How the brain networks of psychopathic criminals functions differently

A strong focus on reward combined with a lack of self-control appears to be linked to the tendency to commit an offence. Brain scans show that this combination occurs in psychopathic criminals, say researchers from Nijmegen in an article in the journal Social Cognitive and Affective Neuroscience.

any criminal offenders display psychopathic traits, such as antisocial and impulsive behaviour. And yet some individuals with psychopathic traits do not commit offences for which they are convicted. As with any other form of behaviour, psychopathic behaviour has a neurobiological basis.

Researchers from the Donders Institute and the Department of Psychiatry at Radboudumc wanted to find out whether the way a psychopath’s brain works is visibly different from that of a non-psychopath. And whether there are differences between the brains of criminal and non-criminal psychopaths.

Reward center more strongly activated

Dirk Geurts, researcher in the Department of Psychiatry at Radboudumc: “We carried out tests on 14 convicted psychopathic individuals, and 20 non-criminal individuals, half of whom had a high score on the psychopathy scale. The participants performed tests while their brain activity was measured in an MRI scanner. We saw that the reward centre in the brains of people with many psychopathic traits (both criminal and non-criminal) were more strongly activated than those in people without psychopathic traits. It has already been proved that the brains of non-criminal individuals with psychopathic traits are triggered by the expectation of reward. This research shows that this is also the case for criminal individuals with psychopathic traits.”

Little self-control and sensitivity to reward

Another interesting difference was discovered between non-criminal people with multiple psychopathic traits and criminal people with psychopathic traits.

Geurts: “There is a difference in the communication between the reward centre and an area in the middle of the forebrain. Good communication between these areas would appear to be a condition for self-control. Our results seem to indicate that the tendency to commit an offence arises from a combination of a strong focus on reward and a lack of self-control. This is the first research project in which convicted criminals were actually examined.”

Predictors of criminal behaviour

Psychopathy consists of several elements. On the one hand, there is a lack of empathy and emotional involvement. On the other hand, we see impulsive and seriously antisocial, egocentric behaviour.

Professor of Psychiatry and coordinator of the research Robbert-Jan Verkes: “Especially the latter character traits seem to be connected with an excessively sensitive reward centre. The presence of these impulsive and antisocial traits predict criminal behaviour more accurately than a lack of empathy. The next relevant question would be: what causes these brain abnormalities? It is probably partly hereditary, but abuse and severe stress during formative years also play a significant role. Follow-up studies will provide more information.

Brain scans in courtrooms?

So what do these findings mean for the free will? If the brain plays such an important role, to what extent can an individual be held responsible for his/her crimes? Will we be seeing brain scans in the courtroom?

Verkes: “For the time being, these findings are only important at group level as they concern variations within the range of normal results. Of course if we can refine these and other types of examinations, we may well see brain scans being used in forensic psychiatric examinations of diminished responsibility in the future.”

http://www.psypost.org/2016/08/brain-network-of-psychopathic-criminal-functions-differently-44202#prettyPhoto

New research shows that hypnosis alters brain activity in several regions


By scanning the brains of subjects while they were hypnotized, researchers at the School of Medicine were able to see the neural changes associated with hypnosis.

By Sarah C.P. Williams

Your eyelids are getting heavy, your arms are going limp and you feel like you’re floating through space. The power of hypnosis to alter your mind and body like this is all thanks to changes in a few specific areas of the brain, researchers at the Stanford University School of Medicine have discovered.

The scientists scanned the brains of 57 people during guided hypnosis sessions similar to those that might be used clinically to treat anxiety, pain or trauma. Distinct sections of the brain have altered activity and connectivity while someone is hypnotized, they report in a study published online July 28 in Cerebral Cortex.

“Now that we know which brain regions are involved, we may be able to use this knowledge to alter someone’s capacity to be hypnotized or the effectiveness of hypnosis for problems like pain control,” said the study’s senior author, David Spiegel, MD, professor and associate chair of psychiatry and behavioral sciences.

A serious science

For some people, hypnosis is associated with loss of control or stage tricks. But doctors like Spiegel know it to be a serious science, revealing the brain’s ability to heal medical and psychiatric conditions.

“Hypnosis is the oldest Western form of psychotherapy, but it’s been tarred with the brush of dangling watches and purple capes,” said Spiegel, who holds the Jack, Samuel and Lulu Willson Professorship in Medicine. “In fact, it’s a very powerful means of changing the way we use our minds to control perception and our bodies.”

Despite a growing appreciation of the clinical potential of hypnosis, though, little is known about how it works at a physiological level. While researchers have previously scanned the brains of people undergoing hypnosis, those studies have been designed to pinpoint the effects of hypnosis on pain, vision and other forms of perception, and not the state of hypnosis itself.

“There had not been any studies in which the goal was to simply ask what’s going on in the brain when you’re hypnotized,” said Spiegel.

Finding the most susceptible

To study hypnosis itself, researchers first had to find people who could or couldn’t be hypnotized. Only about 10 percent of the population is generally categorized as “highly hypnotizable,” while others are less able to enter the trancelike state of hypnosis. Spiegel and his colleagues screened 545 healthy participants and found 36 people who consistently scored high on tests of hypnotizability, as well as 21 control subjects who scored on the extreme low end of the scales.

Then, they observed the brains of those 57 participants using functional magnetic resonance imaging, which measures brain activity by detecting changes in blood flow. Each person was scanned under four different conditions — while resting, while recalling a memory and during two different hypnosis sessions.

“It was important to have the people who aren’t able to be hypnotized as controls,” said Spiegel. “Otherwise, you might see things happening in the brains of those being hypnotized but you wouldn’t be sure whether it was associated with hypnosis or not.”

Brain activity and connectivity

Spiegel and his colleagues discovered three hallmarks of the brain under hypnosis. Each change was seen only in the highly hypnotizable group and only while they were undergoing hypnosis.

First, they saw a decrease in activity in an area called the dorsal anterior cingulate, part of the brain’s salience network. “In hypnosis, you’re so absorbed that you’re not worrying about anything else,” Spiegel explained.

Secondly, they saw an increase in connections between two other areas of the brain — the dorsolateral prefrontal cortex and the insula. He described this as a brain-body connection that helps the brain process and control what’s going on in the body.

Finally, Spiegel’s team also observed reduced connections between the dorsolateral prefrontal cortex and the default mode network, which includes the medial prefrontal and the posterior cingulate cortex. This decrease in functional connectivity likely represents a disconnect between someone’s actions and their awareness of their actions, Spiegel said. “When you’re really engaged in something, you don’t really think about doing it — you just do it,” he said. During hypnosis, this kind of disassociation between action and reflection allows the person to engage in activities either suggested by a clinician or self-suggested without devoting mental resources to being self-conscious about the activity.

Treating pain and anxiety without pills

In patients who can be easily hypnotized, hypnosis sessions have been shown to be effective in lessening chronic pain, the pain of childbirth and other medical procedures; treating smoking addiction and post-traumatic stress disorder; and easing anxiety or phobias. The new findings about how hypnosis affects the brain might pave the way toward developing treatments for the rest of the population — those who aren’t naturally as susceptible to hypnosis.

“We’re certainly interested in the idea that you can change people’s ability to be hypnotized by stimulating specific areas of the brain,” said Spiegel.

A treatment that combines brain stimulation with hypnosis could improve the known analgesic effects of hypnosis and potentially replace addictive and side-effect-laden painkillers and anti-anxiety drugs, he said. More research, however, is needed before such a therapy could be implemented.

The study’s lead author is Heidi Jiang, a former research assistant at Stanford who is currently a graduate student in neuroscience at Northwestern University.

Other Stanford co-authors are clinical assistant professor of psychiatry and behavioral sciences Matthew White, MD; and associate professor of neurology Michael Greicius, MD, MPH.

The study was funded by the National Center for Complementary and Integrative Health (grant RCIAT0005733), the National Institute of Biomedical Imaging and Bioengineering (grant P41EB015891), the Randolph H. Chase, M.D. Fund II, the Jay and Rose Phillips Family Foundation and the Nissan Research Center.

Stanford’s Department of Psychiatry and Behavioral Sciences and Department of Neurology and Neurological Sciences also supported the work.

Jiang H, White MP, Greicius MD, Waelde LC and Spiegel D. Brain Activity and Functional Connectivity Associated with Hypnosis. Cerebral Cortex. 2016 July 28;[Epub ahead of print].

http://med.stanford.edu/news/all-news/2016/07/study-identifies-brain-areas-altered-during-hypnotic-trances.html

How a Wasp Turns Cockroaches into Zombies

By Christie Wilcox

The jewel wasp depends on live cockroaches to provide crucial food for its newly hatched larvae.

To force cockroaches into submission and into a necessary torpor, the wasp has evolved a particular chemical mix that it injects into a roach’s brain to alter its behavior and metabolism.

Many other wasp species also use complex venoms to parasitize spiders, caterpillars and even wasp larvae—sometimes turning them into zombie larva defenders.

I don’t know if cockroaches dream, but i imagine that if they do, jewel wasps feature prominently in their nightmares. These small, solitary tropical wasps are of little concern to us humans; after all, they don’t manipulate our minds so that they can serve us up as willing, living meals to their newborns, as they do to unsuspecting cockroaches. It’s the stuff of horror movies, quite literally; the jewel wasp and similar species inspired the chest-bursting horrors in the Alien franchise. The story is simple, if grotesque: the female wasp controls the minds of the cockroaches she feeds to her offspring, taking away their sense of fear or will to escape their fate. But unlike what we see on the big screen, it’s not some incurable virus that turns a once healthy cockroach into a mindless zombie—it’s venom. Not just any venom, either: a specific venom that acts like a drug, targeting the cockroach’s brain.

Brains, at their core, are just neurons, whether we’re talking human brains or insect brains. There are potentially millions of venom compounds that can turn neurons on or off. So it should come as no surprise that some venoms target the carefully protected central nervous system, including our brains. Some leap their way over physiological hurdles, from remote injection locations around the body and past the blood-brain barrier, to enter their victims’ minds. Others are directly injected into the brain, as in the case of the jewel wasp and its zombie cockroach host.

Making of a zombie

Jewel wasps are a beautiful if terrifying example of how neurotoxic venoms can do much more than paralyze. The wasp, which is often just a fraction of the size of her victim, begins her attack from above, swooping down and grabbing the roach with her mouth as she aims her “stinger”—a modified egg-laying body part called an ovipositor—at the middle of the body, the thorax, in between the first pair of legs. The quick jab takes only a few seconds, and venom compounds work fast, paralyzing the cockroach temporarily so the wasp can aim her next sting with more accuracy. With her long stinger, she targets her mind-altering venom into two areas of the ganglia, the insect equivalent of a brain.

The wasp’s stinger is so well tuned to its victim that it can sense where it is inside the cockroach’s dome to inject venom directly into subsections of its brain. The stinger is capable of feeling around in the roach’s head, relying on mechanical and chemical cues to find its way past the ganglionic sheath (the insect’s version of a blood-brain barrier) and inject venom exactly where it needs to go. The two areas of the roach brain that she targets are very important to her; scientists have artificially clipped them from cockroaches to see how the wasp reacts, and when they are removed, the wasp tries to find them, taking a long time with her stinger embedded in search of the missing brain regions.

Then the mind control begins. First the victim grooms itself, of all things; as soon as the roach’s front legs recover from the transient paralysis induced by the sting to the body, it begins a fastidious grooming routine that takes about half an hour. Scientists have shown that this behavior is specific to the venom, as piercing the head, generally stressing the cockroach, or contact with the wasp without stinging activity did not elicit the same hygienic urge. This sudden need for cleanliness can also be induced by a flood of dopamine in the cockroach’s brain, so we think that the dopaminelike compound in the venom may be the cause of this germophobic behavior. Whether the grooming itself is a beneficial feature of the venom or a side effect is debated. Some believe that the behavior ensures a clean, fungus- and microbe-free meal for the vulnerable baby wasp; others think it may merely distract the cockroach for some time as the wasp prepares the cockroach’s tomb.

Dopamine is one of those intriguing chemicals found in the brains of a broad spectrum of animal life, from insects all the way to humans, and its effects are vital in all these species. In our heads, it’s a part of a mental “reward system”; floods of dopamine are triggered by pleasurable things. Because it makes us feel good, dopamine can be wonderful, but it is also linked to addictive behaviors and the “highs” we feel from illicit substances like cocaine. It’s impossible for us to know if a cockroach also feels a rush of insect euphoria when its brain floods with dopamine—but I prefer to think it does. (It just seems too gruesome for the animal to receive no joy from the terrible end it is about to meet.)

While the cockroach cleans, the wasp leaves her victim in search of a suitable location. She needs a dark burrow where she can leave her child and the zombie-roach offering, and it takes a little time to find and prepare the right place. When she returns about 30 minutes later, the venom’s effects have taken over—the cockroach has lost all will to flee. In principle, this state is temporary: if you separate an envenomated roach from its would-be assassin before the larva can hatch and feed and pupate, the zombification wears off within a week. Unfortunately for the envenomated cockroach, that’s simply too long. Before its brain has a chance to return to normal, the young wasp has already had its fill and killed its host.

The motor abilities of the roach remain intact, but the insect simply doesn’t seem inclined to use them. So the venom doesn’t numb the animal’s senses—it alters how its brain responds to them. Scientists have even shown that the stimuli that normally elicit evasive action, such as touching the roach’s wings or legs, still send signals to the animal’s brain; they just don’t evoke a behavioral response. That’s because the venom mutes certain neurons so they are less active and responsive, leading to the roach’s sudden lack of fear and willingness to be buried and eaten alive. This venom activity requires toxins that target GABA-gated chloride channels.

GABA, or γ-aminobutyric acid, is one of the most important neurotransmitters in insect—and human—brains. If neuron activity is a party, then GABA is a wet blanket; it dampens a neuron’s ability to be triggered through activation of chloride channels. When chloride channels open, they allow negative chloride ions to flow. Because these ions like to hang out with positive ions, if these channels are open when a sodium channel happens to open, chloride ions can cross the membrane at almost the same pace as sodium ions, making it harder for the sodium ions to start the domino cascade that is neuron signaling. Even though a neuron receives the “go” command, the action potential is stopped in its tracks. GABA isn’t a complete inhibitor, however—the chloride channels can’t wholly keep up with the sodium channels, so a strong stimulus can overcome the dampening effect. This dulling system is what the wasp co-opts to make the cockroach do her bidding. Her venom is packed with GABA and two other compounds that also activate the same chloride receptors, β-alanine and taurine. These also work to prevent the reuptake of GABA by neurons, prolonging the effect.

Although these venom compounds can cut the brain activity that would make her prey flee, what they can’t do is make their way to the right parts of the cockroach brain by themselves. That’s why the wasp has to inject them directly into the cockroach’s ganglia. Fortunately for her, in a convenient quirk of nature, the same venom that zombifies roach brains works like magic to produce the transient paralysis needed to line up the cranial injection. GABA, β-alanine and taurine also temporarily shut down motor neurons, so the wasp only needs one venom to complete two very different tasks.

With her prey calm and quiescent, the wasp can replenish her energy by breaking the roach’s antennae and drinking some sweet, nutritious insect blood. Then she leads her victim to its final resting place, using what remains of an antenna as an equestrian uses the reins on a bridle. Once inside her burrow, she attaches one egg to the cockroach’s leg, then seals her offspring and the roach in.

Fresh meals

As if the mind manipulation wasn’t bad enough, the wasp’s venom has one final trick. While the roach awaits its inevitable doom, the venom slows down the roach’s metabolism to ensure it lives long enough to be devoured still fresh. One way metabolism can be measured is by how much oxygen is used up over time, as all animals (including us) use oxygen in the process of creating energy from food or fat stores. Scientists have found that oxygen consumption by cockroaches that have been stung is much lower than that of their healthy roach friends. They thought this might be the result of the reduced movement of the complacent victims, but even when paralysis is induced by using drugs or severing neurons, the stung cockroaches live longer. The key to the prolonged survival seems to be hydration. How exactly the venom acts to keep a roach hydrated is not known, but it ensures that when the wasp larva hatches from its egg, its meal is ready to eat. And soon enough after that, a new wasp emerges from the burrow, leaving the roach carcass behind.

Jewel wasp venom is only one example of neurotoxic venom taken to the extreme. There are more than 130 species in the same wasp genus, including the newly described Ampulex dementor (named for the soul-sucking guards of the magical prison Azkaban in the Harry Potter series). Ampulex belongs to a very large and diverse group of wasps, numbering at least in the hundreds of thousands of species, which are known for some serious mental manipulation. All have a macabre life cycle: as adults, they feed like other wasps and bees, but as larvae, they must feed off other animals. They’re not quite independent, not quite parasites—they’re parasite-ish, or as scientists call them, parasitoids.

Cockroaches are not their only targets; there are parasitoid wasps that lay their eggs in spiders, caterpillars and ants. The temperate Northern Hemisphere wasp Agriotypus will dive underwater to attach her eggs to caddis fly larvae and can remain submerged for up to 15 minutes to accomplish her task. The brave Lasiochalcidia wasps of Europe and Africa throw themselves into the nightmarish jaws of an ant lion, pry them apart and insert their eggs into its throat. There are even wasps called hyperparasitoids that parasitize other wasps like themselves, such as Lysibia species of Europe and Asia, which will sniff out caterpillars parasitized by fellow parasitoid wasps in the genus Cotesia and lay eggs in the freshly pupated wasp larvae. In some cases, multiple wasp species parasitize one another, leading to a Russian doll of parasitic interactions.

And to ensure their safe passage from larva to adulthood, these wasps often gain more than just a meal from their hosts. One of them turns its caterpillar hosts into undead bodyguards that will defend pupating young wasps that just ate through its body. Another species’ larva forces its spider host to spin it a deformed but durable web to protect its cocoon just before killing the arachnid.

Whereas the wasps in this unusual family may have perfected the art of mind control, there are other venomous species whose toxins alter mental states. There are even species whose neurotoxic compounds get through our own blood-brain barrier, a feat that no wasp venom can yet achieve. But unlike cockroaches, we Homo sapiens have a strange affinity for substances that mess with our minds. Although the roaches run from those that would twist their brains, some people are willing to pay upward of $500 for a dose of venom to have a similar experience.

http://www.scientificamerican.com/article/how-a-wasp-turns-cockroaches-into-zombies/?WT.mc_id=SA_SA_20160719_Art_PPV

Brain scan research shows that lack of sleep severely alters brain function

BY DANIEL REED

Sleep deprivation majorly impacts the brain’s connectivity and function, according to a recent study published in NeuroImage. As well as affecting many important networks, sleep deprivation prevented normal changes to brain function between the morning and evening.

Sleep is an essential human state which is necessary for maintaining healthy function throughout the body. Therefore, lack of sleep has severe health-related consequences, with the brain being the most affected organ.

Lack of sleep can negatively affect memory, emotional processing and attentional capacities. For example, sleep deprivation has been shown to disrupt functional connectivity in hippocampal circuits (important for memory), and between the amygdala (important for emotion regulation) and executive control regions (involved in processes such as attention, planning, reasoning and cognitive flexibility). The emotional effects of sleep deprivation can be to both alter response patterns to negative things but also enhance reactivity toward positive things.

The study, led by Tobias Kaufmann of University of Oslo, involved 60 young men who completed three resting state functional magnetic resonance imaging (fMRI) scans – this is used to evaluate connectivity between brain regions when a person is not performing a task.

They were scanned in the morning and evening of the same day – this was to account for changes from morning to evening in normal brain function (diurnal variability). 41 men then underwent total sleep deprivation, whereas the remainder had another night of regular sleep, before they were scanned again the following morning. Finally, behavioural assessments of vigilance and visual attention were assessed.

The findings revealed that sleep deprivation strongly altered the connectivity of many resting-state networks; most clearly affected were networks important for memory (hippocampal networks) and attention (dorsal attention networks), as well as the default mode network (an interconnected set of brain regions active when a person is daydreaming or their mind is wandering).

In fact, they identified a set of 17 brain network connections showing altered brain connectivity. Furthermore, correlation analysis suggested that morning-to-evening connectivity changes returned the next day in the group that had slept the night, but not in the sleep-deprivation group.

The study emphasizes the major impact of sleep deprivation on the brain’s connectivity and function, as well as providing evidence that normal morning-to-evening connectivity changes do not occur after a night without sleep.

http://www.psypost.org/2016/07/brain-scan-research-shows-lack-sleep-severely-alters-brain-function-43977#prettyPhoto

44 year old man discovers he’s been living without 90% of his brain


A scan of the man missing 90% of his brain.

by Paul Ratner

What we think we know about our brains is nothing compared to what we don’t know. This fact is brought into focus by the medical mystery of a 44-year-old French father of two who found out one day that he had most of his brain missing. Instead his skull is mostly full of liquid, with almost no brain tissue left. He has a life-long condition known as hydrocephalus, commonly called “water on the brain” or “water head”. It happens when too much cerebrospinal fluid puts pressure on the brain and the brain’s cavities abnormally increase.

As Axel Cleeremans, a cognitive psychologist at the Université Libre in Brussels, who has lectured about this case, told CBC:

“He was living a normal life. He has a family. He works. His IQ was tested at the time of his complaint. This came out to be 84, which is slightly below the normal range … So, this person is not bright — but perfectly, socially apt”.

The complaint Cleeremans refers to is the original reason the man sought help – he had leg pain. Imagine that – you go to your doctor with a leg cramp and get told that you’re living without most of your brain.

The man continues to live a normal life, being a family man with a wife and kids, while working as a civil servant. All this while having 3 of his main brain cavities filled with only fluid and his brainstem and cerebellum stuck into a small space that they share with a cyst.

What can we learn from this rare case? As Cleeremans points out:

“One of the lessons is that plasticity is probably more pervasive than we thought it was… It is truly incredible that the brain can continue to function, more or less, within the normal range — with probably many fewer neurons than in a typical brain. Second lesson perhaps, if you’re interested in consciousness — that is the manner in which the biological activity of the brain produces awareness… One idea that I’m defending is the idea that awareness depends on the brain’s ability to learn.”

The French man’s story really challenges the idea that consciousness arises in one part of the brain only. Current theories hold that the part of the brain called the thalamus is responsible for our self-awareness. A man living with most of his brain missing does not fit neatly into such hypotheses.

http://bigthink.com/paul-ratner/the-medical-mystery-of-a-man-living-with-90-of-his-brain-missing?utm_source=Big+Think+Weekly+Newsletter+Subscribers&utm_campaign=709f2481ff-Newsletter_072016&utm_medium=email&utm_term=0_6d098f42ff-709f2481ff-41106061

Scientists May Have Discovered What Causes Migraines and a Path toward a Cure

by Philip Perry

Those who get migraines know how painful and debilitating they can be. In extreme cases, they can take you out of commission for days. One in seven suffer from them, making migraines the third most common illness in the world. Symptoms include a pounding headache, sometimes on one side of the head, nausea, vomiting, and sensitivity to light and sound.

A laundry list of causes and triggers have been implicated including genetics, eating certain foods, lack of sleep, hormonal changes, neurological issues, and much more. Though there have been lots of indicators, medical science has been stumped as to what causes them, which has made the development of new therapies difficult. Now, according to a group of scientists at the International Headache Genetics Consortium (IHGC), the cause has most likely been discovered. It all has to do with blood flow. Specifically, blood vessels within the brain becoming restricted may be what causes migraines.

There has been a long running debate as to whether migraines are caused by a neurological problem or a vascular one—having to do with circulation. This study, published in the journal Nature Genetics, is likely to put the controversy to rest, and help researchers develop novel approaches to treat the condition. 59,674 migraine sufferers and 316,078 controls, or those who didn’t get the headaches, participated. They hailed from 12 different countries. All participants were part of previous studies, where they had their DNA or genome scanned.


The part of the brain where migraines originate.

Researchers identified 38 specific genes or loci tied to migraines, 28 of which had never been implicated before. What’s interesting is these same genes are associated with other forms of illness, all in the realm of vascular disease. Due to this, researchers believe blood vessel problems are at the heart of migraines.

Aarno Palotie is the leader of the IHGC. He is also associated with the Center for Human Genome Research at Massachusetts General Hospital, in Boston, and at the Broad Institute of MIT and Harvard. Palotie hailed the discovery. He also said the IHGC’s approach was necessary in achieving it. “Because all of these variants modify the disease risk only slightly, the effect could only be seen when this large amount of samples became available.” Migraines have been difficult to treat. Symptoms and severity run the spectrum, and drugs effective in some patients, have been less potent, or even ineffective in others. Now, researchers have a place to start for developing new drugs, which must somehow target the “regulation of vascular tone.” John-Anker Zwart is another member of IHGC. He hails from the Oslo University Hospital in Norway.

Zwart said, “These genetic findings are the first concrete step towards developing personalized, evidence-based treatments for this very complex disease.” He added, “In the future, we hope this information can be utilized in dividing the patients into different genetic susceptibility groups for clinical drug trials, thus increasing the chances of identifying the best possible treatment for each subgroup.”

Previous studies implicated brain tissue genes. But researchers here say that those studies may not have used enough tissue samples. Another neurological theory was that it had something to do with ion channels in the central nervous system (CNS). This was thought to be an area that warranted more study, until now.

The authors of the IHGC study say that the widespread sharing of data played a critical role in this discovery. Palotie said, “We simply can’t overstate the importance of international collaboration when studying genetics of complex, common diseases.” More studies will now be conducted to understand the pathogenesis or development of migraines and what role each gene plays, in order to find entryways suitable for therapeutic intervention.

http://bigthink.com/philip-perry/scientists-discover-the-cause-of-migraines-and-a-path-toward-a-cure?utm_source=Big+Think+Weekly+Newsletter+Subscribers&utm_campaign=709f2481ff-Newsletter_072016&utm_medium=email&utm_term=0_6d098f42ff-709f2481ff-41106061

The risk of everlasting consequences if our brains don’t get adequate stimulation in our early years

by Bahar Golipour

What is the earliest memory you have?

Most people can’t remember anything that happened to them or around them in their toddlerhood. The phenomenon, called childhood amnesia, has long puzzled scientists. Some have debated that we forget because the young brain hasn’t fully developed the ability to store memories. Others argue it is because the fast-growing brain is rewiring itself so much that it overwrites what it’s already registered.

New research that appears in Nature Neuroscience this week suggests that those memories are not forgotten. The study shows that when juvenile rats have an experience during this infantile amnesia period, the memory of that experience is not lost. Instead, it is stored as a “latent memory trace” for a long time. If something later reminds them of the original experience, the memory trace reemerges as a full blown, long-lasting memory.

Taking a (rather huge) leap from rats to humans, this could explain how early life experiences that you don’t remember still shape your personality; how growing up in a rich environment makes you a smarter person and how early trauma puts you at higher risk for mental health problems later on.

Scientists don’t know whether we can access those memories. But the new study shows childhood amnesia coincides with a critical time for the brain ― specifically the hippocampus, a seahorse-shaped brain structure crucial for memory and learning. Childhood amnesia corresponds to the time that your brain matures and new experiences fuel the growth of the hippocampus.

In humans, this period occurs before pre-school, likely between the ages 2 and 4. During this time, a child’s brain needs adequate stimulation (mostly from healthy social interactions) so it can better develop the ability to learn.

And not getting enough healthy mental activation during this period may impede the development of a brain’s learning and memory centers in a way that it cannot be compensated later.

“What our findings tell us is that children’s brains need to get enough and healthy activation even before they enter pre-school,” said study leader Cristina Alberini, a professor at New York University’s Center for Neural Science. “Without this, the neurological system runs the risk of not properly developing learning and memory functions.”

The findings may illustrate one mechanism that could in part explain scientific research that shows poverty can shrink children’s brains.

Extensive research spanning decades has shown that low socioeconomic status is linked to problems with cognitive abilities, higher risk for mental health issues and poorer performance in school. In recent years, psychologists and neuroscientists have found that the brain’s anatomy may look different in poor children. Poverty is also linked to smaller brain surface area and smaller volume of the white matter connecting brain areas, as well as smaller hippocampus. And a 2015 study found that the differences in brain development explain up to 20 percent of academic performance gap between children from high- and low-income families.

Critical Periods

For the brain, the first few years of life set the stage for the rest of life.

Even though the nervous system keeps some of its ability to rewire throughout life, several biochemical events that shape its core structure happen only at certain times. During these critical periods of the developmental stages, the brain is acutely sensitive to new sights, sounds, experiences and external stimulation.

Critical periods are best studied in the visual system. In the 1960s, scientists David Hubel and Torsten Wiesel showed that if they close one eye of a kitten from birth for just for a few months, its brain never learns to see properly. The neurons in the visual areas of the brain would lose their ability respond to the deprived eye. Adult cats treated the same way don’t show this effect, which demonstrates the importance of critical periods in brain development for proper functioning. This finding was part of the pioneering work that earned Hubel and Wiesel the 1981 Nobel Prize in Physiology or Medicine.

In the new study in rats, the team shows that a similar critical period may be happening to the hippocampus.

Alberini and her colleagues took a close look at what exactly happens in the brain of rats in their first 17 days of life (equivalent to the first three years of a human’s life). They created a memory for the rodents of a negative experience: every time the animals entered a specific corner of their cage, they received a mildly painful shock to their foot. Young rats, like kids, aren’t great at remembering things that happened to them during their infantile amnesia. So although they avoided that corner right after the shock, they returned to it only a day later. In contrast, a group of older rats retained the memory and avoided this place for a long time.

However, the younger rats, had actually kept a trace of the memory. A reminder (such as another foot shock in another corner) was enough to resurrect the memory and make the animals avoid the first corner of the cage.

Researchers found a cascade of biochemical events in the young rats’ brains that are typically seen in developmental critical periods.

“We were excited to see the same type of mechanism in the hippocampus,” Alberini told The Huffington Post.

The Learning Brain And Its Mysteries

Just like the kittens’ brain needed light from the eyes to learn to see, the hippocampus may need novel experiences to learn to form memories.

“Early in life, while the brain cannot efficiently form long-term memories, it is ‘learning’ how to do so, making it possible to establish the abilities to memorize long-term,” Alberini said. “However, the brain needs stimulation through learning so that it can get in the practice of memory formation―without these experiences, the ability of the neurological system to learn will be impaired.”

This does not mean that you should put your kids in pre-pre-school, Alberini told HuffPost. Rather, it highlights the importance of healthy social interaction, especially with parents, and growing up in an environment rich in stimulation. Most kids in developed countries are already benefiting from this, she said.

But what does this all mean for children who grow up exposed to low levels of environmental stimulation, something more likely in poor families? Does it explain why poverty is linked to smaller brains? Alberini thinks many other factors likely contribute to the link between poverty and brain. But it is possible, she said, that low stimulation during the development of the hippocampus, too, plays a part.

Psychologist Seth Pollak of University of Wisconsin at Madison who has found children raised in poverty show differences in hippocampal development agrees.

Pollak believes the findings of the new study represent “an extremely plausible link between early childhood adversity and later problems.”

“We must always be cautious about generalizing studies of rodents to understanding human children,” Pollas added. “But the nonhuman animal studies, such as this one, provide testable hypotheses about specific mechanisms underlying human behavior.”

Although the link between poverty and cognitive performance has been repeatedly seen in numerous studies, scientists don’t have a good handle on how exactly many related factors unfold inside the developing brain, said Elizabeth Sowell, a researcher from the Children’s Hospital Los Angeles. Studies like this one provide “a lot of food for thought,” she added.

http://www.huffingtonpost.com.au/2016/07/24/the-things-you-dont-remember-shape-who-you-are/

Having a socially interactive job helps protect from Alzheimer’s disease.

By Patrick Foster

Lawyers, teachers and doctors have a better chance of fighting off the effects of Alzheimer’s disease, because of the complex nature of their jobs, scientists reported this week.

Researchers found that people whose jobs combined complex thinking with social engagement with others – such as social workers and engineers – were better protected against the onset of Alzheimer’s, compared to those in manual work.

The study came as another report suggested that people with a poor diet could protect themselves against cognitive decline by adopting a mentally stimulating lifestyle.

Both pieces of research, published at the international conference of the Alzheimer’s Association, in Toronto, examined the impact of complex thinking on the onset of the disease.

In the first study, carried out by scientists at the Alzheimer’s Disease Research Centre, in Wisconsin, researchers examined white matter hyperintensities (WMHs) – white spots that appear on brain scans and are associated with Alzheimer’s – in 284 late-middle-aged patients considered at risk of contracting the disease.

They found that people who worked primarily with other people, as opposed to with “things or data”, were less likely to be affected by brain damage indicated by WMHs.

While lawyers, social workers, teachers and doctors were best protected, those who enjoyed the least protection included shelf-stackers, machine operators and labourers.

Elizabeth Boots, a researcher on the project, said: “These findings indicate that participants with higher occupational complexity are able to withstand pathology associated with Alzheimer’s and cerebrovascular disease and perform at a similar cognitive level as their peers.

“This association is primarily driven by work with people, rather than data or things. These analyses underscore the importance of social engagement in the work setting for building resilience to Alzheimer’s disease.”

The second study, carried out by Baycrest Health Sciences, in Toronto, examined the diet of 351 older adults.

Researchers found that those who had a traditional Western diet of red and processed meat, white bread, potatoes and sweets were more likely to experience cognitive decline.

However, those who adhered to such a diet but who had a mentally stimulating lifestyle enjoyed some protection from such decline.

Dr Matthew Parrott, one member of the team, said: “Our results show the role higher educational attainment, mentally stimulating work and social engagement can play in protecting your brain from cognitive decline, counteracting some negative effects of an unhealthy diet.

“This adds to the growing body of evidence showing how various lifestyle factors may combine to increase or protect against vulnerability to Alzheimer’s disease.”

Other research put forward at the convention included a study showing that digital brain training exercises can help stave of Alzheimer’s, and another paper that suggested that some newly-identified genes may also increase resilience to the disease.

Maria C. Carrillo, the chief science officer at the Alzheimer’s Association, said: “These new data add to a growing body of research that suggests more stimulating lifestyles, including more complex work environments with other people, are associated with better cognitive outcomes in later life.

“As each new study emerges, we further understand just how powerful cognitive reserve can be in protecting the brain from disease. Formal education and complex occupation could potentially do more than just slow cognitive decline – they may actually help compensate for the cognitive damage done by bad diet and small vessel disease in the brain.

“It is becoming increasingly clear that in addition to searching for pharmacological treatments, we need to address lifestyle factors to better treat and ultimately prevent Alzheimer’s and other dementias.”

http://www.telegraph.co.uk/news/2016/07/24/stressful-job-it-might-help-you-fight-off-alzheimers/

How the eyes betray your thoughts

By Mo Costandi

It’s sometimes said that the eyes are windows into the soul, revealing deep emotions that we might otherwise want to hide. The eyes not only reflect what is happening in the brain but may also influence how we remember things and make decisions.

Our eyes are constantly moving, and while some of those movements are under conscious control, many of them occur subconsciously. When we read, for instance, we make a series of very quick eye movements called saccades that fixate rapidly on one word after another. When we enter a room, we make larger sweeping saccades as we gaze around. Then there are the small, involuntary eye movements we make as we walk, to compensate for the movement of our head and stabilise our view of the world. And, of course, our eyes dart around during the ‘rapid eye movement’ (REM) phase of sleep.

What is now becoming clear is that some of our eye movements may actually reveal our thought process.

Research published last year shows that pupil dilation is linked to the degree of uncertainty during decision-making: if somebody is less sure about their decision, they feel heightened arousal, which causes the pupils to dilate. This change in the eye may also reveal what a decision-maker is about to say: one group of researchers, for example, found that watching for dilation made it possible to predict when a cautious person used to saying ‘no’ was about to make the tricky decision to say ‘yes’.

Watching the eyes can even help predict what number a person has in mind. Tobias Loetscher and his colleagues at the University of Zurich recruited 12 volunteers and tracked their eye movements while they reeled off a list of 40 numbers.

They found that the direction and size of the participants’ eye movements accurately predicted whether the number they were about to say was bigger or smaller than the previous one – and by how much. Each volunteer’s gaze shifted up and to the right just before they said a bigger number, and down and to the left before a smaller one. The bigger the shift from one side to the other, the bigger the difference between the numbers.

This suggests that we somehow link abstract number representations in the brain with movement in space. But the study does not tell us which comes first: whether thinking of a particular number causes changes in eye position, or whether the eye position influences our mental activity. In 2013, researchers in Sweden published evidence that it’s the latter that may be at work: eye movements may actually facilitate memory retrieval.

They recruited 24 students and asked each one to carefully examine a series of objects displayed to them in one corner of a computer screen. The participants were then told to listen to a series of statements about some of the objects they had seen, such as “The car was facing to the left” and asked to indicate as quickly as possible if each was true or false. Some participants were allowed to let their eyes roam about freely; others were asked to fix their gaze on a cross at the centre of the screen, or the corner where the object had appeared, for example.

The researchers found that those who were allowed to move their eyes spontaneously during recall performed significantly better than those who fixed on the cross. Interestingly, though, participants who were told to fix their gaze in the corner of the screen in which objects had appeared earlier performed better than those told to fix their gaze in another corner. This suggests that the more closely the participants’ eye movements during information encoding corresponded with those that occurred during retrieval of the information, the better they were at remembering the objects. Perhaps that’s because eye movements help us to recall the spatial relationships between objects in the environment at the time of encoding.

These eye movements can occur unconsciously. “When people are looking at scenes they have encountered before, their eyes are frequently drawn to information they have already seen, even when they have no conscious memory of it,” says Roger Johansson, a psychologist at Lund University who led the study.

Watching eye movements can also be used to nudge people’s decisions. One recent study showed – maybe worryingly – that eye-tracking can be exploited to influence the moral decisions we take.

Researchers asked participants complex moral questions such as “Can murder ever be justified?” and then displayed, on a computer screen, alternative answers (“sometimes justifiable” or “never justifiable”). By tracking the participants’ eye movements, and removing the two answer options immediately after a participant had spent a certain amount of time gazing at one of the two options, the researchers found that they could nudge the participants to provide that particular option as their answer.

“We didn’t give them any more information,” says neuroscientist Daniel Richardson of University College London, senior author of study. “We simply waited for their own decision-making processes to unfold and interrupted them at exactly the right point. We made them change their minds just by controlling when they made the decision.”

Richardson adds that successful salespeople may have some insight into this, and use it to be more persuasive with clients. “We think of persuasive people as good talkers, but maybe they’re also observing the decision-making process,” he says. “Maybe good salespeople can spot the exact moment you’re wavering towards a certain choice, and then offer you a discount or change their pitch.”

The ubiquity of eye-tracking apps for smartphones and other hand-held devices raises the possibility of altering people’s decision-making process remotely. “If you’re shopping online, they might bias your decision by offering free shipping at the moment you shift your gaze to a particular product.”

Thus, eye movements can both reflect and influence higher mental functions such as memory and decision-making, and betray our thoughts, beliefs, and desires. This knowledge may give us ways of improving our mental functions – but it also leaves us vulnerable to subtle manipulation by other people.

“The eyes are like a window into our thought processes, and we just don’t appreciate how much information might be leaking out of them,” says Richardson. “They could potentially reveal things that a person might want to suppress, such as implicit racial bias.”

“I can see eye-tracking apps being used for, say, supportive technologies that figure out what phone function you need and then help out,” he adds, “but if they’re left on all the time they could be used to track all sorts of other things. This would provide much richer information, and raises the possibility of unwittingly sharing our thoughts with others.”

http://www.bbc.com/future/story/20150521-how-the-eyes-betray-your-thoughts

Mystery of what sleep does to our brains may finally be solved

By Clare Wilson

It is one of life’s great enigmas: why do we sleep? Now we have the best evidence yet of what sleep is for – allowing housekeeping processes to take place that stop our brains becoming overloaded with new memories.

All animals studied so far have been found to sleep, but the reason for their slumber has eluded us. When lab rats are deprived of sleep, they die within a month, and when people go for a few days without sleeping, they start to hallucinate and may have epileptic seizures.

One idea is that sleep helps us consolidate new memories, as people do better in tests if they get a chance to sleep after learning. We know that, while awake, fresh memories are recorded by reinforcing connections between brain cells, but the memory processes that take place while we sleep have remained unclear.

Support is growing for a theory that sleep evolved so that connections in the brain can be pruned down during slumber, making room for fresh memories to form the next day. “Sleep is the price we pay for learning,” says Giulio Tononi of the University of Wisconsin-Madison, who developed the idea.

Now we have the most direct evidence yet that he’s right. Tononi’s team measured the size of these connections or synapses in brain slices taken from mice. The synapses in samples taken at the end of a period of sleep were 18 per cent smaller than those in samples taken from before sleep, showing that the synapses between neurons are weakened during slumber.

A good night’s sleep

Tononi announced these findings at the Federation of European Neuroscience Societies meeting in Copenhagen, Denmark, last week. “The data was very solid and well documented,” says Maiken Nedergaard of the University of Rochester, who attended the conference.

“It’s an extremely elegant idea,” says Vladyslav Vyazovskiy of the University of Oxford

If the housekeeping theory is right, it would explain why, when we miss a night’s sleep, the next day we find it harder to concentrate and learn new information – we may have less capacity to encode new experiences. The finding suggests that, as well as it being important to get a good night’s sleep after learning something, we should also try to sleep well the night before.

It could also explain why, if our sleep is interrupted, we feel less refreshed the next day. There is some indirect evidence that deep, slow-wave sleep is best for pruning back synapses, and it takes time for our brains to reach this level of unconsciousness.

Waking refreshed

Previous evidence has also supported the housekeeping theory. For instance, EEG recordings show that the human brain is less electrically responsive at the start of the day – after a good night’s sleep – than at the end, suggesting that the connections may be weaker. And in rats, the levels of a molecule called the AMPA receptor – which is involved in the functioning of synapses – are lower at the start of their wake periods.

The latest brain-slice findings that synapses get smaller is the most direct evidence yet that the housekeeping theory is right, says Vyazovskiy. “Structural evidence is very important,” he says. “That’s much less affected by other confounding factors.”

Protecting what matters

Getting this data was a Herculean task, says Tononi. They collected tiny chunks of brain tissue, sliced it into ultrathin sections and used these to create 3D models of the brain tissue to identify the synapses. As there were nearly 7000 synapses, it took seven researchers four years.

The team did not know which mouse was which until last month, says Tononi, when they broke the identification code, and found their theory stood up.

“People had been working for years to count these things. You start having stress about whether it’s really possible for all these synapses to start getting fatter and then thin again,” says Tononi.

The team also discovered that some synapses seem to be protected – the biggest fifth stayed the same size. It’s as if the brain is preserving its most important memories, says Tononi. “You keep what matters.”

https://www.newscientist.com/article/2096921-mystery-of-what-sleep-does-to-our-brains-may-finally-be-solved/