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

By: Alexandria Addesso

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

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



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

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



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

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

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Your Blood Type May Help Protect you From Cognitive Decline

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

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

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

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



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

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

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

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



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

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

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Researchers Find the Existence of another Immune System in Humans

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

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

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

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

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



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

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

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



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

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

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

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

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

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

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



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

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

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

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

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



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

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

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

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

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



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

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

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

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

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

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

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

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

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Understanding the Brain with the Help of Artificial Intelligence

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

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

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

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



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

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



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

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

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Using Virtual Reality to Detect Mild Cognitive Impairment

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

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

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

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



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



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

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

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



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

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Soccer Success in the Young Can Be Measured in the Brain

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

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

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



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

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



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

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

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



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

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The Possible Cause of Flashbacks Discovered

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

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

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

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

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


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

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

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

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

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



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

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

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

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

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

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