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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Parallel Computation Provides Deeper Insight into Brain Function

Unlike experimental neuroscientists who deal with real-life neurons, computational neuroscientists use model simulations to investigate how the brain functions. While many computational neuroscientists use simplified mathematical models of neurons, researchers in the Computational Neuroscience Unit at the Okinawa Institute of Science and Technology Graduate University (OIST) develop software that models neurons to the detail of molecular interactions with the goal of eliciting new insights into neuronal function. Applications of the software were limited in scope up until now because of the intense computational power required for such detailed neuronal models, but recently Dr. Weiliang Chen, Dr. Iain Hepburn, and Professor Erik De Schutter published two related papers in which they outline the accuracy and scalability of their new high-speed computational software, "Parallel STEPS". The combined findings suggest that Parallel STEPS could be used to reveal new insights into how individual neurons function and communicate with each other.

The first paper, published in The Journal of Chemical Physics in August 2016, focusses on ensuring that the accuracy of Parallel STEPS is comparable with conventional methods. In conventional approaches, computations associate with neuronal chemical reactions and molecule diffusion are all calculated on one computational processing unit or 'core' sequentially. However, Dr. Iain Hepburn and colleagues introduced a new approach to perform computations of reaction and diffusion in parallel which can then be distributed over multiple computer cores, whilst maintaining simulation accuracy to a high degree. The key was to develop an original algorithm separated into two parts - one that computed chemical reaction events and the other diffusion events.

"We tested a range of model simulations from simple diffusion models to realistic biological models and found that we could achieve improved performance using a parallel approach with minimal loss of accuracy. This demonstrated the potential suitability of the method on a larger scale," says Dr. Hepburn.



In a related paper published in Frontiers in Neuroinformatics this February, Dr. Weiliang Chen presented the implementation details of Parallel STEPS and investigated its performance and potential applications. By breaking a partial model of a Purkinje cell - one of the largest neurons in the brain - into 50 to 1000 sections and simulating reaction and diffusion events for each section in parallel on the Sango supercomputer at OIST, Dr. Chen and colleagues saw dramatically increased computation speeds. They tested this approach on both simple models and more complicated models of calcium bursts in Purkinje cells and demonstrated that parallel simulation could speed up computations by more than several hundred times that of conventional methods.

"Together, our findings show that Parallel STEPS implementation achieves significant improvements in performance, and good scalability," says Dr. Chen. "Similar models that previously required months of simulation can now be completed within hours or minutes, meaning that we can develop and simulate more complex models, and learn more about the brain in a shorter amount of time."

Dr. Hepburn and Dr. Chen from OIST's Computational Neuroscience Unit, led by Professor Erik De Schutter, are actively collaborating with the Human Brain Project, a world-wide initiative based at École Polytechnique Fédérale de Lausanne (EPFL) in Switzerland, to develop a more robust version of Parallel STEPS that incorporates electric field simulation of cell membranes.

So far STEPS is only realistically capable of modeling parts of neurons but with the support of Parallel STEPS, the Computational Neuroscience Unit hopes to develop a full-scale model of a whole neuron and subsequently the interactions between neurons in a network. By collaborating with the EPFL team and by making use of the IBM 'Blue Gene/Q' supercomputer located there, they aim to achieve these goals in the near future.



"Thanks to modern supercomputers we can study molecular events within neurons in a much more transparent way than before," says Prof. De Schutter. "Our research opens up interesting avenues in computational neuroscience that links biochemistry with electrophysiology for the first time."
Source: Journal of Chemical Physics. Provided by: Okinawa Institute of Science and Technology

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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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The Incredible Benefits of Exercise

Many people hit the gym or pound the pavement to improve cardiovascular health, build muscle, and of course, get a rockin’ bod, but working out has above-the-neck benefits too. For the past decade or so, scientists have pondered how exercising can boost brain function. Regardless of age or fitness level (yup, this includes everyone from mall-walkers to marathoners), studies show that making time for exercise provides some serious mental benefits. Get inspired to exercise by reading up on these unexpected ways that working out can benefit mental health, relationships, and lead to a healthier and happier life overall.

1. Reduce stress. Rough day at the office? Take a walk or head to the gym for a quick workout. One of the most common mental benefits of exercise is stress relief. Working up a sweat can help manage physical and mental stress. Exercise also increases concentrations of norepinephrine, a chemical that can moderate the brain’s response to stress. So go ahead and get sweaty—working out can reduce stress and boost the body’s ability to deal with existing mental tension. Win-win!



2. Boost happy chemicals. Slogging through a few miles on the ‘mill can be tough, but it’s worth the effort! Exercise releases endorphins, which create feelings of happiness and euphoria. Studies have shown that exercise can even alleviate symptoms among the clinically depressed. For this reason, docs recommend that people suffering from depression or anxiety (or those who are just feeling blue) pencil in plenty of gym time. In some cases, exercise can be just as effective as antidepressant pills in treating depression. Don’t worry if you’re not exactly the gym rat type—getting a happy buzz from working out for just 30 minutes a few times a week can instantly boost overall mood.

3. Improve self-confidence. Hop on the treadmill to look (and more importantly, feel) like a million bucks. On a very basic level, physical fitness can boost self-esteem and improve positive self-image. Regardless of weight, size, gender, or age, exercise can quickly elevate a person’s perception of his or her attractiveness, that is, self-worth. How’s that for feeling the (self) love?



4. Enjoy the great outdoors. For an extra boost of self-love, take that workout outside. Exercising in the great outdoors can increase self-esteem even more. Find an outdoor workout that fits your style, whether it’s rock-climbing, hiking, renting a canoe, or just taking a jog in the park. Plus, all that Vitamin D acquired from soaking up the sun (while wearing sunscreen, of course!) can lessen the likelihood of experiencing depressive symptoms. Why book a spa day when a little fresh air and sunshine (and exercise) can work wonders for self-confidence and happiness?

5. Prevent cognitive decline. It’s unpleasant, but it’s true—as we get older, our brains get a little…hazy. As aging and degenerative diseases like Alzheimer’s kill off brain cells, the noggin actually shrinks, losing many important brain functions in the process. While exercise and a healthy diet can’t “cure” Alzheimer’s, they can help shore up the brain against cognitive decline that begins after age 45. Working out, especially between age 25 and 45, boosts the chemicals in the brain that support and prevent degeneration of the hippocampus, an important part of the brain for memory and learning.

6. Alleviate anxiety. Quick Q&A: Which is better at relieving anxiety—a warm bubble bath or a 20-minute jog? You might be surprised at the answer. The warm and fuzzy chemicals that are released during and after exercise can help people with anxiety disorders calm down. Hopping on the track or treadmill for some moderate-to-high intensity aerobic exercise (intervals, anyone?) can reduce anxiety sensitivity. And we thought intervals were just a good way to burn calories!

7. Boost brainpower. Those buff lab rats might be smarter than we think. Various studies on mice and men have shown that cardiovascular exercise can create new brain cells (aka neurogenesis) and improve overall brain performance. Ready to apply for a Nobel Prize? Studies suggest that a tough workout increases levels of a brain-derived protein (known as BDNF) in the body, believed to help with decision making, higher thinking, and learning. Smarty (spandex) pants, indeed.



8. Sharpen memory. Get ready to win big at Go Fish. Regular physical activity boosts memory and ability to learn new things. Getting sweaty increases production of cells in hippocampus responsible for memory and learning. For this reason, research has linked children’s brain development with level of physical fitness (take that, recess haters!). But exercise-based brainpower isn’t just for kids. Even if it’s not as fun as a game of Red Rover, working out can boost memory among grown-ups, too. A study showed that running sprints improved vocabulary retention among healthy adults.

9. Help control addiction. The brain releases dopamine, the “reward chemical” in response to any form of pleasure, be that exercise, sex, drugs, alcohol, or food. Unfortunately, some people become addicted to dopamine and dependent on the substances that produce it, like drugs or alcohol (and more rarely, food and sex). On the bright side, exercise can help in addiction recovery. Short exercise sessions can also effectively distract drug or alcohol addicts, making them de-prioritize cravings (at least in the short term). Working out when on the wagon has other benefits, too. Alcohol abuse disrupts many body processes, including circadian rhythms. As a result, alcoholics find they can’t fall asleep (or stay asleep) without drinking. Exercise can help reboot the body clock, helping people hit the hay at the right time.



10. Increase relaxation. Ever hit the hay after a long run or weight session at the gym? For some, a moderate workout can be the equivalent of a sleeping pill, even for people with insomnia. Moving around five to six hours before bedtime raises the body’s core temperature. When the body temp drops back to normal a few hours later, it signals the body that it’s time to sleep.

11. Get more done. Feeling uninspired in the cubicle? The solution might be just a short walk or jog away. Research shows that workers who take time for exercise on a regular basis are more productive and have more energy than their more sedentary peers. While busy schedules can make it tough to squeeze in a gym session in the middle of the day, some experts believe that midday is the ideal time for a workout due to the body’s circadian rhythms.

12. Tap into creativity. Most people end a tough workout with a hot shower, but maybe we should be breaking out the colored pencils instead. A heart-pumping gym session can boost creativity for up to two hours afterwards. Supercharge post-workout inspiration by exercising outdoors and interacting with nature (see benefit No. 4). Next time you need a burst of creative thinking, hit the trails for a long walk or run to refresh the body and the brain at the same time.

13. Inspire others. Whether it’s a pick-up game of soccer, a group class at the gym, or just a run with a friend, exercise rarely happens in a bubble. And that’s good news for all of us. Studies show that most people perform better on aerobic tests when paired up with a workout buddy. Pin it to inspiration or good old-fashioned competition, nobody wants to let the other person down. In fact, being part of a team is so powerful that it can actually raise athletes’ tolerances for pain. Even fitness beginners can inspire each other to push harder during a sweat session, so find a workout buddy and get moving!

Working out can have positive effects far beyond the gym (and beach season). Gaining self-confidence, getting out of a funk, and even thinking smarter are some of the motivations to take time for exercise on a regular basis.
Source: Sophia Breene for Greatist.com

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Understanding the Obsessive Compulsive Disorder: Conceptual Background and Brain Etiology

Patients suffering from obsessive–compulsive disorder (OCD) experience a combination of anxiety-producing obsessive thought patterns and related compulsive behaviors designed to reduce the distress associated with the obsessions.

Obsessions are recurrent thoughts, impulses, or images that are threatening because they are perceived as either unacceptable or leading to a dreaded outcome, and thus cause marked anxiety. Common obsessional ‘themes’ include contamination (thinking one has contacted dangerous germs or toxins), aggression (image or urge to drive into oncoming traffic or stab one’s spouse), accidental harm (fear that one has hit a pedestrian or doubting whether one turned off the stove), blasphemy (thinking one has offended God by doing a religious ritual incorrectly), and sexuality (intrusive images of having sex with a child or parent). Sometimes an obsession is vague, yet still evokes a looming sense of danger: a ‘bad feeling’ that occurs during an action, or the inexplicable sense that a behavior has not been done correctly. Multiple types of obsessions are found in most affected individuals and can change over time.



Compulsions include behaviors (e.g., hand washing, checking, ordering, or arranging things) and mental actions (e.g., praying, counting, repeating words silently) that are aimed at preventing or neutralizing the threat associated with the obsession, and thus temporarily reduce anxiety. This relief from the distress is highly reinforcing, resulting in the persistent use of compulsions. Compulsive behaviors are often repeated (checking the stove 15 times), or have to be performed according to rules that must be applied rigidly (a sterilization ritual for plates and silverware before meals).

Sometimes compulsions are ‘logically’ linked to the obsessions, as in the case of washing one’s hands in response to a contamination obsession, or driving back to a spot where one fears they may have hit someone. Done once, such behavior might seem reasonable; it is the repetitive, time-consuming, and rigid quality that distinguishes compulsions. Sometimes there is no ‘logical’ action to prevent the obsessional threat so, compulsions develop that are more akin to superstitious rituals. For example, going through doorways can often trigger an obsession (‘bad feeling’). Given no clear antidote to the vague threat, individuals may develop a ritualized compulsion aimed at neutralizing the obsession in some magical way. This might involve having to go through the door on the left side, touching both sides of the threshold 3 times, or passing through the doorway repeatedly until it is accomplished without any ‘bad thoughts.’



Individuals with OCD generally have some degree of insight that their symptoms are excessive or unreasonable. Nonetheless, the disorder is time-consuming, distressing, and severely impairing within the realms of both social and occupational functioning. It is also associated with increased risk of suicide. OCD has an estimated, lifetime prevalence in the general US population of 2–3%, and is equally common in both males and females. The age of onset follows a bimodal distribution: early onset (prepubescent, the majority of cases) and late onset (early 20s). Early-onset cases are more likely to be male, have a family history of OCD, greater symptom severity, and co-occurring tics, OCD spectrum (discussed in section Differential Diagnosis), and disruptive behavioral disorders (e.g., attention deficit hyperactivity disorder).

Differential Diagnosis
It is important to distinguish OCD from worry, intrusive thoughts, and compulsions seen in everyday life. OCD obsessions are experienced as unwanted and anxiety-producing, whereas worry functions more as a mental coping strategy that provides a sense of control and preparation for a perceived future threat. Intrusive thoughts (i.e., suddenly envisioning a family member falling off a cliff while hiking together) are common, but in OCD they occur at a higher frequency, and are experienced as having unusual importance, so are more distressing to the affected individual. Compulsive behaviors are also frequently seen in normal populations in the form of superstitious behavior and repetitive checking. The diagnosis of OCD is made only if they are time consuming or if they result in significant psychosocial impairment or distress.

There are a number of disorders that share the features of OCD, and are sometimes considered as ‘OCD spectrum disorders.’ Disorders such as body dysmorphic disorder, hypochondriasis, and hoarding and eating disorders include obsessive-like fears (that one has a serious illness or is fat), but the thoughts are not experienced themselves as highly intrusive and inappropriate. Derma-tillomania (skin picking) and trichotillomania (hair pulling) have repetitive behaviors that may bring some anxiety relief, but they are neither triggered by obsessions nor have the magical or ritualistic quality of OCD compulsions. Although impulse-control disorders such as kleptomania, pyromania, and pathological gambling also have recurrent thoughts and behaviors that are difficult to resist, the drive tends to be more pleasure-seeking than distress reducing.



Schizophrenia is often characterized by strongly held beliefs that are clearly false (delusions) as well as by stereotyped behaviors. Individuals with OCD, however, generally show considerable insight into their symptoms. In major depression, the depressed individual may have distressing, repetitive thoughts, but these are rarely resisted, and are often focused on a past incident rather than on a current or future threat. Although it has a similar name, obsessive–compulsive personality disorder is actually quite different from OCD. Obsessive–compulsive personality disorder does not involve obsessions or compulsions; rather, it is characterized by a pervasive pattern of maladaptive orderliness, perfectionism, and control.

Other disorders may mimic OCD. Tics and stereotyped movements are similar to compulsions in their appearance but not in their function. Generally, the cognitive elements involved in OCD compulsions are much more complex, whereas in tics and stereotypic movements, the individual does not report any specific reason for the behavior, but only a nonspecific tension that builds until the behavior is performed. Of note, Tourette’s syndrome and OCD are frequently co-occurring disorders, and individuals with Tourette’s should be routinely asked about the presence of obsessions and compulsions.



Etiology
There is converging evidence that OCD involves dysfunction of the corticostriatal-thalamic circuits, which help integrate cognitive and sensorimotor functions, and in particular initiate automatic, procedural behaviors. The high co-occurrence of OCD with Tourette’s – a disorder involving cortical and striatal pathways – is suggestive of a similar etiology. There are also data supporting an association between an autoimmune response to Group A β-hemolytic Streptococcus, affecting the striatal regions, and the acute emergence of OCD, often with tic symptoms (including Tourette’s). The term pediatric autoimmune neuropsychiatric disorder associated with Streptococcus refers to a group of children with this presumed immunological etiology. The role of serotonin in the corticostriatal-thalamic circuits is thought to be important, and several studies suggest that serotonin reuptake inhibitors may normalize activity in these pathways. Medications that boost serotonin activity reliably reduce OCD symptoms. Research also suggests that abnormalities in the glutamate and dopamine systems are involved in OCD as well.

The evidence for a genetic contribution is supported by the monozygotic twin studies showing a concordance rate from 63% to 87%, and first-degree relatives showing rates of OCD in the range of 10–22.5%. No candidate gene has been identified that can reliably account for the broad phenotype of OCD. Animal models of OCD, such as those found naturally in dogs or induced in laboratory mice identify the potential genes for further study.



From the standpoint of neuroimaging, OCD is one of the most investigated illnesses in the anxiety cluster. As of yet, it remains impossible to attribute causality to particular brain structures in the cognitions and clinical features of OCD. In animal models, abnormalities in the orbitofronto-striatal circuits are associated with an impaired ability to modify behavior in response to new information, for example: impaired inhibition of previously important, but now inappropriate response to stimuli. Humans with injuries to the striatum, or areas to which it projects, often develop obsessive –compulsive behaviors. Nevertheless, no consistent structural abnormality has been identified in patients meeting the criteria for OCD. This may suggest that the causative abnormalities are present at the level of a system or network, not at the level of isolated neuroanatomical structures, or because of a marked heterogeneity within the diagnosis. Illnesses with components of compulsive and impulsive behaviors, such as Tourette’s syndrome and trichotillomania, tend to occur in comorbidity with OCD, or cluster with OCD within families. Further research into these disorders of overlapping end phenotype may serve to illuminate the rest of the OCD picture as it relates to the brain structure.
Source: Vimen L. Beckner, University of California San Francisco, and San Francisco Group for Evidence-Based Psychotherapy, San Francisco, CA, USA.

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How humans bond: The Brain Chemistry Revealed

In a new study researches found for the first time that dopamine is involved in human bonding bringing the brain’s reward into understanding of how we form human attachments.

In new research published Monday in the journal Proceedings of the National Academy of Sciences, Northeastern University psychology professor Lisa Feldman Barrett found, for the first time, that the neurotransmitter dopamine is involved in human bonding, bringing the brain's reward system into our understanding of how we form human attachments. The results, based on a study with 19 mother-infant pairs, have important implications for therapies addressing postpartum depression as well as disorders of the dopamine system such as Parkinson's disease, addiction, and social dysfunction.



"The infant brain is very different from the mature adult brain -- it is not fully formed," says Barrett, University Distinguished Professor of Psychology and author of the forthcoming book How Emotions Are Made: The Secret Life of the Brain. "Infants are completely dependent on their caregivers. Whether they get enough to eat, the right kind of nutrients, whether they're kept warm or cool enough, whether they're hugged enough and get enough social attention, all these things are important to normal brain development. Our study shows clearly that a biological process in one person's brain, the mother's, is linked to behavior that gives the child the social input that will help wire his or her brain normally. That means parents' ability to keep their infants cared for leads to optimal brain development, which over the years results in better adult health and greater productivity."

To conduct the study, the researchers turned to a novel technology: a machine capable of performing two types of brain scans simultaneously -- functional magnetic resonance imaging, or fMRI, and positron emission tomography, or PET.

fMRI looks at the brain in slices, front to back, like a loaf of bread, and tracks blood flow to its various parts. It is especially useful in revealing which neurons are firing frequently as well as how different brain regions connect in networks. PET uses a small amount of radioactive chemical plus dye (called a tracer) injected into the bloodstream along with a camera and a computer to produce multidimensional images to show the distribution of a specific neurotransmitter, such as dopamine or opioids.



Barrett's team focused on the neurotransmitter dopamine, a chemical that acts in various brain systems to spark the motivation necessary to work for a reward. They tied the mothers' level of dopamine to her degree of synchrony with her infant as well as to the strength of the connection within a brain network called the medial amygdala network that, within the social realm, supports social affiliation.

"We found that social affiliation is a potent stimulator of dopamine," says Barrett. "This link implies that strong social relationships have the potential to improve your outcome if you have a disease, such as depression, where dopamine is compromised. We already know that people deal with illness better when they have a strong social network. What our study suggests is that caring for others, not just receiving caring, may have the ability to increase your dopamine levels."



Before performing the scans, the researchers videotaped the mothers at home interacting with their babies and applied measurements to the behaviors of both to ascertain their degree of synchrony. They also videotaped the infants playing on their own.

Once in the brain scanner, each mother viewed footage of her own baby at solitary play as well as an unfamiliar baby at play while the researchers measured dopamine levels, with PET, and tracked the strength of the medial amygdala network, with fMRI.

The mothers who were more synchronous with their own infants showed both an increased dopamine response when viewing their child at play and stronger connectivity within the medial amygdala network. "Animal studies have shown the role of dopamine in bonding but this was the first scientific evidence that it is involved in human bonding," says Barrett. "That suggests that other animal research in this area could be directly applied to humans as well."

The findings, says Barrett, are "cautionary." "They have the potential to reveal how the social environment impacts the developing brain," she says. "People's future health, mental and physical, is affected by the kind of care they receive when they are babies. If we want to invest wisely in the health of our country, we should concentrate on infants and children, eradicating the adverse conditions that interfere with brain development."
Source: Materials provided by Northeastern University, original written by Thea Singer.

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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 Internet and your brain are more alike than you think

Salk scientist finds similar rule governing traffic flow in engineered and biological systems. Credit: Salk Institute

A similar rule governs traffic flow in engineered and biological systems, reports a researcher. An algorithm used for the Internet is also at work in the human brain, says the report, an insight that improves our understanding of engineered and neural networks and potentially even learning disabilities.

Although we spend a lot of our time online nowadays -- streaming music and video, checking email and social media, or obsessively reading the news -- few of us know about the mathematical algorithms that manage how our content is delivered. But deciding how to route information fairly and efficiently through a distributed system with no central authority was a priority for the Internet's founders. Now, a Salk Institute discovery shows that an algorithm used for the Internet is also at work in the human brain, an insight that improves our understanding of engineered and neural networks and potentially even learning disabilities.



"The founders of the Internet spent a lot of time considering how to make information flow efficiently," says Salk Assistant Professor Saket Navlakha, coauthor of the new study that appears online in Neural Computation on February 9, 2017. "Finding that an engineered system and an evolved biological one arise at a similar solution to a problem is really interesting."
In the engineered system, the solution involves controlling information flow such that routes are neither clogged nor underutilized by checking how congested the Internet is. To accomplish this, the Internet employs an algorithm called "additive increase, multiplicative decrease" (AIMD) in which your computer sends a packet of data and then listens for an acknowledgement from the receiver: If the packet is promptly acknowledged, the network is not overloaded and your data can be transmitted through the network at a higher rate. With each successive successful packet, your computer knows it's safe to increase its speed by one unit, which is the additive increase part. But if an acknowledgement is delayed or lost your computer knows that there is congestion and slows down by a large amount, such as by half, which is the multiplicative decrease part. In this way, users gradually find their "sweet spot," and congestion is avoided because users take their foot off the gas, so to speak, as soon as they notice a slowdown. As computers throughout the network utilize this strategy, the whole system can continuously adjust to changing conditions, maximizing overall efficiency.

Navlakha, who develops algorithms to understand complex biological networks, wondered if the brain, with its billions of distributed neurons, was managing information similarly. So, he and coauthor Jonathan Suen, a postdoctoral scholar at Duke University, set out to mathematically model neural activity.



Because AIMD is one of a number of flow-control algorithms, the duo decided to model six others as well. In addition, they analyzed which model best matched physiological data on neural activity from 20 experimental studies. In their models, AIMD turned out to be the most efficient at keeping the flow of information moving smoothly, adjusting traffic rates whenever paths got too congested. More interestingly, AIMD also turned out to best explain what was happening to neurons experimentally.

It turns out the neuronal equivalent of additive increase is called long-term potentiation. It occurs when one neuron fires closely after another, which strengthens their synaptic connection and makes it slightly more likely the first will trigger the second in the future. The neuronal equivalent of multiplicative decrease occurs when the firing of two neurons is reversed (second before first), which weakens their connection, making the first much less likely to trigger the second in the future. This is called long-term depression. As synapses throughout the network weaken or strengthen according to this rule, the whole system adapts and learns.

"While the brain and the Internet clearly operate using very different mechanisms, both use simple local rules that give rise to global stability," says Suen. "I was initially surprised that biological neural networks utilized the same algorithms as their engineered counterparts, but, as we learned, the requirements for efficiency, robustness, and simplicity are common to both living organisms and the networks we have built."



Understanding how the system works under normal conditions, could help neuroscientists better understand what happens, when these results are disrupted, for example, in learning disabilities. "Variations of the AIMD algorithm are used in basically every large-scale distributed communication network," says Navlakha. "Discovering that the brain uses a similar algorithm may not be just a coincidence."
Story Source:
Materials provided by Salk Institute.

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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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The Neuropsychology of Religion (Part 2)

Neurological states associated with religious experiences strongly suggest that there are specific regions of the brain that produce them

A New Mind Journal Original
Jaime F. Adriazola
American Graduate University, Washington DC

Hamer and his colleagues used a measure (psychological test) of spiritual development and self-transcendence developed by Robert Cloninger, a psychiatrist at the University of Washington, School of Medicine in St. Louis. Cloninger's "Temperament and Character Inventory" added measures that correlated with the following three traits: self-forgetfulness, transpersonal identification, and mysticism. He administered his temperament test and character inventory on ordinary people, and then analyzed the results using statistical techniques that could find correlations in their responses. It was found that all three traits are highly correlated with each other, and were not as highly correlated with any other aspect of temperament and personality.

Hamer and his colleagues then began to determine whether self-transcendence is a hereditary trait. They did this by administering the ‘Cloninger Temperament and Character Inventory’ on pairs of identical twins and fraternal twins.

They found that identical twins were twice as likely to have very similar scores on the Inventory of Temperament and Characters rather than if they were fraternal twins. This result is consistent with the idea that the personality traits of the Temperament and Character Inventory measures are inherited genetically, since identical twins are twice as genetically related as fraternal twins.



Hamer and his colleagues then compared the results of self-transcendence with measures of environmental influence. They found that similarities and differences in the environment could only explain a small fraction of the differences in the Temperament and Character Inventory scores between identical twins versus fraternal twins.

Finally, Hamer and his colleagues began to determine whether the self-transcendence scores were related to specific genes. To make the long story short, Hamer and his colleagues found that specific mutations of a specific gene were highly correlated with differences in self-transcendence as determined by Cloninger's Temperament and Character Inventory.

The specific gene they found and that correlates with self-transcendence is called “VMAT2”, and is known to encode a protein that wraps and regulates levels of neurochemicals called mono amines that are in the brain. These mono amines regulate our moods and emotions; large amounts of them make us feel energized and euphoric, while an insufficiency of them could result in depression. Further analysis of the correlations between the different forms of the VMAT2 gene and measures of personality showed that differences in the VMAT2 gene were not correlated with other personality differences. Conversely, only self-transcendence correlated with changes in the VMAT2 gene.



Hamer also related the function of the VMAT2 gene to the same type of brain function investigated by Persinger, Ramachandran, Saber, Rabin, D'Aquili, and Newberg. Differences in temporal lobe and limbic system function correlate with differences in monoamine levels in those regions of the brain. Additionally, the differences in brain activity, measured by d'Aquili and Newberg, are also correlated with mono amines that are regulated by the protein encoded by the VMAT2 gene.

In other words, not only is the ability of religious experiences measured by specific regions of the brain and neurochemicals, but a specific gene is responsible for the regulation of those neurochemicals in those regions of the brain.

Again, the specific traits produced as expressions of specific genes are evolutionary adaptations. They exist and do what they do because in the past, individuals who had such traits survived and reproduced more often than those who did not.

It seems clear that the capacity for religious experience is an evolutionary adaptation. However, the capacity for language along with the capacity for religious experience does not cause us to learn a particular religion. Instead, it predisposes us to experience particular sensations in particular circumstances. When we perform a particular religious ritual or see (or hear, or smell, or taste, or touch) a particular religious symbol, and if it is performed or is perceived under the right conditions, we experience a strong surge of emotions which we interpret in the context of our cultural traditions learned.

This explains why religious rituals and symbols provoke powerful emotions in people educated in a tradition that venerates such rituals and symbols. On the other hand, these rituals and symbols virtually have no effect on people who are not educated in those traditions. This also explains why blasphemy is such a heinous sin against religious belief: it undermines the emotional meaning of the ritual or religious symbol, making it as insignificant as it would be for someone who was not educated to experience its effects. This is the difference between the sacred and the profane: sacred actions and their elements produce powerful emotions as profane things do not.



Latest discoveries:
Investigators of the New York State Psychiatric Institute and Columbia University found that the importance of religion or spirituality in individuals may also be related to the thickness of its vertices in the brain. They related the importance of religion or spirituality, but not the frequency of attendance at the 'house of worship', with thicker crusts in the left and right parietal and occipital regions, the right mesial frontal lobe of the right hemisphere, and the cuneus and pre-cuneus in the left hemisphere. The study was published this month in the journalJAMA Psychology. Significantly, this relationship between spiritual importance and cortex thickness was found to be stronger among those who suffered from severe depression. They mentioned that those who expressed a stronger spiritual inclination also showed thicker crusts over the left and right hemispheres. "A thicker cortex associated with a high importance of religion or spirituality can confer resilience to the development of depressive illness in individuals with high familial risk of major depression, possibly expanding a cortical reserve that counteracts to a certain extent the vulnerability, which the cortical thinning raises, to develop depressive family illness."

Significantly, the researchers stated that their findings are simply correlational; as the importance of religion does not necessarily cause greater thickness, or vice versa.



Psychology professor Brick Johnstone also said that, "Finding a neuropsychological basis for spirituality, but is not isolated to a specific area of the brain”. For the study published in the International Journal for the Psychology of Religion, Johnstone and his colleagues studied 20 people with traumatic brain injuries affecting the right parietal lobe, a brain area located a few inches above the right ear. The team interviewed the participants about their spiritual beliefs, wondering how close they felt to a Power, and if they considered their lives to be part of a divine plan.

They found that those participants with more significant lesions in their right parietal lobe expressed a feeling of greater closeness to a higher power. "Neuropsychology researchers have consistently shown that impairment in the right side of the brain diminishes one's focus on the self."



Professor Johnstone also measured the frequency of participants' religious practices, such as attending church or listening to religious programs. Johnstone compared these measures to activity rates in the frontal lobe and found a connection between increased activity in this part of the brain and increased participation in religious practices. "This finding indicates that spiritual experiences are likely to be associated with different parts of the brain." "Certain parts of the brain play more predominant roles, but they all work together to facilitate the spiritual experiences of individuals," Johnstone finally said.

References:
Allen D. MacNeill: Evolutionary Psychology.
D'Aquili: Because God? Brain Science and the Biology of Belief will not leave.
D'Aquili, Eugene G., and Andrew B. Newberg: Mystical Mind: Probing the Biology of
Religious Experience. Minneapolis, MN: Fortress Press.
Dawkins, Richard; The Desilution of God: New York: Mariner Books, 2007. Dennett.
Daniel C .; Breaking the Spell: Religion as a Natural Phenomenon, New York.
Penguin, Hamer, Dean H.: The Gene of God: How Faith is Wired in our Genes.
New York: Doubleday.
Harris, Sam: The End of Faith: Religion, Terror, and the Future of Reason, New York.
Ramachandran, Vilayanur S., and Sandra Blakeslee: Phantoms in the Brain: Probing the
Mysteries of the Human Mind. New York.
Miller L, Vansal R, Wickramaratne P, et al. Neuroanatomical correlates of religiosity and spirituality, one study in adults with high and low familial risk for depression. JAMA Psychiatry.
Johnstone B, Bodling A, Cohen D, et al: The "lack of interest" related to the right parietal lobeas the neuropsychological basis of spiritual transcendence.
International Journal of Psychology of Religion.

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The Neuropsychology of Religion (Part 1)

Neurological states associated with religious experiences strongly suggest that there are specific regions of the brain that produce them

A New Mind Journal Original
Jaime F. Adriazola
American Graduate University, Washington DC

It has been 145 years since Charles Darwin wrote his famous book "The Descent of Man" (1871), where he argued that humans do not have an innate instinct to believe in God. "Belief in God has often been not only the Great, but the most complete of all the distinctions between man and inferior animals. However, it is impossible. . . to hold that this belief is innate or instinctive in men."

This conclusion is based on the general observation that many human cultures do not include in their beliefs a deity that can be interpreted as being, in any way conceptually similar to the Judeo-Christian monotheistic God. However, Darwin went on to point out that ... "The belief in omnipresent spiritual entities seems to be universal; and it seems to have come from a considerable advance of man's reason, and from a greater advance in his faculties of imagination, curiosity, and questioning."



In other words, there seems to be no innate tendency to believe in the monotheistic God of the Judeo-Christian religion or to believe in some supernatural force or entity. Why could this be? Why is atheism not the universal result of the advancement of natural science?

The answer is inescapable. Our minds are adapted to think religiously, rather than rationally, and this is the result of our evolutionary history. The capacity for religious experience is found in all human societies. However, within each society there is considerable variation among individuals to the extent that they have such religious beliefs, and that such beliefs seem to modify their behavior.

Likewise, this ability, as well as human language capacity, has been empirically associated with specific neurological structures of the human nervous system. The capacity for human language and participation in war may be causally linked to specific ecological circumstances. The capacity for religious experience has consequences for those who have it: people who have the ability to believe in the supernatural (and especially to act in those beliefs) under certain circumstances, having high rates of survival and reproduction.



The most likely context for the capacity for religious experience to evolve is the same chronic, though episodic, small-scale warfare observed between our primate cousins ​​and our evolved ancestors. Moreover, not only has the capacity for religious experience been the result of war, but making war itself is more likely.

The capacities for religious experience and war are mutually reinforcing. They are a sort of evolutionary arms race which can be succinctly as a "law": religion facilitates the war, which in turn facilitates religion.

As Darwin said, the ubiquity of religious belief in our species is strong evidence that the capacity for such a belief is a specific evolutionary adaptation of the species. And, like all traits evolved, there is considerable variation within the human groups for this trait. In fact, precisely this variation is the prerequisite for evolution through natural selection.

In addition, the observation that most people, even in our technological culture, believe in the supernatural, essentially without empirical evidence, is strong evidence for the idea that the capacity for such a belief is "wired in our brains." And, like all evolutionary psychological mechanisms, one can ask the question, "What is the use?" Or, "What is the biological function of the capacity for religious belief?" As we shall see, it certainly seems that the evidence points to the conclusion that: "The ability of religious belief increases our ability to participate in war, which in turn improves our fitness."



Michael Persinger, a professor of psychology at Laurentian University in Canada, published “Neuropsychological Bases of Belief in God". In it, Persinger argued that a specific neurological condition known as 'temporal lobe epilepsy' produces psychological states that are similar to the religious experiences of people like Joan of Arc and St. Paul in 'The Road to Damascus'. 'Temporal lobe epilepsy' is different from other forms of temporal lobe epilepsy in which epileptic seizures do not involve seizures, immobility or loss of consciousness. In contrast, a person who has a 'temporal lobe epilepsy' attack observes a change in sensory perception, often involving changes in odors, sounds, tastes, and phantom sensations in the skin. Some people also experience cognitive changes such as 'Déjà Vu' or 'Jamais Vu' during a seizure in ‘temporal lobe epilepsy’, and a significant fraction of these people also experience a greater sense of 'religiosity', including the feeling of a presence Invisible and supernatural.

Researcher Persinger developed a machine, often called the "The God Helmet" (read the full article on 'NewmindJournal.com'), which generates a weak magnetic field in and around the right temporal lobe of a person's brain. Approximately 80 percent of people, in a test of the "Helmet of God", felt the presence of an invisible figure nearby, which is usually interpreted as a supernatural entity, as a figure of God or the spirit of a person absent or dead.



Other researchers, such as Vilayanur S. Ramachandran, have also linked temporal lobe epilepsy and other neurological effects to religious experiences. Ramachandran based his work on the prior research of Norman Geschwind, a clinical psychiatrist. Geschwind described a clinical syndrome, called Geschwind syndrome, which is characterized by hypergraphia (the tendency to write lengthy detailed arguments and descriptions, often on religious subjects), hyper-religiosity, fainting, mutism (the inability to speak at certain events Social), and pedantism (the tendency to extensive discourse, on obscure topics, especially word definitions and the fine points of grammar).

Geschwind hypothesized that this syndrome is a manifestation of a form of mild temporal lobe epilepsy and suggested that it might explain the behavior of some historical hyper-religious figures.

Ramachandran tested the Geschwind hypothesis using a lie detector type device that measures the electrical conductivity of the skin as an indirect indication of emotional arousal. Ramachandran found that people with mild temporal lobe epilepsy reacted differently to religious words than people who did not have temporal lobe epilepsy.

Jeffrey Saver and John Rabin also studied the relationship between temporal lobe epilepsy and extended their recommendations to neurological states generated by the limbic system of the brain and neurochemical states generated by the ingestion of hallucinogenic drugs. They noted that a large amount of Americans have reported having religious experiences, characterized by feelings that included the belief that a specific event "should happen”, were aware of "the presence of God," that "God had responded to their Prayers”, which were being protected (or at least looked at) by an invisible presence (often characterized as the spirit of an absent or dead person), who felt the presence of a" sacred spirit in nature "or" presence Evil "or a deep sense of" oneness with the cosmos."



In particular, many people who had such experiences described a sense of depersonalization (they felt "outside themselves") and a sense of being united or part of their environment. They also noted descriptions of such feelings, often interpreted as religious experiences, by epileptics, such as the Russian writer Fyodor Dostoevsky.

They emphasized that such interpretations were just that: the interpretations were not the causes of such experiences, but rather the cognitive means by which people who had experienced such attacks explained their sensations to themselves. In other words, sensations came first, and subsequently, religious explanations.

Eugene d'Aquili and Andrew Newberg have recently presented an integrative model of the neurobiological underpinnings of religious experience. In his books, 'The Mind Mysticism: Probing the Biology of Religious Experience' and Why God will not go away: 'Brain Science and the Biology of Belief', the books report how their research in the states of Neurological factors associated with religious experiences strongly suggest that there are specific regions of the brain and states that produce such experiences.

This model is based on his research on neurological correlations between brain functions and regions, as well as the religious experiences of devoutly religious mystics and people. They studied these correlations using brain scans and other measures of brain activity using subjects trained in Eastern and Western meditative traditions i.e. (monks, nuns, and priests). They found that these subjects had consistent patterns of brain activity that were different from those not religiously trained, and that these patterns of brain activity were correlated with specific meditation and religious practices.



Researchers D'Aquili and Newberg have pointed out that the center of the greatest religious experience is a sense of wonder, combined with "sensations slightly pleasing to feelings of ecstasy”. They have shown that such sensations can be induced by rhythmic chanting and body movements, combined with loud music and colorful visual displays. Consequently, the factors that induce these sensations produce a condition of sensory overload and excitation of the sympathetic nervous system, together with simultaneous parasympathetic activation, due to the conscious "damping" of the excitation.

Such sensations are common in two contexts: military training and religious training. It is no coincidence that human beings preparing for war use exactly the same types of sensory stimuli described by d'Aquili and Newberg. They have tied such exhibitions to religious activities and demonstrated the deep similarities between religious and secular rituals: "Patriotic rituals ... emphasize the "holiness" of a nation, or a cause, or even a flag… meaningful idea in a visceral experience."

Researcher Dean Hamer found a correlation between a single human gene and a measure of human behavior that correlates strongly with the capacity for religious experiences. Using a combination of molecular genetic techniques, demographic analysis, and epidemiology, Hamer and his colleagues at the National Institutes of Health in Bethesda, Maryland, showed a strong correlation between a specific gene (called VMAT2), and "self-transcendence" which is correlated with religious experience.
………………….End of part 1

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Why Psychology Lost Its Soul? Everything Comes from the Brain

Most functions attributed to the soul can be explained by the brain.

Many people today believed they possess a soul. While conceptions of the soul differ, many would describe it as an “invisible force that appears to animate us”.

It’s often believed the soul can survive death and is intimately associated with a person’s memories, passions and values. Some argue, takes no space and is localized nowhere.
But as a neuroscientist and psychologist, I have no use for the soul. On the contrary, all functions attributable to this kind of soul can be explained by the workings of the brain.



Psychology is the study of behavior. To carry out their work of modifying behavior, such as in treating addiction, phobia, anxiety and depression, psychologists do not need to assume people have souls. For the psychologists, it is not so much that souls do not exist, it is that there is no need for them.
It is said psychology lost its soul in the 1930s. By this time, the discipline fully became a science, relying on experimentation and control rather than introspection.

What is the soul?
It is not only religious thinkers who have proposed that we possess a soul. Some of the most notable proponents have been philosophers, such as Plato (424-348 BCE) and René Descartes in the 17th century.

Plato believed we do not learn new things but recall things we knew before birth. For this to be so, he concluded, we must have a soul.

Centuries later, Descartes wrote his thesis Passions of the Soul, where he argued there was a distinction between the mind, which he described as a “thinking substance”, and the body, “the extended substance”. He wrote:

… because we have no conception of the body as thinking in any way, we have reason to believe that every kind of thought which exists in us belongs to the soul.

One of the many arguments Descartes advanced for the existence of the soul was that the brain, which is a part of the body, is mortal and divisible – meaning it has different parts – and the soul is eternal and indivisible – meaning it is an inseparable whole. Therefore, he concluded they must be different things.

But advances in neuroscience have shown these arguments to be false.

Stripping humans of the soul
In the 1960s, Nobel laureate Roger Sperry showed that the mind and our consciousness are divisible, therefore disproving that aspect of Descartes’ theory.

Sperry studied patients whose corpus callosum, the superhighway connecting the right and left hemispheres, had been severed by surgery aiming to control the spread of epileptic seizures. The surgery blocked or reduced the transfer of perceptual, sensory, motor and cognitive information between the two hemispheres.



Sperry showed each hemisphere could be trained to perform a task, but this experience was not available to the untrained hemisphere. That is, each hemisphere could process information outside the awareness of the other. In essence, this meant the operation produced a double consciousness.

Thus, Descartes cannot be correct in his assertion the brain is divisible but the soul, which can be read as the mind or consciousness, is not. In his effort to prove the existence of the soul in humans, Descartes provided an argument against it.
Rather than endowing rats with souls, psychologists stripped humans of theirs. In 1949, psychologist D.O. Hebb claimed the mind is the integration of the activity of the brain.

Many neurophilosophers have come to the same conclusion as the psychologists, with Patricia Churchland more recently claiming there is no ghost in the machine.



The brain does it all
If the soul is where emotion and motivation reside, where mental activity occurs, sensations are perceived, memories are stored, reasoning takes place and decisions are taken, then there is no need to hypothesize its existence. There is an organ that already performs these functions: the brain.

This idea goes back to the ancient physician Hippocrates (460-377 BCE) who said:

Men ought to know that from nothing else but the brain come joys, delights, laughter and sports, and sorrows, griefs, despondency and lamentations. And by this … we acquire wisdom and knowledge, and see and hear, and know what are foul and what are fair, what are bad and what are good, what are sweet and what are unsavory…

The brain is the organ with a map of our body, the outside world and our experience. Damage to the brain, as in accidents, dementias or congenital malformations, produces a commensurate damage to personality.



Consider one of the functions supposedly – if we listen to Plato – carried out by the soul: memory. A major knock on the head can make you lose your memories of the past several years. If the soul is an immaterial substance separate from our physical being, it should not be injured by the knock. If memory were stored in the soul, it should not have been lost.
The neuronal activity in the brain is responsible for the cognitive and dysfunctions in people with autism; it would be cruel and unethical to blame their hypothetical souls.

Manipulation of the brain is sufficient to alter emotion and mood. The soul is totally superfluous to this process.
The ability of psychotherapeutic drugs to alter mood provides another line of evidence against the presence of the soul. If you produce a chemical imbalance in the brain, such as by depleting dopamine, noradrenaline and serotonin with tetrabenazine, you can induce depression in some people.



Correspondingly, many depressed people can be helped by drugs that increase the function of these neurotransmitters in the brain.

The brain is where thinking takes place, love and hatred reside, sensations become perceptions, personality is formed, memories and beliefs are held, and where decisions are made. As D.K. Johnson said: “There is nothing left for the soul to do.”

Reference: George Paxinos, Visiting/Conjoint Professor of Psychology and Medical Sciences, UNSW & NHMRC Australia Fellow, Neuroscience Research Australia.

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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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The Effects of Advertising on the Brain

By: Alexandria Addesso

Everywhere you turn someone is trying to solicit you for something. On television, the internet, radio, newspapers, billboards and street corners. In big cities such as New York and Los Angeles it is not unlikely to see a whole side of a sprawling high-rise or even sky-skraper be covered in an advertisement. For a capitalist society advertising is the life sustaining blood that keeps consumption going. But could there be more negative side effects from advertising than just an influx of consumerism and slimmer wallets? Could advertising be neurologically affecting the consumer?



Some advertisements grab the viewer or listener via appealing to their sense of reason by stating facts, this method of advertising is called “logical persuasion”. The other type of advertising method is called “non-rational influence” because it may use scenarios that have little to nothing to do with the product but instead depicts instances of fun, pleasure, or sexual appeal.

The brain responds differently to the two types of advertising. A study was done by the University of California in conjunction with the George Washington University in which participants were shown 24 print ads, half were logical persuasion advertising and the other half were non-rational influence. Participants had electrodes attached to different parts of their heads so that researchers could perform an electroencephalogram (EEG) test and watch their brain activity while the ads were viewed. Researchers found that there was much more activity in the orbitofrontal, anterior cingulate regions, the amygdala, and the hippocampus, which are all sections of the brain that deal with emotional processing and decision making, when logical persuasion ads were viewed rather than non-rational influence ads which showed little to none. Meaning that individuals are more likely to resist logical persuasion advertising than non-rational influence advertising because, the latter deals more with the appeal to the subconscious.



Another study was done at the University of North Carolina that focused specifically on the neurological effects of deceptive advertising. In the study participants were shown three different print ads deemed: “highly believable”, “highly deceptive”, and “moderately deceptive” while functional magnetic resonance imaging (fMRI) was utilized to capture images of the brain.

It was uncovered that there is more brain activity occurring when participants viewed moderately deceptive ads, thus making them more frequently believe moderately deceptive advertisement.



The only way to keep from the seductive draw of advertisements is to avoid them
completely. But unless you are completely off-the-grid or blind, dumb, and deaf, this is
nearly impossible to do. The best thing that can be done is to train your brain to become
completely disinterested to any form of conscious solicitation, because unfortunately,
subconscious resistance is nearly impossible.

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