Health and Medicine

neurosciencestuff: Where is My Mind? New Study Looks for the Cortical Conscious Network Our brain is a very complex network, with approximately 100 billion neurons and 100 trillion synapses between the neurons. In order to cope with its enormous complexity, and understand how the brain works and eventually forms our conscious mind, science uses advanced mathematical tools. Ultimately, scientists seek to understand how a global phenomenon such as consciousness can emerge from our neuronal network. A team of Bar-Ilan University physicists, led by Prof. Shlomo Havlin and Prof. Reuven Cohen, used network theory in order to cope with this complexity and to determine how the structure of the human cortical network can support complex data integration and conscious activity. The gray area of the human cortex, the neuron cell bodies, were scanned with MRI imaging and used to form 1,000 nodes in the cortical network. The white matter of the human cortex, the neuron bundles, were scanned with DTI imaging, forming 15,000 links or edges which connected the network’s nodes. In the end of this process, their network was an approximation of the structure of the human cortex. Their research, recently published in New Journal of Physics, attempts to decompose the structural layers of the cortical network to different hierarchies, enabling the identification of the network’s nucleus from which our consciousness could emerge. Previous studies have shown that the human cortex is a network with small world properties, which means that it has many local structures and some shortcuts from global structures which connect faraway areas (similar to the difference between local buses and cross-country trains). The cortex also has many hubs, which are nodes that have a high number of links (like central stations), that are also strongly interconnected between themselves, making it easy to travel between the brain’s information highways. According to Nir Lahav, the lead author of the study, “In order to examine how the structure of the network can support global emerging phenomena, like consciousness, we applied a network analysis called k-shell decomposition. This analysis takes into account the connectivity profile of each node making it easy to uncover different neighborhoods of connections in the cortical network, we called shells.” The most connected neighborhood in the network is termed the network’s nucleus. Lahav explains, “In the process we peel off different shells of the network to get the most connected area of the network, the nucleus. Until today scientists were only interested in the network’s nucleus, but we found that these different shells can hold important information about how the brain integrates information from the local levels of each node to the entire global network. For the first time we can build a comprehensive topological model of our cortex.” This topological model reveals that the network’s nucleus includes 20% of all nodes and that the remaining 80% are strongly connected across all the different shells. Interestingly, when comparing this topology to that of other networks, such as the internet, some noticeable differences can be seen. For instance, in internet network topology almost 25% of the nodes are isolated, meaning they don’t connect to any other shells but the nucleus. In the cortical network, however, there are hardly any isolated nodes. It seems that the cortex is much more connected and efficient than the internet. Looking at all the different shells of the cortical network, the authors were able to define the network’s hierarchical structure and essentially model how information flows within the network. The structure revealed how shells of low connectivity are nodes that typically perform specific functions like face recognition. From there the data are transferred to higher, more connected shells that enable additional data integration, and there regions of the executive network and working memory can be seen. With these areas we can focus on task performance, for example. The integrated information then ‘travels’ to the most connected neighborhood of nodes, the nucleus, which spans across several regions of the cortex. According to Lahav, “It’s an interconnected collective which is densely linked with itself and can perform global functions due to its great amount of global structures that are widespread across the brain.” Which global function might the nucleus serve? The authors suggest the answer is no less than consciousness itself. “The connection between brain activity and consciousness is still a great mystery,” says Lahav. The main hypothesis today is that in order to create conscious activity, the brain must integrate relevant information from different areas of the network. According to this theory, led by Prof. Giulio Tononi, from the University of Wisconsin, if the level of integrated information crosses a certain ‎limit, a new and emergent state is entered, consciousness. This model suggests that consciousness depends on both ‎information integration and information segregation. Loosely speaking, ‎consciousness is generated by a “central” network structure with high ‎capacity for information integration, with the contribution of sub-‎networks that contain specific and segregated information, ‎without being part of the central structure. In other words, certain parts of ‎the brain are more involved than others in what we can ‎call the conscious complex of the brain, yet other connected parts still ‎contribute, working quietly outside the conscious complex. The authors demonstrate how the nucleus and the different shells satisfy all of the requirements of these recent consciousness theories. The different shells calculate and contribute to data integration ‎without actually being part of the conscious complex, while the nucleus receives relevant ‎information from all other hierarchies and integrates it to a unified function using its ‎global interconnected structure. The nucleus could thus be this conscious complex, serving as a platform for consciousness to emerge from the network activity.‎‎ ‎ When the authors examined the different regions that make up the nucleus they revealed that, indeed, these regions have been previously associated with conscious activities. For example, structures within the brain’s midline, which form the majority of the network’s nucleus, were found to be associated with the stream of consciousness and some research, like that of Prof. Georg Northoff from the University of Ottawa, have suggested that these regions are involved with creating our sense of self. “Now we need to use this analysis on the whole brain and not only on the cortex in order to reveal a more exact model of the brain’s hierarchy, and later on to try to understand what exactly are the neuronal dynamics that lead to such global integration and, ultimately, consciousness,“ says Lahav. “Profound questions need a profound answer that can usually be found only in physics. Physics tries to uncover the basic laws of nature by constructing general mathematical equations that can describe as many natural phenomena as possible. These mathematical equations reveal fundamental aspects of reality. If we really want to understand what consciousness is and how the brain works, we have to develop the mathematical equations of our brain and our conscious mind. We are not there yet, in fact we are quite far away from this goal, but I feel that this should be our ‘holy grail’ and we have already begun the process of getting there,” he adds. Via

Salmonella seeks out oxygen-poor regions in the body (cancer tissue), combine that with a protein that causes a strong immune response and… The researchers found that their genetically modified salmonella made its way to several organs in the bodies of mice and also into tumors. The immune system then successfully eradicated the bacteria from the organs while simultaneously attacking the bacteria in the tumors and by extension the tumors themselves. This approach proved successful—11 out of 20 mice were tumor free after 12 days. (via) Via

via HealthandMedicine.orgVia

neurosciencestuff: Infants use prefrontal cortex in learning Researchers have long thought that the region of the brain involved in some of the highest forms of cognition and reasoning – the prefrontal cortex (PFC) – was too underdeveloped in young children, especially infants, to participate in complex cognitive tasks. A new study in the Journal of Neuroscience suggests otherwise. Given the task of learning simple hierarchical rules, babies appeared to employ much the same circuits as adults doing a similar task. The findings suggest that even at the age of 8 months, a baby’s PFC appears properly adapted to the kinds of tasks important to an infant of that age, said study senior author Dima Amso, associate professor of cognitive, linguistic and psychological sciences (CLPS) at Brown University. “The wow factor isn’t ‘Look the PFC works,’” Amso said. “It’s that what seems to be happening is that its function is a really good fit for what these babies need to be mastering at that moment in their development.” Of course babies aren’t yet equipped for writing essays or planning the day’s errands, Amso said, but their brains are properly adapted for learning essential elements in their world and how best to organize them. The PFC is not offline. Instead it’s appropriately mature for the goals of babyhood. An example from bilingualism To make this discovery, Amso, lead author Denise Werchan, fellow CLPS professor Michael Frank and then postdoctoral researcher Anne Collins, who is now assistant professor at the University of California at Berkeley, devised a task initially developed by Collins and Frank to test PFC function in adults. The infant version was made to parallel the circumstance of growing up in a bilingual family. Maybe Mom and her side of the family speak English, while Dad and his family speak Spanish. The babies must learn that different groups of people use different words for the same things. To scientists, this association of some people with one language and other people with another is an example of a “hierarchical rule set.” The person speaking is the higher-level context that determines what language will be used. Babies must learn that Mom and her brother will say “cat” when Dad and his sister will say “gato” to refer to the same family pet. The team wanted to determine how baby brains handle this task. They recruited 37 babies to learn a simple, abstracted version of the bilingual scenario while their brain activity and behavior were gently monitored. On screens before them, babies were shown a face and then an image of a toy. At the same time they’d hear a particular nonsense word in a voice associated with the face, as if the depicted person – call her “person 1” – was calling the depicted toy by that word. Then they’d see a different face with a different associated voice call the same toy by a new word (i.e. as if “person 2” was speaking a different language). Over several rounds, switching back and forth, the babies were exposed to these associations of person 1 with one vocabulary and person 2 with a distinct vocabulary. After that phase the babies were then introduced to person 3 on the screen who used the same words as person 1, but also introduced a few new ones (in the bilingual family metaphor, think of person 3 as Dad’s sister, if person 1 is Dad). If the babies were learning the rules, they’d associate person 3’s new words with person 1, because they were otherwise speaking the same rule set or “language.” In the blink of an eye The researchers tested whether the learning was occurring by next presenting the babies with persons 1 and 2 saying some of the new vocabulary of person 3. Babies who’d been learning should react differently to each instance. They should look longer at the unexpected case of person 2 using a word from the vocabulary of person 3. In fact, that’s what the babies did. On average they gazed a couple of seconds longer at that surprising situation of person 2 using an inconsistent language than they did at the expected case of person 1 speaking like person 3. Meanwhile, the researchers were tracking brain activity by means of a Near Infrared Spectroscopy (NIRS) machine provided, along with technical support, by TechEn, Inc. NIRS safely records brain activity over the scalp and is therefore becoming important to infant research, Amso said. Babies wear a special headband that holds near-infrared sensors over the scalp area of interest. The sensors detect how much infrared light is absorbed by hemoglobin in the blood and therefore report where brain activity is greatest (because that’s where the blood goes). The researchers also tracked the babies’ eye blinks because recent research has found that eye blinks reflect the degree of involvement of the neurotransmitter dopamine. When adults learn hierarchical rules, Frank and Collins have combined experimental data with computer models of brain function to suggest, that the key circuit involved is a connection between the PFC and another region called the striatum. That connection is mediated and reinforced by dopamine. The results of the infrared recording and the eye blink tracking both supported the hypothesis that as the babies were learning they were actively employing the PFC, similarly to adults. Both PFC activity – specifically in the right dorsolateral PFC – and eye blinks were significantly elevated when babies were asked to switch from one “language” to another, which is the most cognitively demanding moment for the PFC during the task. “Once you learn these hierarchical structures, each time you need to access or use one of them you need to update the structure into working memory,” Werchan said. “When the task switches you need to update information into PFC.” Moreover, the degree of the babies’ elevated PFC and eye blink activity predicted how distinctly they responded to the unexpected situation of a person speaking inconsistently with their language – a measure of how well the babies learned the rule structures. Developing a new view of development Amso said the findings suggest that early neurodevelopment should be viewed differently than before. Rather than regarding young brains as immature and less functional, a better perspective may be to regard them as constantly adapting to meet the key challenges they face. When healthy, they are as sophisticated as they need to be. “Atypical development, then, might reflect an inability to adapt to an environmental challenge, or an earlier adaptation because of a negative environment. Amso said. “We and others are probing with these ideas as relevant to PFC development.” Via

neurosciencestuff: American professional golfer Tom Kite said two things about distraction that sum up the findings of a new study on the subject: First, “You can always find a distraction if you’re looking for one.” And, second, “Discipline and concentration are a matter of being interested.” The new research offers evidence that one’s motivation is just as important for sustained attention to a task as is the ease with which the task is done. It also challenges the hypothesis, proposed by some cognitive neuroscientists, that people become more distractible as they tackle increasingly difficult tasks. A report of the new study appears in the Journal of Experimental Psychology: General. “People must almost continuously balance their need for inner focus (reflection, mental effort) with their need for attending to the world,” write the authors of the study, University of Illinois psychology professors Simona Buetti and Alejandro Lleras. “But, when the need for inner focus is high, we may have the impression that we momentarily disengage from the world entirely in order to achieve a heightened degree of mental focus.” Buetti and Lleras designed several experiments to test whether people are more easily distracted when the mental effort required to complete a task goes up, as is generally assumed in their field. The researchers first asked participants to solve math problems of varying difficulty while photographs of neutral scenes – for example, cows in a pasture, a portrait of a man, a cup on a table – flashed on a computer display for three seconds, enticing the subjects to look at them. An eye-tracking device measured the frequency, speed and focus of participants’ eyes as they completed the math problems. The results showed that participants who were engaged in an easy version of the task were more likely to look at the distractors than those engaged in an extremely challenging version. These results run counter to current theories, the researchers said. “This suggests that focus on complex mental tasks reduces a person’s sensitivity to events in the world that are not related to those tasks,” Buetti said. This finding corroborates research on a phenomenon called “inattentional blindness,” in which people involved in an engaging task often fail to notice strange and unexpected events. “Between the inner world of solving a problem and the outer world – what’s going on around you – there seems to be a need to disengage from one when heightened attention to the other is required,” Lleras said. “Interestingly, when participants completed a mix of easy and hard tasks, the difficulty of the task did not seem to affect their distractibility,” Buetti said. This finding led the researchers to hypothesize that the ability to avoid being distracted is not driven primarily by the difficulty of the task, but is likely the result of an individual’s level of engagement with the endeavor. They call this concept the “engagement theory of distractibility.” The team did further studies to test this idea, manipulating subjects’ enthusiasm for the task with financial incentives. To the researchers’ surprise, this manipulation had little effect on participants’ distractibility. However, there were large differences between people in terms of their distractibility. “The more participants struggled with a task, the more they reflexively avoided distraction, irrespective of financial incentive,” Buetti said. “So, the take-home message is: Characteristics of the task itself, like its difficulty, do not alone predict distractibility. Other factors also play a role, like the ease with which we can perform a task, as well as a decision that is internal to each of us: how much we decide to cognitively engage in a task.” Via

neurosciencestuff: Scientists find new path in brain to ease depression Northwestern Medicine scientists have discovered a new pathway in the brain that can be manipulated to alleviate depression. The pathway offers a promising new target for developing a drug that could be effective in individuals for whom other antidepressants have failed. New antidepressant options are important because a significant number of patients don’t adequately improve with currently available antidepressant drugs. The lifetime prevalence of major depressive disorder is between 10 to 20 percent of the population. The study was published Oct. 4 in the journal Molecular Psychiatry. “Identifying new pathways that can be targeted for drug design is an important step forward in improving the treatment of depressive disorders,” said Sarah Brooker, the first author and an M.D./Ph.D student at Northwestern University Feinberg School of Medicine. Brooker did the research in the lab of senior study author Dr. Jack Kessler, a professor of neurology at Feinberg and a Northwestern Medicine neurologist. The aim of the study was to better understand how current antidepressants work in the brain. The ultimate goal is to find new ones that are more effective for people not currently getting relief from existing drugs. In the study, scientists discovered for the first time that antidepressant drugs such as Prozac and tricyclics target a pathway in the hippocampus called the BMP signaling pathway. A signaling pathway is a group of molecules in a cell that work together to control one or more cell functions. Like a cascade, after the first molecule in a pathway receives a signal, it activates another molecule and so forth until the cell function is carried out. Brooker and colleagues showed that Prozac and tricyclics inhibit this pathway and, thereby, trigger stem cells in the brain to produce more neurons. These particular neurons are involved in mood and memory formation. But the scientists didn’t know if blocking the pathway contributed to the drugs’ antidepressant effect because Prozac acts on multiple mechanisms in the brain. After confirming the importance of the BMP pathway in depression, Northwestern scientists tested a brain protein, Noggin, on depressed mice. Noggin is known block the BMP pathway and stimulate new neurons, called neurogenesis. “We hypothesized it would have an antidepressant effect, but we weren’t sure,” Brooker said. They discovered Noggin blocks the pathway more precisely and effectively than Prozac or tricyclics. It had a robust antidepressant effect in mice. Scientists injected Noggin into the mice and observed the effect on mood by testing for depression and anxiety behavior. A sign of depression in mice is a tendency to hang hopelessly when held by the tail, rather than trying to get upright. After receiving Noggin, mice energetically tried to lift themselves up, whereas control mice were more likely to give up and become immobile. The mice were then put in a maze with secluded (safe) and open (less safe) spaces. The Noggin mice were less anxious and explored more mazes than the control mice. “The biochemical changes in the brain that lead to depression are not well understood, and many patients fail to respond to currently available drugs,” said Kessler, also the Ken and Ruth Davee Professor of Stem Cell Biology. “Our findings may not only help to understand the causes of depression, but also may provide a new biochemical target for developing more effective therapies.” Via

jewsee-medicalstudent: Mesentery is now classified as an organ. Researchers have classified a brand-new organ inside our bodies, one that’s been hiding in plain sight in our digestive system this whole time. Although we now know about the structure of this new organ, its function is still poorly understood, and studying it could be the key to better understanding and treatment of abdominal and digestive disease. Known as the mesentery, the new organ is found in our digestive systems, and was long thought to be made up of fragmented, separate structures. But recent research has shown that it’s actually one, continuous organ. The evidence for the organ’s reclassification is now published in The Lancet Gastroenterology & Hepatology. “In the paper, which has been peer reviewed and assessed, we are now saying we have an organ in the body which hasn’t been acknowledged as such to date,” said J Calvin Coffey, a researcher from the University Hospital Limerick in Ireland, who first discovered that the mesentery was an organ. So what is the mesentery? It’s a double fold of peritoneum - the lining of the abdominal cavity - that attaches our intestine to the wall of our abdomen, and keeps everything locked in place. One of the earliest descriptions of the mesentery was made by Leonardo da Vinci, and for centuries it was generally ignored as a type of insignificant attachment. Over the past century, doctors who studied the mesentery assumed it was a fragmented structure made of separate sections, which made it pretty unimportant. But in 2012, Coffey and his colleagues showed through detailed microscopic examinations that the mesentery is actually a continuous structure. And while that doesn’t change the structure that’s been inside our bodies all along, with the reclassification comes a whole new field of medical science that could improve our health outcomes. “When we approach it like every other organ… we can categorise abdominal disease in terms of this organ,” said Coffey. “Now we have established anatomy and the structure. The next step is the function. If you understand the function you can identify abnormal function, and then you have disease. Put them all together and you have the field of mesenteric science … the basis for a whole new area of science.” “This is relevant universally as it affects all of us.” (Source). Via

jewsee-medicalstudent: Mesentery is now classified as an organ. Researchers have classified a brand-new organ inside our bodies, one that’s been hiding in plain sight in our digestive system this whole time. Although we now know about the structure of this new organ, its function is still poorly understood, and studying it could be the key to better understanding and treatment of abdominal and digestive disease. Known as the mesentery, the new organ is found in our digestive systems, and was long thought to be made up of fragmented, separate structures. But recent research has shown that it’s actually one, continuous organ. The evidence for the organ’s reclassification is now published in The Lancet Gastroenterology & Hepatology. “In the paper, which has been peer reviewed and assessed, we are now saying we have an organ in the body which hasn’t been acknowledged as such to date,” said J Calvin Coffey, a researcher from the University Hospital Limerick in Ireland, who first discovered that the mesentery was an organ. So what is the mesentery? It’s a double fold of peritoneum - the lining of the abdominal cavity - that attaches our intestine to the wall of our abdomen, and keeps everything locked in place. One of the earliest descriptions of the mesentery was made by Leonardo da Vinci, and for centuries it was generally ignored as a type of insignificant attachment. Over the past century, doctors who studied the mesentery assumed it was a fragmented structure made of separate sections, which made it pretty unimportant. But in 2012, Coffey and his colleagues showed through detailed microscopic examinations that the mesentery is actually a continuous structure. And while that doesn’t change the structure that’s been inside our bodies all along, with the reclassification comes a whole new field of medical science that could improve our health outcomes. “When we approach it like every other organ… we can categorise abdominal disease in terms of this organ,” said Coffey. “Now we have established anatomy and the structure. The next step is the function. If you understand the function you can identify abnormal function, and then you have disease. Put them all together and you have the field of mesenteric science … the basis for a whole new area of science.” “This is relevant universally as it affects all of us.” (Source). View the full article

medresearch: Researchers Find Biological Explanation for Wheat Sensitivity A new study may explain why people who do not have celiac disease or wheat allergy nevertheless experience a variety of gastrointestinal and extra-intestinal symptoms after ingesting wheat and related cereals. The findings suggest that these individuals have a weakened intestinal barrier, which leads to a body-wide inflammatory immune response. “Our study shows that the symptoms reported by individuals with this condition are not imagined, as some people have suggested,” said study co-author Peter H. Green, MD, the Phyllis and Ivan Seidenberg Professor of Medicine at Columbia University Medical Center (CUMC) and director of the Celiac Disease Center. “It demonstrates that there is a biological basis for these symptoms in a significant number of these patients.” In the new study, the CUMC team examined 80 individuals with non-celiac gluten or wheat sensitivity (NCWS), 40 individuals with celiac disease, and 40 healthy controls. Despite the extensive intestinal damage associated with celiac disease, blood markers of innate systemic immune activation were not elevated in the celiac disease group. This suggests that the intestinal immune response in celiac patients is able to neutralize microbes or microbial components that may pass through the damaged intestinal barrier, thereby preventing a systemic inflammatory response against highly immunostimulatory molecules. The NCWS group was markedly different. They did not have the intestinal cytotoxic T cells seen in celiac patients, but they did have a marker of intestinal cellular damage that correlated with serologic markers of acute systemic immune activation. The results suggest that the identified systemic immune activation in NCWS is linked to increased translocation of microbial and dietary components from the gut into circulation, in part due to intestinal cell damage and weakening of the intestinal barrier. Read more Funding: This study was supported by grants from the National Center for Advancing Translational Sciences, National Institutes of Health (UL1 TR000040), and the Stanley Medical Research Institute. Raise your voice in support of expanding federal funding for life-saving medical research by joining the AAMC’s advocacy community. Via

medresearch: Researchers Find Biological Explanation for Wheat Sensitivity A new study may explain why people who do not have celiac disease or wheat allergy nevertheless experience a variety of gastrointestinal and extra-intestinal symptoms after ingesting wheat and related cereals. The findings suggest that these individuals have a weakened intestinal barrier, which leads to a body-wide inflammatory immune response. “Our study shows that the symptoms reported by individuals with this condition are not imagined, as some people have suggested,” said study co-author Peter H. Green, MD, the Phyllis and Ivan Seidenberg Professor of Medicine at Columbia University Medical Center (CUMC) and director of the Celiac Disease Center. “It demonstrates that there is a biological basis for these symptoms in a significant number of these patients.” In the new study, the CUMC team examined 80 individuals with non-celiac gluten or wheat sensitivity (NCWS), 40 individuals with celiac disease, and 40 healthy controls. Despite the extensive intestinal damage associated with celiac disease, blood markers of innate systemic immune activation were not elevated in the celiac disease group. This suggests that the intestinal immune response in celiac patients is able to neutralize microbes or microbial components that may pass through the damaged intestinal barrier, thereby preventing a systemic inflammatory response against highly immunostimulatory molecules. The NCWS group was markedly different. They did not have the intestinal cytotoxic T cells seen in celiac patients, but they did have a marker of intestinal cellular damage that correlated with serologic markers of acute systemic immune activation. The results suggest that the identified systemic immune activation in NCWS is linked to increased translocation of microbial and dietary components from the gut into circulation, in part due to intestinal cell damage and weakening of the intestinal barrier. Read more Funding: This study was supported by grants from the National Center for Advancing Translational Sciences, National Institutes of Health (UL1 TR000040), and the Stanley Medical Research Institute. Raise your voice in support of expanding federal funding for life-saving medical research by joining the AAMC’s advocacy community. View the full article

r3almonster: Our brain “includes several distinct dopamine systems, one of which plays a major role in reward-motivated behavior.”. This is quite fascinating that the availability of this information is present within our society, also revealing, the major record labels in the Music Industry are well aware of this. In an article published by The Nuero Organization at McGill University by Anita Kar, states “The team at The Neuro measured dopamine release in response to music that elicited “chills”, changes in skin conductance, heart rate, breathing, and temperature that were correlated with pleasurability ratings of the music. ‘Chills’ or ‘musical frisson’ is a well established marker of peak emotional responses to music.” If one was unaware, you probably aren’t now because these scientists have proven that music has a biological effect on our physical bodies. Kar also adds "PET and fMRI brain imaging techniques, revealed that dopamine release is greater for pleasurable versus neutral music, and that levels of release are correlated with the extent of emotional arousal and pleasurability ratings. Dopamine is known to play a pivotal role in establishing and maintaining behavior that is biologically necessary.” We are literally, becoming stimulated at a deeply internal level, from every song that’s brought us joy in our lives, resulting in the development emotional and behavioral patterns to embed into our psyche. This may come to no surprise to some of us who’ve re-lived a heart break when listening to a mid 2000’s r&b song. Also consider, us humans are developing, subconsciously, a rewarding/pleasurable sensation to certain songs which causes us to phase lock at least momentarily into a specific frequency. Dr. Robert Zatorre, neuroscientist at The Neuro. "These findings provide neurochemical evidence that intense emotional responses to music involve ancient reward circuitry in the brain,”….“To our knowledge, this is the first demonstration that an abstract reward such as music can lead to dopamine release.” It should be noted that music, has been a highly influential factor in every single culture regardless of geographic location. Our mental consent has been imprinted into the collective psyche as a human family for thousands of years. If this is the first abstract reward to lead to a dopamine release (in contemporary studies), other objects have the potential to do so as well. "The study also showed that two different brain circuits are involved in anticipation and experience, respectively: one linking to cognitive and motor systems, and hence prediction, the other to the limbic system, and hence the emotional part of the brain.” If this study proves anything beside what I’ve eluded to above, at bare minimum, music has a profound effect on our brain as well as the rest of our physical body(at least) . I implore you to further research the effects of music which is major influence within our lives daily! By Andrew Millan Via

r3almonster: Our brain “includes several distinct dopamine systems, one of which plays a major role in reward-motivated behavior.”. This is quite fascinating that the availability of this information is present within our society, also revealing, the major record labels in the Music Industry are well aware of this. In an article published by The Nuero Organization at McGill University by Anita Kar, states “The team at The Neuro measured dopamine release in response to music that elicited “chills”, changes in skin conductance, heart rate, breathing, and temperature that were correlated with pleasurability ratings of the music. ‘Chills’ or ‘musical frisson’ is a well established marker of peak emotional responses to music.” If one was unaware, you probably aren’t now because these scientists have proven that music has a biological effect on our physical bodies. Kar also adds "PET and fMRI brain imaging techniques, revealed that dopamine release is greater for pleasurable versus neutral music, and that levels of release are correlated with the extent of emotional arousal and pleasurability ratings. Dopamine is known to play a pivotal role in establishing and maintaining behavior that is biologically necessary.” We are literally, becoming stimulated at a deeply internal level, from every song that’s brought us joy in our lives, resulting in the development emotional and behavioral patterns to embed into our psyche. This may come to no surprise to some of us who’ve re-lived a heart break when listening to a mid 2000’s r&b song. Also consider, us humans are developing, subconsciously, a rewarding/pleasurable sensation to certain songs which causes us to phase lock at least momentarily into a specific frequency. Dr. Robert Zatorre, neuroscientist at The Neuro. "These findings provide neurochemical evidence that intense emotional responses to music involve ancient reward circuitry in the brain,”….“To our knowledge, this is the first demonstration that an abstract reward such as music can lead to dopamine release.” It should be noted that music, has been a highly influential factor in every single culture regardless of geographic location. Our mental consent has been imprinted into the collective psyche as a human family for thousands of years. If this is the first abstract reward to lead to a dopamine release (in contemporary studies), other objects have the potential to do so as well. "The study also showed that two different brain circuits are involved in anticipation and experience, respectively: one linking to cognitive and motor systems, and hence prediction, the other to the limbic system, and hence the emotional part of the brain.” If this study proves anything beside what I’ve eluded to above, at bare minimum, music has a profound effect on our brain as well as the rest of our physical body(at least) . I implore you to further research the effects of music which is major influence within our lives daily! By Andrew Millan View the full article

currentsinbiology: Antibiotic restores cell communication in brain areas damaged by Alzheimer’s disease New research from the Djavad Mowafaghian Centre for Brain Health at UBC has found a way to partially restore brain cell communication around areas damaged by plaques associated with Alzheimer’s disease. The findings, published this week in Nature Communications, demonstrate a possible target and a potential drug treatment to reduce damage to the brain that occurs in the early stages of Alzheimer’s disease. Using Ceftriaxone, an FDA-approved antibiotic used to treat bacterial infections, researchers were able to reduce synaptic disruption and clear the lines of neuronal communication in mice. Amyloid plaques of -amyloid deposits develop in brain regions of patients with Alzheimer’s disease, These plaques are linked to the damage found in Alzheimer’s disease because they prevent cell communication and are toxic to nerve cells. The researchers found that the brain areas around these plaques show high levels of glutamate, a signaling molecule essential to communication between brain cells, accompanying high levels of hyperactivity in glia, the brain’s support cells. It’s in this glutamate-rich environment that communication between neurons is changed or disrupted, causing neurons to die in the later stages of the disease. “By imaging the glial cells and glutamate itself around the plaques, we were able to see that the cells were not able to ‘remove’ the glutamate accumulating in these brain areas. By using Ceftriaxone, we were able to up-regulate glutamate transport,” explains Dr. MacVicar, principal investigator and professor of psychiatry. “By restoring glutamate levels, we were able to mostly restore neuronal activity.” The team’s findings have implications for treatment of early symptoms of Alzheimer’s disease. J. K. Hefendehl et al, Mapping synaptic glutamate transporter dysfunction in vivo to regions surrounding Aβ plaques by iGluSnFR two-photon imaging, Nature Communications (2016). DOI: 10.1038/ncomms13441 Via

currentsinbiology: Antibiotic restores cell communication in brain areas damaged by Alzheimer’s disease New research from the Djavad Mowafaghian Centre for Brain Health at UBC has found a way to partially restore brain cell communication around areas damaged by plaques associated with Alzheimer’s disease. The findings, published this week in Nature Communications, demonstrate a possible target and a potential drug treatment to reduce damage to the brain that occurs in the early stages of Alzheimer’s disease. Using Ceftriaxone, an FDA-approved antibiotic used to treat bacterial infections, researchers were able to reduce synaptic disruption and clear the lines of neuronal communication in mice. Amyloid plaques of -amyloid deposits develop in brain regions of patients with Alzheimer’s disease, These plaques are linked to the damage found in Alzheimer’s disease because they prevent cell communication and are toxic to nerve cells. The researchers found that the brain areas around these plaques show high levels of glutamate, a signaling molecule essential to communication between brain cells, accompanying high levels of hyperactivity in glia, the brain’s support cells. It’s in this glutamate-rich environment that communication between neurons is changed or disrupted, causing neurons to die in the later stages of the disease. “By imaging the glial cells and glutamate itself around the plaques, we were able to see that the cells were not able to ‘remove’ the glutamate accumulating in these brain areas. By using Ceftriaxone, we were able to up-regulate glutamate transport,” explains Dr. MacVicar, principal investigator and professor of psychiatry. “By restoring glutamate levels, we were able to mostly restore neuronal activity.” The team’s findings have implications for treatment of early symptoms of Alzheimer’s disease. J. K. Hefendehl et al, Mapping synaptic glutamate transporter dysfunction in vivo to regions surrounding Aβ plaques by iGluSnFR two-photon imaging, Nature Communications (2016). DOI: 10.1038/ncomms13441 View the full article

medresearch: Study: Nanoparticles Could Help Overcome Treatment-Resistant Breast Cancer Researchers at the University of Cincinnati (UC) College of Medicine have been able to generate multifunctional RNA nanoparticles that could overcome treatment resistance in breast cancer, potentially making existing treatments more effective in these patients. The study, published in the Dec. 14, 2016, online edition of American Chemical Society’s ACS Nano and led by Xiaoting Zhang, PhD, associate professor in the Department of Cancer Biology at the UC College of Medicine, shows that using a nanodelivery system to target HER2-positive breast cancer and stop production of the protein MED1 could slow tumor growth, stop cancer from spreading and sensitize the cancer cells to treatment with tamoxifen, a known therapy for estrogen-driven cancer. MED1 is a protein often produced at abnormally high levels in breast cancer cells that when eliminated is found to stop cancer cell growth. HER2-positive breast cancer involves amplification of a gene encoding, or programming, the protein known as human epidermal growth factor receptor 2, which also promotes the growth of cancer cells. MED1 co-produces (co-expresses) and co-amplifies with HER2 in most cases, and Zhang’s previous studies have shown their interaction plays key roles in anti-estrogen treatment resistance. “These findings are highly promising for potential clinical treatment of advanced metastatic and tamoxifen-resistant human breast cancer. Further studies are still needed and hopefully soon we’ll be able to test our nanoparticles in clinical trials at the UC Cancer Institute’s Comprehensive Breast Cancer Center.” Read more Funding: This study was supported by the UC Cancer Institute Drake Pilot Award, Ride Cincinnati, a Cincinnati Cancer Center Pilot Grant, the Susan G. Komen Career Catalyst Research Grant (KG110028), the National Institutes of Health (R01CA197865, R01 EB019036) and the U.S. Department of Defense Idea Award (W81XWH-15-1-0052). Raise your voice in support of expanding federal funding for life-saving medical research by joining the AAMC’s advocacy community. Via

medresearch: Study: Nanoparticles Could Help Overcome Treatment-Resistant Breast Cancer Researchers at the University of Cincinnati (UC) College of Medicine have been able to generate multifunctional RNA nanoparticles that could overcome treatment resistance in breast cancer, potentially making existing treatments more effective in these patients. The study, published in the Dec. 14, 2016, online edition of American Chemical Society’s ACS Nano and led by Xiaoting Zhang, PhD, associate professor in the Department of Cancer Biology at the UC College of Medicine, shows that using a nanodelivery system to target HER2-positive breast cancer and stop production of the protein MED1 could slow tumor growth, stop cancer from spreading and sensitize the cancer cells to treatment with tamoxifen, a known therapy for estrogen-driven cancer. MED1 is a protein often produced at abnormally high levels in breast cancer cells that when eliminated is found to stop cancer cell growth. HER2-positive breast cancer involves amplification of a gene encoding, or programming, the protein known as human epidermal growth factor receptor 2, which also promotes the growth of cancer cells. MED1 co-produces (co-expresses) and co-amplifies with HER2 in most cases, and Zhang’s previous studies have shown their interaction plays key roles in anti-estrogen treatment resistance. “These findings are highly promising for potential clinical treatment of advanced metastatic and tamoxifen-resistant human breast cancer. Further studies are still needed and hopefully soon we’ll be able to test our nanoparticles in clinical trials at the UC Cancer Institute’s Comprehensive Breast Cancer Center.” Read more Funding: This study was supported by the UC Cancer Institute Drake Pilot Award, Ride Cincinnati, a Cincinnati Cancer Center Pilot Grant, the Susan G. Komen Career Catalyst Research Grant (KG110028), the National Institutes of Health (R01CA197865, R01 EB019036) and the U.S. Department of Defense Idea Award (W81XWH-15-1-0052). Raise your voice in support of expanding federal funding for life-saving medical research by joining the AAMC’s advocacy community. View the full article

neurosciencestuff: (Image caption: A visualization of the brain, reconstructed from MRI scans, shows tracts of white matter connecting different regions of the brain to one another. A new study that uses computational modeling to investigate brain stimulation finds that stimulating network hubs - areas of the brain that are strongly connected to other parts via white matter - results in the global activation of many brain regions. Credit: Jean Vettel, Army Research Laboratory/PLOS Computational Biology) New study describes what happens when the brain is artificially stimulated Stimulating the brain via electricity or other means may help to ease the symptoms of various neurological and psychiatric disorders, with the method already being used to treat conditions from epilepsy to depression. But what really happens when doctors zap the brain? Little is known about what makes this technique effective, or which areas of the brain should be targeted to treat different diseases. A new study led by the University of Pennsylvania and the University at Buffalo marks a step forward in filling these gaps in knowledge. The research describes how the stimulation of a single region of the brain affects the activation of other regions and large-scale activity within the brain. “We don’t have a good understanding of the effects of brain stimulation,” said first author Sarah Muldoon, PhD, assistant professor of mathematics in the University at Buffalo College of Arts and Sciences and a core faculty member in UB’s Computational and Data-Enabled Science and Engineering (CDSE) Program. “When a clinician has a patient with a certain disorder, how can they decide which parts of the brain to stimulate? Our study is a step toward better understanding how brain connectivity can better inform these decisions.” “If you look at the architecture of the brain, it appears to be a network of interconnected regions that interact with each other in complicated ways. The question we asked in this study was how much of the brain is activated by stimulating a single region. We found that some regions have the ability to steer the brain into a variety of states very easily when stimulated, while other regions have less of an effect,” said Danielle S. Bassett, PhD, Eduardo D. Glandt Faculty Fellow and associate professor of bioengineering in the University of Pennsylvania School of Engineering and Applied Science. The research was performed in collaboration with cognitive neuroscientist Jean M. Vettel, PhD, of the Army Research Laboratory; control theorist Fabio Pasqualetti of the University of California, Riverside; Scott T. Grafton, MD, and Matthew Cieslak of the University of California, Santa Barbara; and Shi Gu of the University of Pennsylvania Department of Psychiatry. The study was published Sept. 9 in PLOS Computational Biology. The study used a computational model to simulate brain activity in eight individuals whose brain architecture was mapped using data derived from diffusion spectrum imaging, a type of brain image taken by an MRI scanner. The research examined the impact of stimulating each of 83 regions within each subject’s brain. While results varied by person, common trends emerged. Network hubs — areas of the brain that are strongly connected to other parts of the brain via the brain’s white matter — displayed what researchers call a “high functional effect”: Stimulating these regions resulted in the global activation of many brain regions. This effect was particularly notable in two sub-networks of the brain that are known to contain multiple regional hubs: the subcortical network (which is composed of regions that evolved relatively early on and are critical for emotion processing) and the default mode network (which is composed of regions that evolved later and are critical for self-referential processing when a person is at rest, or not completing any task). Stimulating regions in the subcortical network culminated in global changes, in which a diversity of areas within a subject’s brain lit up. Stimulating regions in the default mode network also led easily to a plethora of new brain states, though the patterns of activation were constrained by the brain’s underlying architecture — by the white matter links between the nodes of the network and other parts of the brain. Despite this limitation, the network’s agility supports the idea that the brain at “rest” is well suited for shifting quickly into an array of new states geared toward completing specific tasks. In contrast to regions within the default mode network and subcortical networks, more weakly connected areas, such as in the sensory and association cortex, had a more limited effect on brain activity when activated. These patterns suggest that doctors could pursue two classes of therapies when it comes to brain stimulation: a “broad reset” that alters global brain dynamics, or a more targeted approach that focuses on the dynamics of just a few regions. The study confirms the findings of past research by Bassett and others on the controllability of the brain’s structural networks. In contrast to past work that used linear modeling to arrive at results, the new study employed nonlinear models that more accurately reflect the brain’s complex activity, Muldoon said. Via

neurosciencestuff: (Image caption: A visualization of the brain, reconstructed from MRI scans, shows tracts of white matter connecting different regions of the brain to one another. A new study that uses computational modeling to investigate brain stimulation finds that stimulating network hubs - areas of the brain that are strongly connected to other parts via white matter - results in the global activation of many brain regions. Credit: Jean Vettel, Army Research Laboratory/PLOS Computational Biology) New study describes what happens when the brain is artificially stimulated Stimulating the brain via electricity or other means may help to ease the symptoms of various neurological and psychiatric disorders, with the method already being used to treat conditions from epilepsy to depression. But what really happens when doctors zap the brain? Little is known about what makes this technique effective, or which areas of the brain should be targeted to treat different diseases. A new study led by the University of Pennsylvania and the University at Buffalo marks a step forward in filling these gaps in knowledge. The research describes how the stimulation of a single region of the brain affects the activation of other regions and large-scale activity within the brain. “We don’t have a good understanding of the effects of brain stimulation,” said first author Sarah Muldoon, PhD, assistant professor of mathematics in the University at Buffalo College of Arts and Sciences and a core faculty member in UB’s Computational and Data-Enabled Science and Engineering (CDSE) Program. “When a clinician has a patient with a certain disorder, how can they decide which parts of the brain to stimulate? Our study is a step toward better understanding how brain connectivity can better inform these decisions.” “If you look at the architecture of the brain, it appears to be a network of interconnected regions that interact with each other in complicated ways. The question we asked in this study was how much of the brain is activated by stimulating a single region. We found that some regions have the ability to steer the brain into a variety of states very easily when stimulated, while other regions have less of an effect,” said Danielle S. Bassett, PhD, Eduardo D. Glandt Faculty Fellow and associate professor of bioengineering in the University of Pennsylvania School of Engineering and Applied Science. The research was performed in collaboration with cognitive neuroscientist Jean M. Vettel, PhD, of the Army Research Laboratory; control theorist Fabio Pasqualetti of the University of California, Riverside; Scott T. Grafton, MD, and Matthew Cieslak of the University of California, Santa Barbara; and Shi Gu of the University of Pennsylvania Department of Psychiatry. The study was published Sept. 9 in PLOS Computational Biology. The study used a computational model to simulate brain activity in eight individuals whose brain architecture was mapped using data derived from diffusion spectrum imaging, a type of brain image taken by an MRI scanner. The research examined the impact of stimulating each of 83 regions within each subject’s brain. While results varied by person, common trends emerged. Network hubs — areas of the brain that are strongly connected to other parts of the brain via the brain’s white matter — displayed what researchers call a “high functional effect”: Stimulating these regions resulted in the global activation of many brain regions. This effect was particularly notable in two sub-networks of the brain that are known to contain multiple regional hubs: the subcortical network (which is composed of regions that evolved relatively early on and are critical for emotion processing) and the default mode network (which is composed of regions that evolved later and are critical for self-referential processing when a person is at rest, or not completing any task). Stimulating regions in the subcortical network culminated in global changes, in which a diversity of areas within a subject’s brain lit up. Stimulating regions in the default mode network also led easily to a plethora of new brain states, though the patterns of activation were constrained by the brain’s underlying architecture — by the white matter links between the nodes of the network and other parts of the brain. Despite this limitation, the network’s agility supports the idea that the brain at “rest” is well suited for shifting quickly into an array of new states geared toward completing specific tasks. In contrast to regions within the default mode network and subcortical networks, more weakly connected areas, such as in the sensory and association cortex, had a more limited effect on brain activity when activated. These patterns suggest that doctors could pursue two classes of therapies when it comes to brain stimulation: a “broad reset” that alters global brain dynamics, or a more targeted approach that focuses on the dynamics of just a few regions. The study confirms the findings of past research by Bassett and others on the controllability of the brain’s structural networks. In contrast to past work that used linear modeling to arrive at results, the new study employed nonlinear models that more accurately reflect the brain’s complex activity, Muldoon said. View the full article

neurosciencestuff: A new scientific study reveals one way to stop proteins from triggering an energy failure inside nerve cells during Huntington’s disease. Huntington’s disease is an inherited genetic disorder caused by mutations in the gene that encodes huntingtin protein. Approximately 30,000 Americans have mutant huntingtin protein which can impair energy-producing parts of nerve cells called mitochondria. The mutant protein destroys nerve cells and slowly chips away at a person’s ability to walk, speak, and control their behavior. Xin Qi, PhD, assistant professor of physiology and biophysics at Case Western Reserve University School of Medicine has been looking for proteins that interact with mutant huntingtin to better understand the initial steps of Huntington’s disease progression. “Because mitochondrial dysfunction has been proposed to play an important role in the pathogenesis of Huntington’s disease,” said Qi, “we investigated the binding proteins of mutant huntingtin on mitochondria.” His recent study published in Nature Communications characterized one protein, valosin-containing protein (VCP) that Qi’s research team found in high abundance inside nerve cell mitochondria. Qi and colleagues discovered that VCP is recruited to nerve cell mitochondria by mutant huntingtin protein. The researchers showed that mice with mutant huntingtin had mitochondria full of VCP, as did nerve cells donated by people with Huntington’s disease. The VCP inside mitochondria only interacted with mutant, but not healthy huntingtin protein. According to Qi, “In Huntington’s disease, the VCP-mutant huntingtin binding is greatly increased. This abnormal binding causes more VCP accumulation on the mitochondria,” Nerve cells with VCP-mutant huntingtin interacting inside them became dysfunctional and self-destructed. “We found that VCP is a key player in mitochondria-associated autophagy, a mitochondria self-eating process. Over-accumulation of VCP on mitochondria thus results in a great loss of mitochondria, which leads to neuronal cell death due to lack of energy supply.” explained Qi. The researchers worked to identify ways to prevent VCP from heading to nerve cell mitochondria and interacting with mutant huntingtin protein once inside. The team identified the regions of VCP and mutant huntingtin that were interacting. They cleverly designed a small protein, or peptide, with the same regions to disrupt the VCP-mutant huntingtin protein interaction. In nerve cells exposed to their peptide, VCP and mutant huntingtin bound the peptide instead of each other. Nerve cells exposed to the novel peptide had healthier mitochondria than unexposed cells. In fact, the peptide prevented VCP from relocating to mitochondria at all, and prevented nerve cell death. Qi wanted to determine if the peptide had more than subcellular effects, and if it could be used therapeutically to prevent Huntington’s disease symptoms. The researchers administered the peptide to mice with Huntington’s-like disease and assessed mouse motor skills. Huntington’s-like mice exhibit spontaneous movement including excessive clasping, poor coordination, and decreased lifespan. Mice treated with the novel peptide did not experience these symptoms and appeared healthy. Qi concluded that the peptide reduced nerve cell impairment caused by Huntington’s disease in the animal model. The study successfully countered harmful effects of mutant huntingtin and protected nerve cells in several models of Huntington’s disease. According to Qi, the interfering peptide developed in the study “suggests a potential therapeutic option for treatment of Huntington’s disease, a disease with no treatment available.” The next step for the researchers will be to optimize the potentially therapeutic peptide for use in human studies. Via

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