Earlier research revealed that proteins involved in the complement system are found near synapses during development and are necessary for pruning. To see if these same proteins are used by microglia to shape neuronal connections, the researchers disrupted complement pathway proteins that are found only in the brain’s immune cells. Their results indicate that these complement proteins signal the microglia to trim away synapses, and suggest that immune system pathways are key to proper synaptic pruning.

"The concept that microglia prune synapses using immune system pathways has been difficult to prove,” said Edmund Talley, Ph.D., program director at the National Institute of Neurological Disorders and Stroke, “This exquisitely careful and meticulous research confirms the role of microglia in brain development, plasticity and learning.”

Dr. Stevens said the study sheds light on the role of microglia in the normal brain, and supports further investigations into the role of microglia in brain disease. “Almost every neurodegenerative brain disease involves several interesting common denominators,” she said. “It’s becoming increasingly recognized that early synapse loss is a hallmark of many neurodegenerative diseases.”

Provided by NIH/National Institute of Neurological Disorders and Stroke

Source: medicalxpress.com

May 23, 2012

When grabbing a coffee mug out of a cluttered cabinet or choosing a pen to quickly sign a document, what brain processes guide your choices?

New research from Carnegie Mellon University’s Center for the Neural Basis of Cognition (CNBC) shows that the brain’s visual perception system automatically and unconsciously guides decision-making through valence perception. Published in the journal Frontiers in Psychology, the review hypothesizes that valence, which can be defined as the positive or negative information automatically perceived in the majority of visual information, integrates visual features and associations from experience with similar objects or features. In other words, it is the process that allows our brains to rapidly make choices between similar objects.

The findings offer important insights into consumer behavior in ways that traditional consumer marketing focus groups cannot address. For example, asking individuals to react to package designs, ads or logos is simply ineffective. Instead, companies can use this type of brain science to more effectively assess how unconscious visual valence perception contributes to consumer behavior.

To transfer the research’s scientific application to the online video market, the CMU research team is in the process of founding the start-up company neonlabs through the support of the National Science Foundation (NSF) Innovation Corps (I-Corps).

"This basic research into how visual object recognition interacts with and is influenced by affect paints a much richer picture of how we see objects," said Michael J. Tarr, the George A. and Helen Dunham Cowan Professor of Cognitive Neuroscience and co-director of the CNBC. “What we now know is that common, household objects carry subtle positive or negative valences and that these valences have an impact on our day-to-day behavior.”

Tarr added that the NSF I-Corps program has been instrumental in helping the neonlabs’ team take this basic idea and teaching them how to turn it into a viable company. “The I-Corps program gave us unprecedented access to highly successful, experienced entrepreneurs and venture capitalists who provided incredibly valuable feedback throughout the development process,” he said.

NSF established I-Corps for the sole purpose of assessing the readiness of transitioning new scientific opportunities into valuable products through a public-private partnership. The CMU team of Tarr, Sophie Lebrecht, a CNBC and Tepper School of Business postdoctoral fellow, Babs Carryer, an embedded entrepreneur at CMU’s Project Olympus, and Thomas Kubilius, president of Pittsburgh-based Bright Innovation and adjunct professor of design at CMU, were awarded a $50,000, six-month grant to investigate how understanding valence perception could be used to make better consumer marketing decisions. They are launching neonlabs to apply their model of visual preference to increase click rates on online videos, by identifying the most visually appealing thumbnail from a stream of video. The web-based software product selects a thumbnail based on neuroimaging data on object perception and valence, crowd sourced behavioral data and proprietary computational analyses of large amounts of video streams.

"Everything you see, you automatically dislike or like, prefer or don’t prefer, in part, because of valence perception," said Lebrecht, lead author of the study and the entrepreneurial lead for the I-Corps grant. "Valence links what we see in the world to how we make decisions."

Lebrecht continued, “Talking with companies such as YouTube and Hulu, we realized that they are looking for ways to keep users on their sites longer by clicking to watch more videos. Thumbnails are a huge problem for any online video publisher, and our research fits perfectly with this problem. Our approach streamlines the process and chooses the screenshot that is the most visually appealing based on science, which will in the end result in more user clicks.”

Today (May 23), Lebrecht will join the other 23 I-Corps project teams in Palo Alto, Calif., for the final presentation of each team’s I-Corps journey from basic science idea to real-world business application. She will present neonlabs’ solution, outlining the customer landscape, competition and business model.

Carnegie Mellon is well known for its entrepreneurial culture. The university’s Greenlighting Startups initiative, a portfolio of five business incubators, is designed to speed company creation at CMU. In the past 15 years, Carnegie Mellon faculty and students have helped to create more than 300 companies and 9,000 jobs; the university averages 15 to 20 new startups each year.

"CMU has been an amazing place to build neonlabs," Lebrecht said. "There’s a great intellectual community and facilities here as well as people unbelievably experienced in tech transfer and startups who have been so incredibly generous with their time."

Provided by Carnegie Mellon University

Source: medicalxpress.com

May 23rd, 2012

Well-connected brains make you smarter in older age
Brains that maintain healthy nerve connections as we age help keep us sharp in later life, new research funded by the charity Age UK has found

Brains that maintain healthy nerve connections as we age help keep us sharp in later life, new research funded by the charity Age UK has found.

Older people with robust brain ‘wiring’, that is, the nerve fibres that connect different, distant brain areas, can process information quickly and that this makes them generally smarter, the study suggests.

According to the findings, joining distant parts of the brain together with better wiring improves mental performance, suggesting that intelligence is not found in a single part of the brain.

However a loss of condition of this wiring or ‘white matter’, the billions of nerve fibres that transmit signals around the brain, can negatively affect our intelligence by altering these networks and slowing down our processing speed.

The research by the University of Edinburgh shows for the first time that the deterioration of white matter with age is likely to be a significant cause of age-related cognitive decline.

The research team used three different brain imaging techniques in compiling the results, including two that have never been used before in the study of intelligence.

Healthy nerve connections in the brain help to reduce mental decline and dementia in older people. Image by Flickr user Brian Auer. See below for attribution.

These techniques measure the amount of water in brain tissue, indicate structural loss in the brain, and show how well the nerve fibres are insulated.

The researchers examined scans and results of thinking and reaction time tests from 420 people in the Lothian Birth Cohort of 1936, a group of nearly 1100 people whose intelligence & general health have been tracked since they were 11

The research was part of the Disconnected Mind Project, a large study of the causes of people’s differences in cognitive ageing, led by Professor Ian Deary.

Study author Doctor Lars Penke said “Our results suggest a first plausible way how brain structure differences lead to higher intelligence. The results are exciting for our understanding of human intelligence differences at all ages.”

“They also suggest a clear target for seeking treatment for mental difficulties, be they pathological or age-related. That the brain’s nerve connections tend to stay the same throughout the brain means we can now look at factors that affect the overall condition of the brain, like its bloody supply.”

Professor Deary said that uncovering the secrets of good thinking skills in old age is a high priority. “The research team is now looking at what keeps the brain’s connections healthy. We value our thinking skills, and research should address how we might retain them or slow their decline with age.”

Doctor Mark Bastin, who co-authored the study, said “These findings are exciting as they show how quantitative brain imaging can provide novel insights into the links between brain structure and cognitive ability. This is a key research area given the importance of identifying strategies for retaining good mental ability into older age.”

Professor James Goodwin, Head of Research at Age UK, said: “This research is very exciting as it could have a real impact on tackling mental decline in later life, including dementia. With new understanding on how the brain functions we can work out why mental faculties decline with age in some people and not others and look at what can be done to improve our minds’ chances of ageing better.”

Source: Neuroscience News