Alzheimer’s Disease: Possibly Caused From Haywire Immune System Eating Brain Connections?

By: Alexandria Addesso

Memory loss and absent-mindedness has long been seen as an inevitable flaw that comes with old age. Although there is a slew of medications on the market that are prescribed for those suffering from Alzheimer’s Disease, none seem to change it by too large of a margin. This has led scientists to rethink what in particular is the root cause of Alzheimer’s.

New studies done on laboratory test rodents have found that there is a marked loss of synapses, which are a junction between two nerve cells, consisting of a minute gap across which impulses pass by diffusion of a neurotransmitter. Specifically synapses that are located in brain regions that are highly significant and key to memory.



These junctions between nerve cells are where neurotransmitters are released to spark the brain’s electrical activity. Currently, all pharmaceutical drugs on the market for the treatment of Alzheimer’s, focus on eliminating β amyloid, a protein that forms telltale sticky plaques around neurons in people with the disease. But, more β amyloid does not always mean more severe symptoms such as memory loss or poor attention.

Researchers at the University of Virginia, School of Medicine, in Charlottesville found that a protein called ‘C1q’ sets off a series of chemical reactions that ultimately mark a synapse for destruction. After this occurs immune cells called microglia-glial cells derived from mesoderm that function as macrophages (scavengers) in the central nervous system and form part of the reticuloendothelial system, destroy or “eat” the synapse.



“It is beautiful new work brings into light what’s happening in the early stage of the disease,” said one of the researchers at the University of Virginia School of Medicine neuroscientist Jonathan Kipnis.

These findings could mean that treatment that blocks C1q could be pivotal and highly successful in fighting Alzheimer’s Disease. When researchers gave the laboratory rodent test subjects an antibody to stop the destruction of cells by microglia, synapse loss did not appear. This could also mean a slowing in cognitive decline, but according to Edward Ruthazer, a neuroscientist at the Montreal Neurological Institute and Hospital in Canada, using microglia as such a central role to fight the disease is “still on the controversial side.”

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Your Blood Type May Help Protect you From Cognitive Decline

A pioneering study conducted by leading researchers at the University of Sheffield has revealed that blood types play a role in the development of the nervous system and may cause a higher risk of developing cognitive decline.

The research, carried out in collaboration with the IRCCS San Camillo Hospital Foundation in Venice, shows that people with an ‘O’ blood type have more grey matter in their brain, which helps to protect against diseases such as
Alzheimer’s, than those with ‘A’, ‘B’ or ‘AB’ blood types.

Research fellow Matteo De Marco and Professor Annalena Venneri, from the University’s Department of Neuroscience, made the discovery after analyzing the results of 189 Magnetic Resonance Imaging (MRI) scans from healthy volunteers.
The researchers calculated the volumes of grey matter within the brain and explored the differences between different blood types.

The results, published in The Brain Research Bulletin, show that individuals with an ‘O’ blood type have more grey matter in the posterior proportion of the cerebellum.



In comparison, those with ‘A’, ‘B’ or ‘AB’ blood types had smaller grey matter volumes in temporal and limbic regions of the brain, including the left hippocampus, which is one of the earliest part of the brain damaged by Alzheimer’s disease.

These findings indicate that smaller volumes of grey matter are associated with non-‘O’ blood types.

As we age a reduction of grey matter volumes is normally seen in the brain, but later in life this grey matter difference between blood types will intensify as a consequence of ageing.

“The findings seem to indicate that people who have an ‘O’ blood type are more protected against the diseases in which volumetric reduction is seen in temporal and middle-temporal regions of the brain like with Alzheimer’s disease for instance,” said Matteo DeMarco.



“However additional tests and further research are required as other biological
mechanisms might be involved.”

Professor Annalena Venneri added: “What we know today is that a significant difference in volumes exists, and our findings confirm established clinical observations. In all likelihood the biology of blood types influences the development of the nervous system. We now have to understand how and why this occurs.”
Source: Neuroscience News / Amy Pullan – University of Sheffield

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Researchers Find the Existence of another Immune System in Humans

The good news is that doctors can determine which antigens a patient’s cancer cells release. By targeting sequestered antigens – the ones unknown to the immune system – doctors could greatly increase vaccines’ chances of success. NeuroscienceNews.com image is credited to United States Department of Health and Human Services and is for illustrative purposes only.

A groundbreaking new study reveals an unexpected interaction between men’s testes and the immune system. Additionally, the findings could help explain the development of certain autoimmune disorders and why some cancer vaccines are ineffective.

Unexpected connection likely sabotaging vaccines designed to treat cancer.
The University of Virginia, School of Medicine, has again shown that a part of the body thought to be disconnected from the immune system actually interacts with it, and that discovery helps explain cases of male infertility, certain autoimmune diseases and even the failure of cancer vaccines.

Scientists developing such vaccines may need to reconsider their work in light of the new findings or risk unintentionally sabotaging their own efforts. UVA’s Kenneth Tung, MD, said that many vaccines likely are failing simply because researchers are picking the wrong targets – targets that aren’t actually foreign to the immune system and thus won’t provoke the desired immune responses.

Overturning Orthodoxy
Tung, of UVA’s Beirne B. Carter Center for Immunology Research, and a team of collaborators have discovered an unexpected interaction between men’s testes and the immune system. While science textbooks insist the testes are barricaded from the immune system by an impenetrable wall of cells, the researchers have determined there’s actually a very small door in that wall, a door that appears to open in only one direction.



The team discovered that the testes release some, but not all, of the antigens – substances that can spur an immune response – that are created during the production of sperm. Because the testes release these antigens naturally, the immune system ignores them. That’s a normal, healthy response, but it also may explain why cancer vaccines are failing. Cancer vaccines target antigens, so if vaccine developers rely on antigens that are ignored by the immune system, the vaccine won’t work.

“In essence, we believe the testes antigens can be divided into those which are sequestered [behind the barrier] and those that are not,” Tung said. “Antigens which are not sequestered would not be very good cancer vaccine candidates.”

The good news is that doctors can determine which antigens a patient’s cancer cells release. By targeting sequestered antigens – the ones unknown to the immune system – doctors could greatly increase vaccines’ chances of success.



Treating Infertility
The finding also may prove important for couples seeking to have children. Up to 12 percent of men who suffer from infertility have an autoimmune response to their own reproductive cells. That means their immune systems are attacking their sperm, essentially. Tung and his collaborators shed light on what may be happening, showing that a particular step during the creation of sperm is responsible for determining whether the sperm antigens will spark an immune response. Cells called “regulatory T cells” then help control the immune system’s response to the non-sequestered antigens. In men who are infertile because of an autoimmune disorder, something is going wrong with the process, leading the immune system to attack when it shouldn’t. With that knowledge, doctors may be able to develop new treatments for the autoimmune disorders and the resulting infertility.

Rethinking the Immune System
The discovery of the unknown immune interaction comes less than two years after UVA’s Jonathan Kipnis and Antoine Louveau rewrote textbooks when they discovered that the brain has a direct connection to the immune system, a connection long thought not to exist. That discovery could have profound effects in the quest to defeat diseases ranging from Alzheimer’s to multiple sclerosis.
Source: University of Virginia Health System.

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Autism diagnosis by brain scan? It’s time for a reality check

Recent reports that it might be possible to use MRI to identify at-risk children are exciting, but we are still a long way from autism diagnosis by brain scan

A brain scan for autism would be a major step forward. But is the hype justified?

What if I told you that we can now identify babies who are going to develop autism based on a simple brain scan? This, in essence, is the seductive pitch for a study published last week in the journal Nature, and making headlines around the world.

Early identification and diagnosis is one of the major goals of autism research. By definition, people with autism have difficulties with social interaction and communication. But these skills take many years to develop, even in typically developing (i.e., non-autistic) children. Potential early signs of autism are extremely difficult to pick out amidst the natural variation in behavior and temperament that exists between all babies.
A brain scan for autism would be a major step forward. But is the hype justified? Are we really on the brink of a new era in autism diagnostics? Without wishing to detract from the efforts of everyone involved in the study, it’s important to look at the results critically, both in terms of the scientific findings and their potential implications for clinical practice.



The study, led by Heather Cody Hazlett at the University of North Carolina, was part of a larger research program investigating the development of babies who have an older sibling with autism. Because autism runs in families, these babies are much more likely to develop autism than babies from the general population.

The babies were given MRI brain scans at 6, 12, and 24 months of age and were then assessed for autism. As expected for this “high risk” sample, around 1 in 5 met the diagnostic criteria. The researchers were then able to look back at the brain scans to see if there were any differences between the autistic and the non-autistic babies.

Hazlett and colleagues first looked at three measures of overall brain size: the total volume of the brain; its total surface area; and the average thickness of the cortex (the brain’s outer layer). Consistent with previous studies of older children, the autistic babies had slightly larger brain volume and greater surface area. However, these effects were only statistically significant for the last scan at 24 months.

Most autistic infants had brains that wouldn’t set them apart from non-autistic infants. In other words, overall brain size isn’t in itself a very good predictor of whether or not an individual baby will go on to an autism diagnosis.

So Hazlett and colleagues tried a different approach, calculating the volume and surface area for 78 different regions within each infant’s brain. They did this twice: once for the 6 month scan and again for the 12 month scan, giving them 312 data points, or “features”, for each baby.



Next, they fed that information (plus the sex and skull volume of each baby) into a computer that they trained to differentiate between the autistic and non-autistic babies.

Importantly, they only trained it on 90% of the babies at a time. They then fed in the brain features from the remaining 10% and asked the computer to predict the diagnosis of each baby. They did this 10 times, leaving out a different subgroup of babies each time.

The computer correctly diagnosed 30 of 34 autistic babies in the sample and incorrectly flagged just 7 of 145 non-autistic babies. So the excitement is understandable.

Of 34 babies with autism, 30 were correctly identified. False positives occurred for 7 out of 145 non-autistic babies.

However, as the researchers themselves note, the study really needs to be replicated. Because it was a first-of its-kind, the researchers would necessarily have been feeling their way, making decisions as they went along. This tweaking inevitably biases the outcome towards a more compelling result. But having learnt the lessons from this first study, researchers are now in a position to preregister any replication attempt, nailing down all the details before they begin. If the current results are robust, they should replicate even without the tweaking.



Assuming the results do hold up, the next big question is whether this approach actually translates to real life clinical applications. Will we really see the everyday use of MRI scans to predict whether or not babies have or will develop autism?

An important practical consideration is the requirement for brain scans to be acquired at both 6 and 12 months. MRI scanners are noisy and claustrophobic. Any movement and the scan is ruined. The researchers scanned the babies while they were asleep but, despite their best efforts, only around half of the babies had two useable scans. Once we add the babies with incomplete data to the picture, the results start to look less useful. In particular, only 30 of the 70 autistic babies in the study could be identified based on their brain scans.

Including babies with incomplete data, only 30 out of 70 babies with autism were correctly identified.

As a final point, the use of MRI scans for autism detection is unlikely to be of much practical benefit beyond high-risk populations. This is simply an issue of numbers. In the general population, it’s estimated that one person in 68 has autism. In the figure below, I’ve assumed that the computer maintains the same ability to differentiate between autistic and non-autistic brains but is now faced with 67 non-autistic babies for every one autistic baby.

Assuming an estimate of 1 in 68 people having autism, in order to identify the 30 babies with autism in the original sample, we would need to scan a total of 4760 babies.

We’d still miss the other 40 autistic babies. And because of the scaling up, 132 non-autistic babies would incorrectly test positive. In other words, 81% of babies who tested positive would not actually be autistic.

These are, of course, inexact back-of-the-envelope calculations. The computer algorithm may perform much better when it is trained to differentiate between autistic and low risk babies. And there are, no doubt, ways of improving the success rate of scanning. But it illustrates the profound challenges in translating the research finding into widespread clinical practice. For now at least, it’s time to dial back the hype. We are still a very long way from autism diagnosis by brain scan.

But from a scientific point of view, I remain excited by these findings. They’re part of a growing body of evidence for subtle differences in the brains of young infants who go on to be diagnosed with autism. Some of these findings are perhaps more robust than others, but each represents an important step towards a greater understanding of the developmental origins of autism in the
Source: Jon Brock, The Guardian

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Understanding the Brain with the Help of Artificial Intelligence

Neurobiologists aim to decode the brain’s circuitry with the help of artificial neural networks. NeuroscienceNews.com image is credited to Julia Kuhl.

Researchers have trained neural networks to accelerate the reconstruction of neural circuits.

How does consciousness arise? Researchers suspect that the answer to this question lies in the connections between neurons. Unfortunately, however, little is known about the wiring of the brain. This is due also to a problem of time: tracking down connections in collected data would require man-hours amounting to many lifetimes, as no computer has been able to identify the neural cell contacts reliably enough up to now. Scientists from the Max Planck Institute of Neurobiology in Martinsried plan to change this with the help of artificial intelligence. They have trained several artificial neural networks and thereby enabled the vastly accelerated reconstruction of neural circuits.

Neurons need company. Individually, these cells can achieve little, however when they join forces neurons form a powerful network which controls our behaviour, among other things. As part of this process, the cells exchange information via their contact points, the synapses. Information about which neurons are connected to each other when and where is crucial to our understanding of basic brain functions and superordinate processes like learning, memory, consciousness and disorders of the nervous system. Researchers suspect that the key to all of this lies in the wiring of the approximately 100 billion cells in the human brain.



To be able to use this key, the connectome, that is every single neuron in the brain with its thousands of contacts and partner cells, must be mapped. Only a few years ago, the prospect of achieving this seemed unattainable. However, the scientists in the Electrons – Photons – Neurons Department of the Max Planck Institute of Neurobiology refuse to be deterred by the notion that something seems “unattainable”. Hence, over the past few years, they have developed and improved staining and microscopy methods which can be used to transform brain tissue samples into high-resolution, three-dimensional electron microscope images. Their latest microscope, which is being used by the Department as a prototype, scans the surface of a sample with 91 electron beams in parallel before exposing the next sample level. Compared to the previous model, this increases the data acquisition rate by a factor of over 50. As a result an entire mouse brain could be mapped in just a few years rather than decades.

Although it is now possible to decompose a piece of brain tissue into billions of pixels, the analysis of these electron microscope images takes many years. This is due to the fact that the standard computer algorithms are often too inaccurate to reliably trace the neurons’ wafer-thin projections over long distances and to identify the synapses. For this reason, people still have to spend hours in front of computer screens identifying the synapses in the piles of images generated by the electron microscope.



Training for neural networks
However the Max Planck scientists led by Jörgen Kornfeld have now overcome this obstacle with the help of artificial neural networks. These algorithms can learn from examples and experience and make generalizations based on this knowledge. They are already applied very successfully in image process and pattern recognition today. “So it was not a big stretch to conceive of using an artificial network for the analysis of a real neural network,” says study leader Jörgen Kornfeld. Nonetheless, it was not quite as simple as it sounds. For months the scientists worked on training and testing so-called Convolutional Neural Networks to recognize cell extensions, cell components and synapses and to distinguish them from each other.

Following a brief training phase, the resulting SyConn network can now identify these structures autonomously and extremely reliably. Its use on data from the songbird brain showed that SyConn is so reliable that there is no need for humans to check for errors. “This is absolutely fantastic as we did not expect to achieve such a low error rate,” says Kornfeld with obvious delight at the success of SyConn, which forms part of his doctoral study. And he has every reason to be delighted as the newly developed neural networks will relieve neurobiologists of many thousands of hours of monotonous work in the future. As a result, they will also reduce the time needed to decode the connectome and, perhaps also, the consciousness, by many years.
Source: Max Planck Institute / Neuroscience.news

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Using Virtual Reality to Detect Mild Cognitive Impairment

The VSM payment screen (screenshot from the English version of the application). NeuroscienceNews.com image is credited to Aristotle University of Thessaloniki (AUTH).

Researchers report mild cognitive impairment can be remotely detected with the help of a self-administered brain training game.

Mild cognitive impairment (MCI), a condition that often predates Alzheimer’s disease (AD), can be remotely detected through a self-administered virtual reality brain training game.

Greek researchers demonstrated the potential of a self-administered virtual supermarket cognitive training game for remotely detecting mild cognitive impairment (MCI), without the need for an examiner, among a sample of older adults. MCI patients suffer from cognitive problems and often encounter difficulties in performing complex activities such as financial planning. They are at a high risk for progressing to dementia however early detection of MCI and suitable interventions can stabilize the patients’ condition and prevent further decline.



It has been shown that virtual reality game-based applications and especially virtual supermarkets can detect MCI. Past studies have utilized user performance in such applications along with data from standardized neuropsychological tests in order to detect MCI. The team that conducted this study was the first scientific team to achieve reliable MCI detection using a virtual reality game-based application on its own. In that previous study , administration of the virtual super market (VSM) exercise was conducted by an examiner. The present study eliminated the need for an examiner by calculating the average performance of older adults using a special version of the VSM application, the VSM Remote Assessment Routine (VSM-RAR), at home on their own, for a period of one month. It is the first instance where a self-administered virtual reality application was used to detect MCI with a high degree of reliability.



The research team included scientists from the Aristotle University of Thessaloniki (AUTH), the Centre for Research and Technology Hellas/Information Technologies Institute (CERTH/ITI), the Greek Association of Alzheimer’s Disease and Related Disorders (GAADRD) and the Network Aging Research (NAR) of the University of Heidelberg.

In an article published in the Journal of Alzheimer’s Disease, the researchers have indicated that the virtual supermarket remote assessment routine (VSM-RAR) application displayed a correct classification rate (CCR) of 91.8% improving VSM’s CCR as assessed in the previous VSM study while achieving a level of diagnostic accuracy similar to the most accurate standardized neuropsychological tests, which are considered the gold standard for MCI detection.

Self-administered computerized cognitive training exercises/games are gaining popularity among older adults as an easy and enjoyable means of maintaining cognitive health. Such applications are especially popular among older adults who consider themselves healthy and are not inclined to visit specialized memory clinics for cognitive assessment. If self-administered games and exercises could also detect cognitive disorders, initial cognitive screening could be conducted remotely. The wide implementation of this method of remote screening would facilitate the detection of cognitive impairment at the MCI stage thus allowing for more efficient therapeutic interventions.



This preliminary study indicates that automated, remote MCI screening is feasible. This method could be utilized to screen the majority of the older adult population, as it dramatically lowers examination-related costs. The social and economic benefits, especially caregiver and healthcare service burden, of the early detection of cognitive disorders could be enormous. At the same time, as older adults are becoming increasingly computer savvy, it is important to create software that meets their needs and allows them to remain healthy and active. Out team continues its research on the VSM with the aim of improving its usability, shortening its administration time and supplementing the science behind VSM with additional data.
Source: Stelios Zygouris – IOS Press
Image Source: NeuroscienceNews.com image is credited to Aristotle University of Thessaloniki (AUTH).

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Soccer Success in the Young Can Be Measured in the Brain

Executive functions are special control functions in the brain that allow us to adapt to an environment in a perpetual state of change. They include creative thinking in order to quickly switch strategy, find new, effective solutions and repress erroneous impulses. The functions are dependent on the brain’s frontal lobes, which continue to develop until the age of 25. NeuroscienceNews.com image is adapted from Karolinska Institute press release.

Cognitive function can be quantified and linked to how well a child performs in a game of soccer, researchers report.

The working memory and other cognitive functions in children and young people can be associated with how successful they are on the football pitch, a new study from Karolinska Institutet, Sweden, shows. Football clubs that focus too much on physical attributes therefore risk overlooking future stars.



Physical attributes such as size, fitness and strength in combination with ball control have long been considered critical factors in the hunt for new football talent. The third, slightly elusive factor of “game intelligence” — to always be at the rights place at the right time — has been difficult to measure. In 2012, researchers at Karolinska Institutet provided a possible scientific explanation for the phenomenon, and showed that the so-termed “executive cognitive functions” in adult players could be associated with their success on the pitch. In a new study, which is published in the scientific journal PLOS ONE, they show that cognitive faculties can be similarly quantified and linked to how well children and young people do in the game.

“This is interesting since football clubs focus heavily on the size and strength of young players,” says study leader Predrag Petrovic, at Karolinska Institutet’s Department of Clinical Neuroscience. “Young players who have still to reach full physical development rarely get a chance to be picked as potential elite players, which means that teams risk missing out on a new Pele, Maradona or Messi.”



Executive functions are special control functions in the brain that allow us to adapt to an environment in a perpetual state of change. They include creative thinking in order to quickly switch strategy, find new, effective solutions and repress erroneous impulses. The functions are dependent on the brain’s frontal lobes, which continue to develop until the age of 25.

For this present study, the researchers measured certain executive functions in 30 elite footballers aged between 12 and 19, and then cross-referenced the results with the number of goals they scored during two years. The metrics were taken in part using the same standardized tests used in healthcare. Strong results for several executive functions were found to be associated with success on the pitch, even after controlling for other factors that could conceivably affect performance. The clearest link was seen for simpler forms of executive function, such as working memory, which develops relatively early in life.

“This was expected since cognitive function is less developed in young people than it is in adults, which is probably reflected in how young people play, with fewer passes that lead to goals,” says Predrag Petrovic.
The young elite players also performed significantly better than the average population in the same age group on several tests of executive function. Whether these faculties are inherited or can be trained remains the object of future research, as does the importance of the different executive functions for the various positions on the field.



“We think that the players’ positions on the pitch are linked to different cognitive profiles,” continues Dr Petrovic. “I can imagine that trainers will start to use cognitive tests more and more, both to find talented newcomers and to judge the position they should play in.”
Source: Karolinska Institute
Image Source: NeuroscienceNews.com image is adapted from Karolinska Institute press release.
Original Research: Full open access research for “Core executive functions are associated with success in young elite soccer players” by Torbjörn Vestberg, Gustaf Reinebo, Liselotte Maurex, Martin Ingvar, Predrag Petrovic in PLOS ONE. Neuroscience.news

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The Possible Cause of Flashbacks Discovered

Traumatic events can stop the brain storing the context in which they took place.

Remembering the past is an important function and defines who we are. In some situations though, the normal processes that store our experiences into memory can go wrong. After experiencing a distressing event, people can develop memory disturbances where they re-experience the event in the form of flashbacks – distressing vivid images that involuntarily enter consciousness, as happens in post-traumatic stress disorder.

Our latest study shows that a distressing experience has opposite effects in two different parts of the brain: the amygdala and the hippocampus. The amygdala, a region of the brain involved in emotion, seemed to strongly encode the negative content of an experience while the hippocampus, which is involved in storing new memories, is only weakly activated.

When remembering something from the past, we can bring to mind what we were doing, the people we were with, and where the event took place. An important aspect of memory is that these separate pieces of information are bound together as a single memory so that all of it can easily be recalled at a later time. But when experiencing a distressing event, the normal processes that help to integrate this information in memory can be disrupted.

The hippocampus is crucial for forming these associations so that all parts of a memory can be later retrieved as a single event (and damage to this brain region can stop a person from forming new memories). In contrast, the amygdala is involved in processing emotional information and making basic responses to things associated with fear, such as recoiling from a snake or spider.


The hippocampus. The brain region involved in consolidating new memories.

People who have suffered a trauma often have difficulty remembering the context of the event. We thought that, while processing in the amygdala might be increased during a negative experience, processing in the hippocampus might be decreased, disrupting the way it binds the different aspects of the experience together as a single memory.

To test this idea we showed 20 volunteers pairs of pictures and asked them to remember the pictures while lying in an MRI scanner. Some of the pictures were of traumatic
scenes, such as a badly injured person.

The volunteers’ memory of the pictures was then tested in two ways. First, they were shown one picture from each pair and asked if they recognized previously seeing it. Second, if the picture was recognized, we then asked whether they could remember what other picture had been part of the original pair.

When asked whether they recognized the individual pictures, people showed better memory for previously seen pictures that were negative (traumatic) compared with pictures that were neutral, such as a person sitting at an office desk. Improved memory for negative pictures related to increased activity in the amygdala. In contrast, their memory for remembering what pictures were presented together as a pair was worse when one of the pictures was negative.



We also found that activity in the hippocampus was reduced by the presence of negative pictures suggesting that its function in storing the associations between the pictures was impaired. This imbalance could lead to strong memories for the negative content of an event that is not properly stored with the other parts of the event and the context in which it took place.

Implications for psychotherapy
This work supports the view that experiencing a traumatic event might alter how memory works. The re-experiencing of intrusive images in post-traumatic stress disorder might happen because of strengthened memory for the negative aspects of a trauma but not their context – that is, the location where the event occurred or the time it occurred. This may result in the person involuntarily retrieving the traumatic event “out of context” and experiencing it as though it was in the present.

In this case, therapy should focus on strengthening or recreating appropriate contextual associations for the negative event. This view is supported by current psychotherapies where a person is taken back to the place where the traumatic event took place to help in strengthening memory for the context.

These findings also highlight potential issues with eyewitness testimony as trauma sufferers with poorly contextualized memories are likely to provide a fragmented report of an event.

The author of this James Bisby, Research Associate, University College London. This article was originally published in The Conversation under a Creative Commons Attribution

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Personality Traits Linked to Differences in Brain Structure

Researchers report on how differences in cortical anatomy relates to each of the five factors of personality.

Our personality may be shaped by how our brain works, but in fact the shape of our brain can itself provide surprising clues about how we behave – and our risk of developing mental health disorders – suggests a study published today.

According to psychologists, the extraordinary variety of human personality can be broken down into the so-called ‘Big Five’ personality traits, namely neuroticism (how moody a person is), extraversion (how enthusiastic a person is), openness (how open-minded a person is), agreeableness (a measure of altruism), and conscientiousness (a measure of self-control).

In a study published today in the journal Social Cognitive and Affective Neuroscience, an international team of researchers from the UK, US, and Italy have analyzed a brain imaging dataset from over 500 individuals that has been made publicly available by the Human Connectome Project, a major US initiative funded by the National Institutes of Health. In particular, the researchers looked at differences in the brain cortical anatomy (the structure of the outer layer of the brain) as indexed by three measures – the thickness, area, and amount of folding in the cortex – and how these measures related to the Big Five personality traits.


The researchers looked at differences in the brain cortical anatomy (the structure of the outer layer of the brain) as indexed by three measures – the thickness, area, and amount of folding in the cortex – and how these measures related to the Big Five personality traits. NeuroscienceNews.com image is adapted from the University of Cambridge press release.

“Evolution has shaped our brain anatomy in a way that maximizes its area and folding at the expense of reduced thickness of the cortex,” explains Dr. Luca Passamonti from the Department of Clinical Neurosciences at the University of Cambridge. “It’s like stretching and folding a rubber sheet – this increases the surface area, but at the same time the sheet itself becomes thinner. We refer to this as the cortical stretching hypothesis”.

“Cortical stretching is a key evolutionary mechanism that enabled human brains to expand rapidly while still fitting into our skulls, which grew at a slower rate than the brain,” adds Professor Antonio Terracciano from the Department of Geriatrics at the Florida State University. “Interestingly, this same process occurs as we develop and grow in the womb and throughout childhood, adolescence, and into adulthood: the thickness of the cortex tends to decrease while the area and folding increase.”
In addition, as we get older, neuroticism goes down – we become better at handling emotions. At the same time, conscientiousness and agreeableness go up – we become progressively more responsible and less antagonistic.

The researchers found that high levels of neuroticism, which may predispose people to develop neuropsychiatric disorders, were associated with increased thickness as well as reduced area and folding in some regions of the cortex such as the prefrontal-temporal cortices at the front of the brain.


The researchers found that high levels of neuroticism, which may predispose people to develop neuropsychiatric disorders, were associated with increased thickness as well as reduced area and folding in some regions of the cortex such as the prefrontal-temporal cortices at the front of the brain. Credit: The researchers/University of Cambridge.

In contrast, openness, which is a personality trait linked with curiosity, creativity and a preference for variety and novelty, was associated with the opposite pattern, reduced thickness and an increase in area and folding in some prefrontal cortices.
“Our work supports the notion that personality is, to some degree, associated with brain maturation, a developmental process that is strongly influenced by genetic factors,” says Dr. Roberta Riccelli from Italy.

“Of course, we are continually shaped by our experiences and environment, but the fact that we see clear differences in brain structure which are linked with differences in personality traits suggests that there will almost certainly be an element of genetics involved,” says Professor Nicola Toschi from the University ‘Tor Vergata’ in Rome. “This is also in keeping with the notion that differences in personality traits can be detected early on during development, for example in toddlers or infants.”

The volunteers whose brains were imaged as part of the Human Connectome Project were all healthy individuals aged between 22 and 36 years with no history of neuro-psychiatric or other major medical problems. However, the relationship between differences in brain structure and personality traits in these people suggests that the differences may be even more pronounced in people who are more likely to experience neuro-psychiatric illnesses.

“Linking how brain structure is related to basic personality traits is a crucial step to improving our understanding of the link between the brain morphology and particular mood, cognitive, or behavioral disorders,” adds Dr. Passamonti. “We also need to have a better understanding of the relation between brain structure and function in healthy people to figure out what is different in people with neuropsychiatric disorders.”
This is not the first time the researchers have found links between our brain structure and behavior. A study published by the group last year found that the brains of teenagers with serious antisocial behavior problems differ significantly in structure to those of their peers.

Source: University of Cambridge.

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New Breakthrough: The new Treatment strategies for Bipolar Disorder and Epilepsy

Summary: A new study looks at how a gene associated with bipolar disorder affects the balance between inhibition and excitation; revealing a link with epilepsy.

People with bipolar disorder suffer from excessive emotional highs and lows that can cycle uncontrollably, severely distorting their awareness of self and others, impairing social and work ability and causing high risk of suicide. Current treatments are only partly effective. Researchers at Baylor College of Medicine have used mouse models and advanced molecular mapping studies in both mouse and human to learn how a gene associated with bipolar disorder controls the balance between brain excitation and inhibition and shown for the first time that it also is linked to epilepsy.

The findings, appearing recently in the early online edition of Molecular Psychiatry, open new treatment strategies for both bipolar disorder and epilepsy.

“We became very interested in a gene called ‘ankyrin 3’, or ANK3, a decade ago when we discovered it coded for a partner of two other genes that are mutated in some people with epilepsy. Soon afterward, ANK3 was connected with bipolar disorder by genetic testing of thousands of psychiatric patient volunteers around the world,” said Dr. Edward C. Cooper, associate professor of neurology, molecular and human genetics, and neuroscience at Baylor. “Although there are important differences, we noted similarities between bipolar disorder and epilepsy: both cycle, both are risk factors for the other, and both are currently treated using many of the same drugs. Reasons behind these overlaps were mysterious, and the specific parts of the ANK3 gene linked with bipolar had no known function. We decided to take a much closer look at the human brain and mice with bipolar-like behavior. In our study we found that reduced expression of one type of ANK3 removes a brake on the output of brain neurons, leading to excesses in firing in circuits for emotions, memory and epilepsy.”



Proteins coded by ANK3. Blue: output cells. Yellow: nerve impulse trigger zones of output cells. White: Inhibitory neurons that hold back output. Red: trigger zones with a different type of ANK3 protein, lost in bipolar disorder and epilepsy. NeuroscienceNews.com image is credited to the researchers.

Within each ANK3 gene are bits of DNA containing information coding for several different proteins. The research team found that, in both mice and human, different ANK3-coded proteins were expressed on brain cells responsible for increasing output (excitation) and holding back output (inhibition). Working with Cooper, Baylor genetics graduate student Angel Lopez discovered that an ANK3 type found in lower amounts in bipolar disorder patients was selectively lost by inhibitory neurons, lowering their output. Activity of neighboring excitatory cells proved unaffected. So, what scientists call “excitation/inhibition” balance, was shifted in the direction of excessive excitation.

When Lopez and colleagues engineered mice to lose this inhibitory form of ANK3, they found that the imbalance caused both frequent epileptic seizures and an increased risk of sudden death across the lifespan.

“This showed us that imbalance in ANK3 function can result not only in excessive circuit sensitivity and output leading to bipolar
disorder, but also severe epilepsy,” Cooper said.

Although diagnosis and care for bipolar disorder and epilepsy often are viewed as distinctly psychiatric and neurological issues, respectively, the study highlights an example of common genetic and biological underpinnings at a frontier between medical disciplines. The results open the door to additional lab and clinical research and could lead to new treatment options for both conditions by targeting ANK3 and its molecular partners in the brain.



“Our work also provides an example of how conducting and participating in unbiased human genetic studies, such as those that implicated ANK3 in bipolar disorder, can illuminate unforeseen connections between disease categories and the benefits of research that crosses disciplinary borders” said Cooper.
Source: Neuroscience News, Baylor College of Medicine

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Experimental Treatment for Parkinson’s Symptoms Shows Early Promise

Depicted is a reconstruction of bi-hemispheric DBS electrodes that have been surgically placed into the most common target structure for treatment of Parkinson Disease, the sub-thalamic nucleus (orange). Other subcortical structures include the red nucleus (green), the substantia ‘nigra’ (yellow), the internal (cyan) and external (blue) pallidum and the striatum (red). A stimulation volume is modeled by applying 2V (at 1000Ω impedance) to the second-uppermost contact of the left electrode. Structural ‘fibertracts’ traversing through this volume are visualized and cortical regions that they connect with the stimulation volume are selected from an automatic anatomical labeling atlas and visualized. NeuroscienceNews.com image is credited to Andreashorn and is for illustrative purposes only

DBS Plus, a new version of deep brain stimulation, shows promise in helping to relieve Parkinson’s symptoms.

About 14 years ago, Bill Crawford noticed a persistent twitching in one of his fingers that was interfering with his rehearsal time as the music pastor at Porter Memorial Church.
“It was driving me crazy,” said the 57-year-old Lexingtonian.

He’d noticed a few other things too, like weakness. He had mentioned it to his primary care physician, who ordered heart and lung function tests, but both were negative.

Finally, however, he was so weak that he could no longer ride his bike. “I just couldn’t seem to go,” he said. So he made an appointment with a neurologist.

After a few minutes with Crawford, the neurologist asked him to return on Monday – and bring his wife Lisa with him.

On that dreadful day, the neurologist told Bill that he had Parkinson’s disease. At the time, Bill was just 44 years old.

“Obviously not what you want to hear,” Crawford said. “But then I began to think of Michael J. Fox and all he had accomplished, and I thought I could do that too.”

Eventually, though, the medicines that helped Bill control his Parkinson’s symptoms began to lose their effectiveness.

“There is no cure for Parkinson’s, and treatments we currently have at our disposal can only reduce symptoms,” explained Dr. John T. Slevin, a specialist at UK HealthCare’s Kentucky Neuroscience Institute, who began treating Crawford in 2006. “The disease progression inevitably overcomes the drugs’ capacity to alleviate the rigidity and tremor that are hallmarks of Parkinson’s.”

That meant that Crawford would go into what he called “full body charley horses” – sudden, painful involuntary spasms that left him paralyzed and lying on the floor for as much as 45 minutes.

“It was the pits,” Crawford said. Sometimes at the last minute he would be unable to conduct
musical performances at church services, which was particularly disheartening. “I didn’t want to be a spectacle.”

It was then that Slevin suggested a treatment called Deep Brain Stimulation and connected Crawford with UK HealthCare neurosurgeon Dr. Craig van Horne.

Deep Brain Stimulation (DBS) is a surgical procedure used to treat the problems associated with Parkinson’s disease. The procedure involves implanting electrodes into the brain that are connected to a small, pacemaker-like device implanted in the chest. These electrodes produce electrical signals that override the abnormal electrical impulses caused by the disease, which attacks and breaks down nerve cells in the brain.



The procedure isn’t suitable for everyone and requires thorough psychological testing and motion studies to ensure that a patient is ready for DBS. “I wasn’t sure I would qualify,” Crawford said. “But I knew this was my last chance.”

Crawford considers it a blessing that he was, in fact, qualified to receive DBS. But then came an additional surprise: after further testing, van Horne told Crawford that he was qualified to participate in a study for a new version of DBS called “DBS Plus.”

Van Horne explains that the central nervous system – which is comprised of the brain and spinal cord – is unable to heal itself after injury or disease. However, peripheral nerves from the rest of the body are able to regenerate.

“Our study is designed to test whether taking a small part of peripheral nerve tissue and putting it in the brain would prompt healing in the areas of the central nervous system damaged by Parkinson’s,” he said.

With DBS Plus, van Horne and his team (Greg Gerhard, PhD, and George Quintero, PhD,) take a small piece of nerve tissue from the patient’s ankle and implant it in their brain. Because the tissue is from a patient’s own body there are no concerns about rejection, and because the experimental treatment is applied during a procedure that was declared safe and effective by U.S. Food and Drug Administration (FDA) almost two decades ago, DBS Plus is considered relatively safe with only minimal additional risk.



Nonetheless, van Horne is cautious about the process of enrolling patients in the study.
“It’s more ethical, in my opinion, to wait until after a patient qualifies for the basic DBS before I tell them about my study,” he said. “I don’t want patients to elect to do DBS just because they want DBS Plus.”

And van Horne says he was thrilled that Crawford qualified for the study.
“When I met Bill for the first time, he was lying paralyzed on the floor in the treatment room,” van Horne recalled. “It was a startling and heart-breaking sight.”
Crawford received DBS Plus in August 2015. His family can’t get over the dramatic changes in his mobility.

“I’m climbing ladders now, I can plan our church’s worship time, I can lead the services, I can still lead others in worship,” he said.

The charley horses have gone away, and Crawford now takes just one or two pills a day, down from 12 before the surgery. A before and after video of Crawford walking the halls outside van Horne’s office is astonishing.

To date, 34 patients have participated in the DBS Plus study with encouraging results. Of the 17 patients that are 12 months out from their procedure, 65 percent of them have shown a clinically important improvement in motor performance as a result of the graft.



Van Horne is quick to point out that the study needs to be tested on a larger sample size at many other medical centers around the country before it can be deemed a viable treatment. Furthermore, he cautions, while 12-month results are promising, it’s important to evaluate effectiveness over a longer term. But assuming all goes as well as it has so far, DBS Plus shows promise as a means of slowing down the disease process.

Van Horne and his team garner no financial benefit from DBS Plus, which adds just a fraction of cost to the DBS surgery that is already covered by most insurance plans. “Our payback is the gratification we receive in seeing our patients do well,” van Horne said.

Crawford understands that DBS Plus isn’t a cure for his Parkinson’s, but is delighted to have a little more time to enjoy life.

“‘Feeling the beat’ is critical to my work as a musician, and my Parkinson’s had begun to take that away from me,” he said. “I couldn’t even snap my fingers with the music anymore.”
But, said Crawford, as he woke up from the surgery, he instinctively began to tap his fingers like a metronome. Two members of the team, Julie Gurwell, the PA responsible for programming the DBS equipment, and Ann Hanley, a Parkinson’s patient who personally accompanies patients through their surgeries, were sitting with him, and they asked him what he was doing.

“I was too emotional to explain but I managed to say ‘I can feel the beat.’ And they high-fived each other.”
Source: Laura Dawahare – University of Kentucky
NEUROSCIENCE NEWSJANUARY 6, 2017

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Alzheimer: Rejuvenating the brain's disposal system

A characteristic feature of Alzheimer's disease is the presence of so called amyloid plaques in the patient's brain -- aggregates of misfolded proteins that clump together and damage nerve cells. Researchers have now discovered a strategy to help the brain remove amyloid plaques.

A characteristic feature of Alzheimer's disease is the presence of so called amyloid plaques in the patient's brain -- aggregates of misfolded proteins that clump together and damage nerve cells. Although the body has mechanisms to dispose these aggregates, it apparently cannot keep up with the load in the diseased brain. Researchers from the German Center for Neurodegenerative Diseases (DZNE), Munich and the Ludwig Maximillian’s University (LMU) Munich have now discovered a strategy to help the brain remove amyloid plaques. More precisely: they uncovered a factor that can activate microglial cells to engulf newly forming clumps in the brain. Microglia are the scavenger cells of the brain's immune system that function in keeping the brain tidy and free of any damaging material. The work is published today in The EMBO Journal.
Plaques form when protein pieces called beta-amyloid (BAY-tuh AM-uh-loyd) clump together. Beta-amyloid comes from a larger protein found in the fatty membrane surrounding nerve cells. Beta-amyloid is chemically "sticky" and gradually builds up into plaques.

The most damaging form of beta-amyloid may be groups of a few pieces rather than the plaques themselves. The small clumps may block cell-to-cell signaling at synapses. They may also activate immune system cells that trigger inflammation and devour disabled cells.



Previous research addressing the function of microglia in Alzheimer's disease was hampered by methodological constraints. Researchers often used microglial cells cultured in a dish, but only microglia from newborn mice survive outside the body. However, young microglia is not ideal to investigate an age-related illness, especially since it was known that microglia change in the course of the disease. All in all, the role of microglia in clearing the brain of amyloid plaques was still under debate.

The research team from Munich, headed by Christian Haass and Sabina Tahirovic, devised a new tissue culture system to address these issues. The scientists took aged brain tissue from mouse model of Alzheimer's disease and co-cultured it with tissue from younger brains. They observed that, within a few days of culturing, amyloid plaques were starting to clear away.
A detailed analysis of this process revealed that microglia from the aging tissue, were engulfing the plaques on site but they received some long-distance assistance from the younger tissue in the dish. In fact, young microglia is secreting factors that helped old microglia rejuvenate, resume cell division and take up their work: clear the brain from plaques. One of the factors that reactivated aged microglia is called "granulocyte-macrophage colony stimulating factor" or GM-CSF for short. The researchers found that GM-CSF alone could do the job.



GM-CSF has previously been reported to reduce plaques and improve cognition in a mouse model of Alzheimer's disease. However, it is not yet known if GM-CSF could potentially work as a new drug for Alzheimer's disease in humans. Caution is advised, because activating microglia may also have its downsides. Microglia secreted small proteins that induce inflammatory reactions and may harm neurons. The new model system of Tahirovic, Haass and their colleagues, however, can be explored further to search for additional factors that enhance the clearance of amyloid plaques.

Story Source:
Materials provided by EMBO
Journal Reference:
Daria A, Colombo A, Llovera G, Hampel H, Willem M, Liesz A, Haass C, Tahirovic S. Young microglia restore amyloid plaque clearance of aged microglia. The EMBO Journal, 2016

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Brain Circuit indispensable to the sleep-wake cycle has been identified

Stanford University School of Medicine scientists have identified a brain circuit that's indispensable to the sleep-wake cycle. This same circuit is also a key component of the reward system, an archipelago of interconnected brain clusters crucial to promoting behavior necessary for animals, including humans, to survive and reproduce.

It makes intuitive sense that the reward system, which motivates goal-directed behaviors such as fleeing from predators or looking for food, and our sleep-wake cycle would coordinate with one another at some point. You can't seek food in your sleep, unless you're an adept sleepwalker. Conversely, getting out of bed is a lot easier when you're excited about the day ahead of you.



But until this study, no precise anatomical location for this integration of the brain's reward and arousal systems has been pinpointed, said Luis De Lecea, PhD, professor of psychiatry and behavioral sciences.

The researchers' findings will be published online Sept. 5 in Nature Neuroscience. De Lecea is the senior author. The lead author is postdoctoral scholar Ada Eban-Rothschild, PhD.
"This has potential huge clinical relevance," De Lecea said. "Insomnia, a multibillion-dollar market for pharmaceutical companies, has traditionally been treated with drugs such as benzodiazepines that nonspecifically shut down the entire brain. Now we see the possibility of developing therapies that, by narrowly targeting this newly identified circuit could induce much higher-quality sleep."

Some 25 to 30 percent of American adults are affected by sleep disturbances of one type or another, according to the National Institutes of Health. In addition, disruption of the sleep-wake rhythm typifies many different neuropsychiatric disorders and is understood to exacerbate them.



One of the first questions a psychiatrist asks a patient, said De Lecea, is, "How's your sleep?"

Similarity across vertebrates
The reward system's circuitry is similar in all vertebrates, from fish, frogs and falcons to fishermen and fashion models. A chemical called dopamine plays a crucial role in firing up this circuitry.

Neuroscientists know that a particular brain structure, the ventral tegmental area, or VTA, is the origin of numerous dopamine-secreting nerve fibers that run in discrete tracts to many different parts of the brain. A plurality of these fibers go to the nucleus acumens, a forebrain structure particularly implicated in generating feelings of pleasure in anticipation of, or response to, obtaining a desired objective.

"Since many reward-circuit-activating drugs such as amphetamines that work by stimulating dopamine secretion also keep users awake, it's natural to ask if dopamine plays a key role in the sleep-wake cycle as well as in reward," Eban-Rothschild said. "But, in part due to existing technical limitations, earlier experimental literature has unearthed little evidence for the connection and, in fact, has suggested that this circuit probably wasn't so important."



For the new study, the investigators employed male laboratory mice bioengineered in several respects to enable the use of advanced technologies to remotely excite, suppress and monitor activity in the dopamine-secreting nerve cells from the mice's VTA. The researchers also measured the mice's overall brain activity and muscle tone to determine the mice's relative stages of asleep or arousal. They used video cameras to view the mice's behavior.

Observed in mice
Overall, activity in the dopamine-secreting nerve cells emanating from the VTA rose on waking and stayed elevated when mice were awake. Conversely, this activity ramped down when mice transitioned into sleep, remaining low while they slumbered. Activating this nerve-cell population was enough to rouse the animals from a sound sleep and keep them awake for long periods, even during a point in the mice's diurnal cycle when they'd ordinarily be bunking down. Control animals, whose VTA activity wasn't similarly jacked up, built little nests from pellets of materials placed in all the mice's cages and then promptly dropped off.



When instead the scientists suppressed activity in the same nerve-cell population during the typically active period of the mice's 24-hour cycle, the mice conked out, snoozing through the presence of surefire arousal triggers: delicious high-fat chow, a female or fear-inducing fox urine.

Mice in an unfamiliar cage ordinarily explore their new surroundings energetically. And indeed, VTA-suppressed mice stayed awake for the first 45 minutes of the hour they spent in a new cage. But Eban-Rothschild noticed something: They spent that waking time building nests.
"They were really careful about it," she noted. Once they were satisfied with what they'd built, they dozed off.

This wasn't just some stereotyped behavior guaranteed to emerge when VTA activity was inhibited, Eban-Rothschild added. "If we put the nest they'd already built in their usual cage into the novel cage, they climbed in and went right to sleep."



Control mice in the unfamiliar cage ran around, either ignoring the pellet of nesting materials placed inside or scattering those materials all over the cage.

Nest-making activities
Eban-Rothschild analyzed video footage of the animals' behavior in their novel environments, and correlated 1-second video segments with recorded brain activity during the corresponding time frame. She saw that actions directly connected to building nests were marked by reduced VTA activity, while actions that weren't were associated with higher levels of VTA activity.
"We knew stimulating the brain's dopamine-related circuitry would increase goal-directed behaviors such as food- and sex-seeking" said Eban-Rothschild. "But the new study shows that at least one complex behavior is induced not by stimulating, but by inhibiting, this very circuit. Interestingly, this behavior -- nest building -- is essential to a mouse's preparation for sleep."

Nobody had noticed that before, said De Lecea. "This is the first finding of a sleep-preparation starter site in the brain. It's likely we humans have one, too. If we're disrupting this preparation by, say, reading email or playing videogames, which not only give off light but charge up our emotions and get our VTA dopaminergic circuitry going, it's easy to see why we're likely to have trouble falling asleep."



Noting that this anticipatory phase is often at the root of many people's sleeping problems, De Lecea suggested that the newly identified circuit could be a target for pharmacological intervention to help people ease into sleep.

"We have plenty of drugs that counter dopamine," he said. "Perhaps giving a person the right dose, at just the right time, of a drug with just the right pharmacokinetic properties so its effect will wear off at the right time would work a lot better than bombarding the brain with benzodiazepines, such as Valium, that knock out the entire brain."

He said he also sees the possibility that drugs targeting the VTA's dopamine-secreting nerve cells could benefit those suffering from neurological conditions such as schizophrenia or bipolar disorder that are characterized by sleep-wake cycle disturbances.

"It could be that merely solving the sleep-wake part will clear up a lot of symptoms," De Lecea said.
Source: Stanford University Medical Center

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Hearing ‘Meaningful’ Sounds Decreases Performance on Cognitive Tasks

Open office plans are becoming increasingly common in the workplace — offering a way to optimize available space and encourage dialogue, interaction and collaboration among employees. However, a new study suggests that productive work-related conversations might actually decrease the performance of other employees within earshot — more so than other random, meaningless noises.

The results of the study, led by Takahiro Tamesue, an associate professor at Yamaguchi University in Japan, will be described during the 172nd Meeting of the Acoustical Society of America and the 5th Joint Meeting with Acoustical Society of Japan, being held Nov. 28-Dec. 2, 2016 in Honolulu, Hawaii.

In their work, the researchers investigated the impact of meaningless and meaningful noises on selective attention and cognitive performance in volunteers, as well as the degree of subjective “annoyingness” of those noises.

The experiments were based on the so-called “odd-ball” paradigm — a test used to examine selective attention and information processing ability.

“In the odd-ball paradigm, subjects detect and count rare target events embedded in a series of repetitive events. To complete the odd-ball task it is necessary to regulate attention to a stimulus,” Tamesue explained. Tamesue’s laboratory focuses on improving auditory environments by analyzing the physiological and psychological effects of noise.

In one trial, a visual odd-ball paradigm, subjects observed pictures flashing on a PC monitor as meaningless (for example, a pseudo voice-noise consisting of a pink noise with a spectrum closely resembling that of speech) and meaningful sounds (male and female speech) were played to both ears through headphones. The most frequent image — appearing 20 percent of the time — was 10 x 10 centimeter-square green image; the most infrequent was a red square. The subjects had to count the number of times the red image flashed on the screen over a 10-minute period. In a second trial, an auditory odd-ball paradigm, the subjects had to detect and count an infrequently played noise — a 2,000-Hertz tone — amid a series of 1,000-Hz tones. At the end of the trial, the subjects also rated their level of annoyance at each sound, on a seven-point scale.



During this and other experiments, the subjects’ brain waves were measured through electrodes placed on their scalp. In particular, the researchers looked at two parts of the electroencephalograph (EEG) waveforms generated during the trials. The first, the so-called N100 component of event-related potentials (ERPs, brain responses caused by particular sensations, thoughts or motions), peaks about 100 milliseconds after a stimulus is presented. The second, the P300 component of ERPs, peaks around 300 milliseconds after the presentation of a stimulus.

“The N100 is thought to represent the activation of neural assemblies involved in the analysis of incoming sensory information,” Tamesue said. “The P300 is thought to reflect the resolution of uncertainty or the perceptual decision that an expected signal has occurred. The peak amplitude and latency of this component is related to selective attention and working memory.”

In their work, the researchers investigated the impact of meaningless and meaningful noises on selective attention and cognitive performance in volunteers, as well as the degree of subjective “annoyingness” of those noises. NeuroscienceNews.com image is for illustrative purposes only.

The study revealed that more meaningful noises, such as music and conversation, had a stronger effect on levels of subjective annoyance than meaningless noises — and led to a greater decline in performance on cognitive tasks involving memory or arithmetic tests. In addition, when meaningful noise such as speech was presented to the subjects, their EEG measurements showed large reductions in the P100 and P300 components, indicating that selective attention to cognitive tasks was influenced by the degree of meaningfulness of the noise. The effect was most pronounced during the auditory odd-ball paradigm test.



The experiments suggest that when designing sound environments in spaces used for cognitive tasks — such as the workplace or schools — it is appropriate to consider not only the sound level, but also meaningfulness of the noise that is likely to be present, Tamesue said. “Surrounding conversations often disturb the business operations conducted in such open offices. Because it is difficult to soundproof an open office, a way to mask meaningful speech with some other sound would be of great benefit for achieving a comfortable sound environment,” he said.

Source: Acoustical Society of America
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: The study was presented at the 172nd Meeting of the Acoustical Society of America in Honolulu, Hawaii.

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The Phenomenon named ‘Sixth Sense’ has been Scientifically Explained

We’ve all had that feeling that somebody is watching us – even if we’re not looking directly at their eyes. Sometimes we even experience a feeling of being watched by someone completely outside our field of vision. But how can we explain this phenomenon without resorting to pseudoscientific explanations like extrasensory perception (or a “sixth sense”)?

The human fascination with eyes lies at the heart of the issue. Eyes are the window into the soul, goes the saying. And it’s no wonder we’re so interested in them – the human brain is highly tuned to lock onto the gaze of others. It’s been suggested that there’s a widespread neural network in the brain just dedicated to the processing of gaze. Scientists have already identified a specialized group of neurons in the macaque brain that fire specifically when a monkey is under the direct gaze of another.

We also appear to be wired for gaze perception. The mechanism that detects eyes and shifts our attention towards them may be innate – newborns just two to five days old prefer staring at faces with direct gaze, for example, (over averted gaze).

It’s not just our brains that are specialized to draw us to the gaze of others – our eyes are also exceptionally formed to catch attention and easily reveal the direction of gaze. Indeed, our eye structure is distinct from almost all other species. The area of our eye surrounding our pupil (the sclera) is very large and completely white. This makes it very easy to discern the direction of someone’s gaze. In many animals, by contrast, the pupil takes up a lot of the eye, or the sclera is darker. This is thought to be an adaptation to camouflage the eye in predators – cleverly hiding the direction of gaze from potential prey.



But why is gaze so important that it needs all this specialized processing? Basically, eyes provide us with insights into when something meaningful is happening. Shifts in attention from another person are able to, almost reflexively redirect our attention in line with their gaze. Our heightened attention to gaze is thought to have evolved to support cooperative interactions between humans, and is argued to form the foundation for many of our more complex social skills.

Disturbances of normal gaze processing are seen across a wide range of conditions. For example, people on the autistic spectrum spend less time in general fixating on the eyes of others. They also have more trouble extracting information from eyes, such as emotion or intentions, and are less able to tell when someone is looking directly at them. On the other extreme, highly socially anxious people tend to fixate on eyes more than those with low anxiety, even though they show increased physiological fear reactions when under the direct gaze of another.

You may not realize it, but eye gaze affects something so primitive as our psychological reactions to other people. It is a large cue in establishing social dominance. Also, here’s a tip: direct gaze makes people appear more trustworthy and attractive (you’re welcome). This also seems to apply to animals. One study suggested that dogs may have evolved to adaptively react to our gaze preferences. It found that dogs in a shelter that gaze at humans while furrowing their inner brows (momentarily making their eyes look larger) get adopted significantly faster than dogs that didn’t.



Gaze also helps unconsciously regulate turn-taking in our conversations – people more often than not look away while talking (as compared to when listening), and we typically exchange a mutual gaze with our partner to indicate a changeover between talking and listening. Try messing with this natural gaze flux – you will probably weird out your conversational partner.

The truth about gaze detection
Because the human eye gaze is optimized for easy detection, it is often easy for us to work out whether someone is looking at us. For example, if someone sitting right opposite you on the train is looking at you, you can register the direction of their gaze without looking directly at them. However, it turns out we can only reliably detect such gaze within our degree of our central fixation point.

However, we can use other cues to tell when someone is looking at us in our peripheral vision. Typically we also rely on the position or movement of their head (such as a turn towards you). We also rely on head or body cues when the potential watcher is in the dark or is wearing sunglasses. But, interestingly, you may not be right about being watched as often as you think. It turns out that in uncertain situations, people systematically overestimate the likelihood that the other person is looking at them. This may be an adaptation to prepare us for interactions that are about to occur, particularly if the interaction may be threatening.



But what about the feeling that someone outside your field of vision such as behind you is watching? Is it really possible to “sense” that? This has long been a source of scientific investigation (the first study on this was published in 1898) – probably because this idea is very popular. Some studies have found that up to 94% of people report that they have experienced the feeling of eyes upon them and turned around to find out they were indeed being watched.

Sadly for those who wish we were X-men, it appears much of the body of research supporting the “psychic staring effect” appears to be suffering from methodological issues, or unexplained experimenter effects. For example, when certain experimenters act as the watcher in these experiments, they seem to be more “successful” at getting people to detect their stares than other experimenters. It is almost certainly an unconscious bias, perhaps due to initial interactions with the experimenter.

Memory biases may also come into play. If you feel like you are being watched, and turn around to check – another person in your field of view might notice you looking around and shift their gaze to you. When your eyes meet, you assume this individual has been looking all along. Situations where this happens are more memorable than when you look around to find no one looking at you.

So remember – the next time you think someone you can’t see is watching you, it could be your mind playing tricks on you, no matter how real it feels.
Source: Harriet Dempsey-Jones, Postdoctoral Researcher in Clinical Neuroscience, University of Oxford

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Breakthrough in the production of dopamine neurons for Parkinson’s

New studies may help to explain the path from stem cells to dopamine neurons.

The Lund experiments use modern global gene expression studies to better understand the path from a stem cell to a dopamine neuron. NeuroscienceNews.com image is credited to university at Buffalo.

The first transplantation of stem cells in patients with Parkinson’s disease is almost within reach. However, it remains a challenge for researchers to control stem cells accurately in the lab in order to achieve successful and functional stem cell therapies for patients.

“Dopamine is an organic chemical of the catecholamine and phenethylamine families that plays several important roles in the brain and body. It is an amine synthesized by removing a carboxyl from a molecule of its precursor chemical L-DOPA, which is synthesized in the brain and kidneys. Dopamine is also synthesized in plants and most multicellular animals.”



“In our preclinical assessments of stem cell-derived dopamine neurons we noticed that the outcome in animal models varied dramatically, even though the cells were very similar at the time of transplantation. This has been frustrating and puzzling, and has significantly delayed the establishment of clinical cell production protocols,” says Malin Parmar who led the study conducted at Lund University as part of the EU network Neuro-Stem-cell-Repair.

The Lund experiments use modern global gene expression studies to better understand the path from a stem cell to a dopamine neuron. The data has been generated in close collaboration with a team of scientists at Karolinska Institute lead by Professor Thomas Perlmann, and is closely linked with a second study from the same cluster of scientists. The second study sheds new light on how dopamine neurons are formed during development, and what makes them different from other similar and neigh boring neurons.

This new insight has enabled a streamlined differentiation process resulting in pure populations of dopamine neurons of high quality.



“We have identified a specific set of markers that correlate with high dopaminergic yield and graft function after transplantation in animal models of Parkinson’s disease. Guided by this information, we have developed a better, and more accurate methods for producing dopamine cells for clinical use in a reproducible way,” says first author Agnete Kirkeby.

The new results, published in two back-to-back articles in the leading journal in the field, Cell Stem Cell, propel stem cell therapy for Parkinson’s disease towards clinical application. The first transplants are expected to be only a few years away.Source: Lund University.

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Deep Learning: A Giant Step for Robots

The prospect of robots that can learn for themselves — through artificial intelligence and adaptive learning — has fascinated scientists and movie-goers alike. Films like Short Circuit, Terminator, Millennial Man, Chappie and Ex Machina flirt with the idea of a machine intelligence beyond the restricted rules of a set program.

Robots today can be programmed to reliably carry out a straightforward task over and over, such as installing a part on an assembly line. But a robot that can respond appropriately to changing conditions without specific instructions for how to do so has remained an elusive goal.

A robot that could learn from experience would be far more versatile than one needing detailed, baked-in instructions for each new act. It could rely on what artificial intelligence researchers call deep learning and reinforcement learning.



Deep learning enables the robot to perceive its immediate environment, including the location and movement of its limbs. Reinforcement learning means improving at a task by trial and error. A robot with these two skills could refine its performance based on real-time feedback.

For the past 15 years, Berkeley robotics researcher Pieter Abbeel has been looking for ways to make robots learn. In 2010 he and his students programmed a robot they named BRETT (Berkeley Robot for the Elimination of Tedious Tasks) to pick up different sized towels, figure out their shape and neatly fold them.

The key instructions allowed the robot to visualize the towel’s limp shape when held by one gripper and its outline when held by two. It may not seem like much but the challenge was daunting for the robot. After as many as a hundred trials — holding a towel in different places each time — BRETT knew the towel’s size and shape and could start folding. A YouTube video of BRETT’s skills was viewed hundreds of thousands of times.

“The algorithms instructed the robot to perform in a very specific set of conditions, and although it succeeded, it took 20 minutes to fold each towel,” laughs Abbeel, associate professor of electrical engineering and computer science.




“We stepped back and asked ‘How can we make it easier to equip robots with the ability to perfect new skills so that we can apply the learning process to many different skills?’”

This year in a first for the field Abbeel gave a new version of BRETT the ability to improve its performance through both deep learning and reinforcement learning. The deep learning component employs so-called neural networks to provide moment-to-moment visual and sensory feedback to the software that controls the robot’s movements.

With these programmed skills, BRETT learned to screw a cap onto a bottle, to place a clothes hanger on a rack and to pull out a nail with the claw end of a hammer.

Its onboard camera allowed BRETT to pinpoint the nail to be extracted, as well as the position of its own arms and hands. Through trial and error, it learned to adjust the vertical and horizontal position of the hammer claw as well as maneuver the angle to the right position to pull out the nail.

The deep reinforcement learning strategy opens the way for training robots to carry out increasingly complex tasks. The achievement gained widespread attention, including an article in The New York Times.



BRETT learned to complete his chores in 30 to 40 trials, with each attempt taking only a few seconds. Still, he has more trial and error ahead: Learning to screw a cap on a bottle doesn’t prepare him to screw a lid on a jar. Instead, he re-starts learning as if he had never mastered caps and bottles. Abbeel has begun research aimed at enabling robots to do something humans take for granted, generalize from one task to another.

Starting this year, the Bakar Fellows Program will support Abbeel’s lab with $75,000 a year for five years to help him refine the deep-learning strategy and move the research towards commercial viability. In addition to financial support, the Bakar Fellows Program provides mentoring in such crucial areas as the intricacies of venture capital and strategies to secure intellectual property rights.

“The Bakar support will allow us to improve the robot’s deep-learning ability and to apply a learned skill to new tasks,” Abbeel says.

Applications for such a skilled robot might range from helping humans with tedious housekeeping chores all the way to assisting in highly detailed surgery. In fact, Abbeel says, “Robots might even be able to teach other robots.”
Source: NEUROSCIENCE NEWS

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New devices emulate Human Biological Synapses

A new type of nano device for computer microprocessors is being developed that can mimic the functioning of a biological synapse -- the place where a signal passes from one nerve cell to another in the body, report scientists.

Memristive devices are electrical resistance switches that can alter their resistance based on the history of applied voltage and current. These devices can store and process information and offer several key performance characteristics that exceed conventional integrated circuit technology.

Engineers at the University of Massachusetts Amherst are leading a research team that is developing a new type of nanodevice for computer microprocessors that can mimic the functioning of a biological synapse -- the place where a signal passes from one nerve cell to another in the body. The work is featured in the advance online publication of Nature Materials.

Such neuromorphic computing in which microprocessors are configured more like human brains is one of the most promising transformative computing technologies currently under study.



J. Joshua Yang and Qiangfei Xia are professors in the electrical and computer engineering department in the UMass Amherst College of Engineering. Yang describes the research as part of collaborative work on a new type of memristive device.
Memristive devices are electrical resistance switches that can alter their resistance based on the history of applied voltage and current. These devices can store and process information and offer several key performance characteristics that exceed conventional integrated circuit technology.

"Memristors have become a leading candidate to enable neuromorphic computing by reproducing the functions in biological synapses and neurons in a neural network system, while providing advantages in energy and size," the researchers say.
Neuromorphic computing -- meaning microprocessors configured more like human brains than like traditional computer chips -- is one of the most promising transformative computing technologies currently under intensive study. Xia says, "This work opens a new avenue of neuromorphic computing hardware based on memristors.”

They say that most previous work in this field with ‘memristors’ has not implemented diffusive dynamics without using large standard technology found in integrated circuits commonly used in microprocessors, microcontrollers, static random access memory and other digital logic circuits.



The researchers say they proposed and demonstrated a bio-inspired solution to the diffusive dynamics that is fundamentally different from the standard technology for integrated circuits while sharing great similarities with synapses. They say, "Specifically, we developed a diffusive-type ‘memristor’ where diffusion of atoms offers a similar dynamics and the needed time-scales as its bio-counterpart, leading to a more faithful emulation of actual synapses, i.e., a true synaptic emulator."

The researchers say, "The results here provide an encouraging pathway toward synaptic emulations using diffusive ‘memristors’ for neuromorphic computing."
Source: UMass Amherst

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Breakthrough in Neuroscience: Stimulating Neurons Could Protect Against Brain Damage

Researchers have discovered a previously unknown mechanism that allows neural networks to protect against the spread of secondary brain damage as seen in TBI and ischemic stroke.

A breakthrough in understanding how brain damage spreads – and how it could potentially be limited – has been made through collaboration between neuroscientists and engineers at the Universities of Dundee and Strathclyde.

They have uncovered a previously unknown mechanism in the brain that allows networks of neurons to protect against the kind of spreading secondary damage seen in cases of strokes and traumatic brain injuries.

“If this network activity could be triggered clinically as soon as possible then major brain damage could be minimized and recovery periods shortened,” said Doctor Christopher Connolly, Reader in Neurobiology in the University of Dundee’s School of Medicine.



“Although this is basic laboratory research, it does now re-open the door to the possibility of stopping ongoing brain damage.

“Slow acting neuroprotection is well known but approaches to induce protection require at least 24 hours’ notice to be effective. This is of no practical use in a clinical emergency situation such as a stroke or traumatic brain injury, so current treatment options are limited to aiding the recovery processes.

“We have identified that neuronal networks react to an insult by sending rapid – in minutes – warning signals in an attempt to protect against the toxicity that causes brain damage. If that could be recruited clinically then it would give us a tool to deploy quickly in cases where brain damage was a risk.

“Where we can’t protect neurons quickly, we can recruit the help of surrounding neurons to do this for us. It is a case of `If you need a job done quickly, ask the expert’ and in this instance the experts are the neurons themselves.”



Laboratory-based modelling also showed that the rapid use of benzodiazepines (Valium) appeared to mimic the protection offered by the neuron networks.

“This is something we certainly need to test further but it does suggest the possibility of an effective and immediate pharmacological treatment for stroke,” said Doctor Connolly.

Image of the microfluidic device developed to determine activity-dependent spreading neurotoxic and neuroprotective signaling. Five parallel cell culture chambers recreate in vivo disease conditions. NeuroscienceNews.com image is adapted from the University of Strathclyde press release.

Doctor Connolly worked on the project with Doctor Michele Zagnoni, Senior Lecturer in Electronic and Electrical Engineering at the University of Strathclyde.

Doctor Zagnoni said, “Using microfluidic technology, we were able to produce in-vitro neuronal networks to investigate spreading toxicity in the brain, which is the cause of brain damage even after an initial trauma.

“Through this process we were able to demonstrate how the spread of this toxicity is driven. In doing that we also uncovered a previously unknown, fast acting, neuroprotective signaling mechanism.

“This mechanism utilizes the innate capacity of the surrounding neuronal networks (grown in the laboratory) to provide protection against the spreading toxicity. By stimulating that network, then theoretically we could limit the spread of brain damage. That requires further work, but it is an exciting and important possibility.”



The results of the research are published in the journal Scientific Reports.

The project examined the process known as acute secondary neuronal cell death, which is seen in neurodegenerative disease, cerebral ischemia (stroke) and traumatic brain injury (TBI) and drives spreading neurotoxicity into surrounding, undamaged, brain areas.

Source: University of Strathclyde.

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Legal Dope: Everyone's on opioids

By: Alexandria Addesso

The human race has long had a love affair with euphoria. Drugs and other substances have long been used to reached such a state. Currently prescription pills seem to be the drug of choice. Being that they are considered legal, to a degree, many people feel that they are safer than the average street drug, which has led everyone from soccer moms to teenagers picking up the pill popping habit.

Common prescription painkillers include morphine, codeine, oxycodone, hydrocodone, methadone, fentanyl, meperidine, hydrocodone, and acetaminophen. But what exactly do these prescription pills contain? Most prescription pills that are abused are painkiller drugs. These drugs are known as opioids. Heroin is also an opioid. According to drugabuse.gov, a recent study showed that nearly half of young heroin users surveyed reported that they started out using prescription pills.



So why are such dangerous drugs on the market and so easily accessible to anyone with a prescription? Because the market for them is insane! In the past 25 years the number of prescriptions written for opioids went from about 71 million to 206 million in the United States alone, which is a win for pharmaceutical companies.

Currently the United States consumes about 75 percent of all the prescription pills in the world despite only making up 5 percent of the globe’s population. Yet most users are not those receiving prescriptions. Prescription pills, has become a full blown black market with thousands of doctors being busted every year for over-prescribing these dangerous drugs. Those wholesaling such drugs can make as much as any other drug kingpins if not a lot, lot more. Business is good for those who sell these prescription drugs because the price is high. But once the user becomes so addicted and low on funds that they can no longer afford the pricy pills, heroin is a cheap alternative. As mentioned early heroin, like prescription painkillers, is an opioid and thus creates the same “high” just to different degrees.



Heroin has long been demonized by society, but these prescription pills have not. If we could shift the “safe” and “normalized” usage associated with painkillers to that of the connotation that comes with heroin, we could possibly change the culture.

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