The memories of near death experiences (NDE): more real than reality?

University of Liège researchers have demonstrated that the physiological mechanisms triggered during NDE lead to a more vivid perception not only of imagined events in the history of an individual but also of real events which have taken place in their lives! These surprising results – obtained using an original method which now requires further investigation – are published in PLOS ONE.

Seeing a bright light, going through a tunnel, having the feeling of ending up in another ‘reality’ or leaving one’s own body are very well known features of the complex phenomena known as ‘Near-Death Experiences ‘ (NDE), which people who are close to death can experience in particular. Products of the mind? Psychological defence mechanisms? Hallucinations? These phenomena have been widely documented in the media and have generated numerous beliefs and theories of every kind. From a scientific point of view, these experiences are all the more difficult to understand in that they come into being in chaotic conditions, which make studying them in real time almost impossible. The University of Liège’s researchers have thus tried a different approach.

Working together, researchers at the Coma Science Group (Directed by Steven Laureys) and the University of Liège’s Cognitive Psychology Research (Professor Serge Brédart and Hedwige Dehon), have looked into the memories of NDE with the hypothesis that if the memories of NDE were pure products of the imagination, their phenomenological characteristics (e.g., sensorial, self referential, emotional, etc. details) should be closer to those of imagined memories. Conversely, if the NDE are experienced in a way similar to that of reality, their characteristics would be closer to the memories of real events.

The researchers compared the responses provided by three groups of patients, each of which had survived (in a different manner) a coma, and a group of healthy volunteers. They studied the memories of NDE and the memories of real events and imagined events with the help of a questionnaire which evaluated the phenomenological characteristics of the memories. The results were surprising. From the perspective being studied, not only were the NDEs not similar to the memories of imagined events, but the phenomenological characteristics inherent to the memories of real events (e.g. memories of sensorial details) are even more numerous in the memories of NDE than in the memories of real events.

The brain, in conditions conducive to such phenomena occurring, is prey to chaos. Physiological and pharmacological mechanisms are completely disturbed, exacerbated or, conversely, diminished. Certain studies have put forward a physiological explanation for certain components of NDE, such as Out-of-Body Experiences, which could be explained by dysfunctions of the temporo-parietal lobe. In this context the study published in PLOS ONE suggests that these same mechanisms could also ‘create’ a perception – which would thus be processed by the individual as coming from the exterior – of reality. In a kind of way their brain is lying to them, like in a hallucination. These events being particularly surprising and especially important from an emotional and personal perspective, the conditions are ripe for the memory of this event being extremely detailed, precise and durable.

Numerous studies have looked into the physiological mechanisms of NDE, the production of these phenomena by the brain, but, taken separately, these two theories are incapable of explaining these experiences in their entirety. The study published in PLOS ONE does not claim to offer a unique explanation for NDE, but it contributes to study pathways which take into account psychological phenomena as factors associated with, and not contradictory to, physiological phenomena.

Brain scans predict which criminals are more likely to reoffend

In a twist that evokes the dystopian science fiction of writer Philip K. Dick, neuroscientists have found a way to predict whether convicted felons are likely to commit crimes again from looking at their brain scans. Convicts showing low activity in a brain region associated with decision-making and action are more likely to be arrested again, and sooner.

Kent Kiehl, a neuroscientist at the non-profit Mind Research Network in Albuquerque, New Mexico, and his collaborators studied a group of 96 male prisoners just before their release. The researchers used functional magnetic resonance imaging (fMRI) to scan the prisoners’ brains during computer tasks in which subjects had to make quick decisions and inhibit impulsive reactions.

The scans focused on activity in a section of the anterior cingulate cortex (ACC), a small region in the front of the brain involved in motor control and executive functioning. The researchers then followed the ex-convicts for four years to see how they fared.

Among the subjects of the study, men who had lower ACC activity during the quick-decision tasks were more likely to be arrested again after getting out of prison, even after the researchers accounted for other risk factors such as age, drug and alcohol abuse and psychopathic traits. Men who were in the lower half of the ACC activity ranking had a 2.6-fold higher rate of rearrest for all crimes and a 4.3-fold higher rate for nonviolent crimes. The results are published in the Proceedings of the National Academy of Sciences.

There is growing interest in using neuroimaging to predict specific behaviour, says Tor Wager, a neuroscientist at the University of Colorado in Boulder. He says that studies such as this one, which tie brain imaging to concrete clinical outcomes, “provide a new and so far very promising way” to find patterns of brain activity that have broader implications for society.

But the authors themselves stress that much more work is needed to prove that the technique is reliable and consistent, and that it is likely to flag only the truly high-risk felons and leave the low-risk ones alone. “This isn’t ready for prime time,” says Kiehl.

Wager adds that the part of the ACC examined in this study “is one of the most frequently activated areas in the human brain across all kinds of tasks and psychological states”. Low ACC activity could have a variety of causes — impulsivity, caffeine use, vascular health, low motivation or better neural efficiency — and not all of these are necessarily related to criminal behaviour.

Crime prediction was the subject of Dick’s 1956 short story “The Minority Report” (adapted for the silver screen by Steven Spielberg in 2002), which highlighted the thorny ethics of arresting people for crimes they had yet to commit.

Brain scans are of course a far cry from the clairvoyants featured in that science-fiction story. But even if the science turns out to be reliable, the legal and social implications remain to be explored, the authors warn. Perhaps the most appropriate use for neurobiological markers would be for helping to make low-stakes decisions, such as which rehabilitation treatment to assign a prisoner, rather than high-stakes ones such as sentencing or releasing on parole.

“A treatment of [these clinical neuroimaging studies] that is either too glibly enthusiastic or over-critical,” Wager says, “will be damaging for this emerging science in the long run.”

New mechanism for long-term memory formation discovered

UC Irvine neurobiologists have found a novel molecular mechanism that helps trigger the formation of long-term memory. The researchers believe the discovery of this mechanism adds another piece to the puzzle in the ongoing effort to uncover the mysteries of memory and, potentially, certain intellectual disabilities.

In a study led by Marcelo Wood of UC Irvine’s Center for the Neurobiology of Learning & Memory, the team investigated the role of this mechanism – a gene designated Baf53b – in long-term memory formation. Baf53b is one of several proteins making up a molecular complex called nBAF.

Mutations in the proteins of the nBAF complex have been linked to several intellectual disorders, including Coffin-Siris syndrome, Nicolaides-Baraitser syndrome and sporadic autism. One of the key questions the researchers addressed is how mutations in components of the nBAF complex lead to cognitive impairments.

In their study, Wood and his colleagues used mice bred with mutations in Baf53b. While this genetic modification did not affect the mice’s ability to learn, it did notably inhibit long-term memories from forming and severely impaired synaptic function.

“These findings present a whole new way to look at how long-term memories form,” said Wood, associate professor of neurobiology & behavior. “They also provide a mechanism by which mutations in the proteins of the nBAF complex may underlie the development of intellectual disability disorders characterized by significant cognitive impairments.”

How does this mechanism regulate gene expression required for long-term memory formation? Most genes are tightly packaged by a chromatin structure – chromatin being what compacts DNA so that it fits inside the nucleus of a cell. That compaction mechanism represses gene expression. Baf53b, and the nBAF complex, physically open the chromatin structure so specific genes required for long-term memory formation are turned on. The mutated forms of Baf53b did not allow for this necessary gene expression.

“The results from this study reveal a powerful new mechanism that increases our understanding of how genes are regulated for memory formation,” Wood said. “Our next step is to identify the key genes the nBAF complex regulates. With that information, we can begin to understand what can go wrong in intellectual disability disorders, which paves a path toward possible therapeutics.”

Findings appear online today in Nature Neuroscience.

Alterations in brain activity in children at risk of schizophrenia predate onset of symptoms

Research from the University of North Carolina has shown that children at risk of developing schizophrenia have brains that function differently than those not at risk.

Brain scans of children who have parents or siblings with the illness reveal a neural circuitry that is hyperactivated or stressed by tasks that peers with no family history of the illness seem to handle with ease.

Because these differences in brain functioning appear before neuropsychiatric symptoms such as trouble focusing, paranoid beliefs, or hallucinations, the scientists believe that the finding could point to early warning signs or “vulnerability markers” for schizophrenia.

“The downside is saying that anyone with a first degree relative with schizophrenia is doomed. Instead, we want to use our findings to identify those individuals with differences in brain function that indicate they are particularly vulnerable, so we can intervene to minimize that risk,” said senior study author Aysenil Belger, PhD, associate professor of psychiatry at the UNC School of Medicine.

The UNC study, published online on March 6, 2013, in the journal Psychiatry Research: Neuroimaging, is one of the first to look for alterations in brain activity associated with mental illness in individuals as young as nine years of age.

Individuals who have a first degree family member with schizophrenia have an 8-fold to 12-fold increased risk of developing the disease. However, there is no way of knowing for certain who will become schizophrenic until symptoms arise and a diagnosis is reached. Some of the earliest signs of schizophrenia are a decline in verbal memory, IQ, and other mental functions, which researchers believe stem from an inefficiency in cortical processing – the brain’s waning ability to tackle complex tasks.

In this study, Belger and her colleagues sought to identify what if any functional changes occur in the brains of adolescents at high risk of developing schizophrenia. She performed functional magnetic resonance imaging (fMRI) on 42 children and adolescents ages 9 to 18, half of which had relatives with schizophrenia and half of which did not. Study participants each spent an hour and a half playing a game where they had to identify a specific image – a simple circle – out of a lineup of emotionally evocative images, such as cute or scary animals. At the same time, the MRI machine scanned for changes in brain activity associated with each target detection task.

Belger found that the circuitry involved in emotion and higher order decision making was hyperactivated in individuals with a family history of schizophrenia, suggesting that the task was stressing out these areas of the brain in the study subjects.

“This finding shows that these regions are not activating normally,” she says. “We think that this hyperactivation eventually damages these specific areas in the brain to the point that they become hypoactivated in patients, meaning that when the brain is asked to go into high gear it no longer can.”

Belger is currently exploring what kind of role stress plays in the changing mental capacity of adolescents at high risk of developing schizophrenia. Though only a fraction of these individuals will be diagnosed with schizophrenia, Belger thinks it is important to pinpoint the most vulnerable people early to explore interventions that may stave off the mental illness.

“It may be as simple as understanding that people are different in how they cope with stress,” says Belger. “Teaching strategies to handle stress could make these individuals less vulnerable to not just schizophrenia but also other neuropsychiatric disorders.”

Human brain research made easier by database

Researchers will be able to access samples from more than 7,000 donated human brains to help study major brain diseases, thanks to a new on-line database, launched by the Medical Research Council (MRC) today.

The UK Brain Banks Network database speeds up access to donated brain samples held across 10 brain banks in the UK and allows researchers studying Multiple Sclerosis, Alzheimer’s, Parkinson’s and a range of other neurodegenerative and developmental diseases to track down human tissue samples for their work.

Thanks to a unique collaboration between the MRC and five leading charities, the database will help scientists from academia and industry investigate the underlying causes of major brain diseases and understand how they take hold in our bodies.

Although scientists can model diseases in the lab, to fully understand dementia and other brain-related disorders they need to study human brain tissue. A lot of research relies on donated brain tissue stored in brain banks across the UK. Until today, researchers had to apply to each brain bank in turn to find out if they held the samples they needed and find the ‘control’ samples (donated brains free from disease) for comparison – a long and drawn out process. Now samples can be found with the click of a button from one source.

Professor James Ironside, Director of the MRC UK Brain Banks Network, said:

“The database is the result of four years of painstaking planning and data analysis by very dedicated people. It will enable quick and easy access for researchers who are already working on neurological or psychiatric disease (perhaps in animal models or cells) and would like to translate their findings into human tissue and is very useful for those who are planning a grant application. The brain banks have already been given ethical approval, cutting out the need for researchers to go through a separate ethics application.

We must remember that vital research would not be possible without the generosity of those individuals who donate their brains to medical research. We’re working hard to make sure that the access for researchers studying brain samples is much easier. The next step is to improve the systems for those wishing to donate their brain to medical research.”

Five leading charities helped to supply data for the database; the MS Society, Parkinson’s UK, Alzheimer’s Society, Alzheimer’s Research UK and Autistica.

For more information about the database visit: http://www.mrc.ac.uk/brainbanksnetwork

How two brain areas interact to trigger divergent emotional behaviors

New research from the University of North Carolina School of Medicine for the first time explains exactly how two brain regions interact to promote emotionally motivated behaviors associated with anxiety and reward.

The findings could lead to new mental health therapies for disorders such as addiction, anxiety, and depression. A report of the research was published online by the journal, Nature, on March 20, 2013.

Located deep in the brain’s temporal lobe are tightly packed clusters of brain cells in the almond shaped amygdala that are important for processing memory and emotion. When animals or people are in stressful situations, neurons in an extended portion of the amygdala called the bed nucleus of the stria terminalis, or BNST, become hyperactive.

But, almost paradoxically, neurons in the BNST, which modulate fear and anxiety, reach into a portion of the midbrain that’s involved in behavioral responses to reward, the ventral tegmental area, or VTA.

“For many years it’s been known that dopamine neurons in the VTA are involved in reward processing and motivation. For example, they’re activated during exposure to drugs of abuse and naturally rewarding experiences,” says study senior author Garret Stuber, PhD, assistant professor in the departments of Psychiatry and Cell Biology and Physiology, and the UNC Neuroscience Center.  “On the one hand, you have this area of the brain – the BNST – that’s associated with aversion and anxiety, but it’s in direct communication with a brain reward center. We wanted to figure out exactly how these two brain regions interact to promote different types of behavioral responses related to anxiety and reward.”

In the past, researchers have tried to get a glimpse into the inner workings of the brain using electrical stimulation or drugs, but those techniques couldn’t quickly and specifically change only one type of cell or one type of connection. But optogenetics, a technique that emerged about seven years ago, can.

In the technique, scientists transfer light-sensitive proteins called “opsins” – derived from algae or bacteria that need light to grow – into the mammalian brain cells they wish to study. Then they shine laser beams onto the genetically manipulated brain cells, either exciting or blocking their activity with millisecond precision.

Brain Mapping Reveals Neurological Basis of Decision-Making in Rats

Scientists at UC San Francisco have discovered how memory recall is linked to decision-making in rats, showing that measurable activity in one part of the brain occurs when rats in a maze are playing out memories that help them decide which way to turn. The more they play out these memories, the more likely they are to find their way correctly to the end of the maze.

In their study, reported this week in the journal Neuron, the UCSF researchers implanted electrodes directly on a region of the rat brain known as the hippocampus, which is already known to play a key role in the formation and recall of memory. This same region is active when animals are learning, and it is damaged in people who have Alzheimer’s and post-traumatic stress disorder.

The study showed that when the rats paused before an upcoming choice, sometimes the hippocampus was more active and sometimes it was less active. When it was more active it did a better job of recalling memories of places the animal could go next, and the animal was more likely to go to the right place.

“We know that considering possibilities is important for decision-making, but we haven’t really known how this happens in the brain,” said neuroscientist Loren Frank, PhD, who led the research. Frank is an associate professor of physiology and a member of the UCSF Center for Integrative Neuroscience at UCSF.

The work builds upon several years of investigations in Frank’s laboratory that have shown how activity in the hippocampus is a fundamental constituent of memory retrieval. Their recent work shows that this activity is not just about remembering the past – it is also important for thinking about the future. When the brain does a better job of thinking about future possibilities, it makes better decisions.

Next, the team wants to tease out why sometimes the hippocampus does not do a good job of playing out future options. Problems with memory and decision-making are central to age-related cognitive decline, and a deeper understanding of how this works could pave the way for interventions that make the brain work better.