Study Finds Pedophiles’ Brains Wired to Find Children Attractive

Pedophiles’ brains are “abnormally tuned” to find young children attractive, according to a new study published this week. The research, led by Jorge Ponseti at Germany’s University of Kiel, means that it may be possible to diagnose pedophiles in the future before they are able to offend.

The findings, published in scientific journal Biology Letters, discovered that pedophiles have the same neurological reaction to images of those they find attractive as those of people with ordinary sexual predilections, but that all the relevant cerebral areas become engaged when they see children, as opposed to fellow adults. The occipital areas, prefrontal cortex, putamen, and nucleus caudatus become engaged whenever a person finds another attractive, but the subject of this desire is inverted for pedophiles.

While studies into the cognitive wiring of sex offenders have long been a source of debate, this latest research offers some fairly conclusive proof that there is a neural pattern behind their behavior.

The paper explains: “The human brain contains networks that are tuned to face processing, and these networks appear to activate different processing streams of the reproductive domain selectively: nurturing processing in the case of child faces and sexual processing in the case of sexually preferred adult faces. This implies that the brain extracts age-related face cues of the preferred sex that inform appropriate response selection in the reproductive domains: nurturing in the case of child faces and mating in the case of adult faces.”

Usually children’s faces elicit feelings of caregiving from both sexes, whereas those of adults provide stimuli in choosing a mate. But among pedophiles, this trend is skewed, with sexual, as opposed to nurturing, emotions burgeoning.

The study analyzed the MRI scans of 56 male participants, a group that included 13 homosexual pedophiles and 11 heterosexual pedophiles, exposing them to “high arousing” images of men, women, boys, and girls. Participants then ranked each photo for attractiveness, leading researchers to their conclusion that the brain network of pedophiles is activated by sexual immaturity.

The critical new finding is that face processing is also tuned to face cues revealing the developmental stage that is sexually preferred,” the paper reads.

Dr. James Cantor, associate professor at the University of Toronto’s Faculty of Medicine, said he was “delighted” by the study’s results. “I have previously described pedophilia as a ‘cross-wiring’ of sexual and nurturing instincts, and this data neatly verifies that interpretation.”

Cantor has undertaken extensive research into the area, previously finding that pedophiles are more likely to be left-handed, 2.3 cm shorter than the average male, and 10 to 15 IQ points lower than the norm.

He continued: “This [new] study is definitely a step in the right direction, and I hope other researchers repeat this kind of work. There still exist many contradictions among scientists’ observations, especially in identifying exactly which areas of the brain are the most central to pedophilia. Because financial support for these kinds of studies is quite small, these studies have been quite small, permitting them to achieve only incremental progress. Truly definitive studies about what in the brain causes pedophilia, what might detect it, and what might prevent it require much more significant support.”

Ponseti said that he hoped to investigate this area further by examining whether findings could be emulated when images of children’s faces are the sole ones used. This could lead to gauging a person’s predisposition to pedophilia far more simply than any means currently in place. “We could start to look at the onset of pedophilia, which is probably in puberty at about 12 or 14 years [old],” he told The Independent.

While Cantor is correct in citing the less than abundant size of the study, the research is certainly significant in providing scope for future practicable testing that could reduce the number of pedophilic crimes committed. By being able to run these tests and examine a person’s tendency toward being sexually attracted to underage children, rehabilitative care and necessary precautions could be taken to safeguard children and ensure that those at risk of committing a crime of this ilk would not be able to do so.

http://www.thedailybeast.com/articles/2014/05/23/study-finds-pedophiles-brains-wired-to-find-children-attractive.html#

New research shows molecular mechanism by which neuronal projections can regenerate after injury

The mechanisms that drive axon regeneration after central nervous system (CNS) injury or disease are proposed to recapitulate, at least in part, the developmental axon growth pathways. This hypothesis is bolstered by a new study by O’Donovan et al. showing that activation of a B-RAF kinase signaling pathway is sufficient to promote robust axon growth not only during development but also after injury.

B-RAF was previously shown to be essential for developmental axon growth but it was not known if additional signaling pathways are required. In this study, the authors demonstrate that activation of B-RAF alone is sufficient to promote sensory axon growth during development. Using a conditional B-RAF gain-of-function mouse model, the authors elegantly prove that B-RAF has a cell-autonomous role in the developmental axon growth program. Notably, activated B-RAF promoted overgrowth of embryonic sensory axons projecting centrally in the spinal cord, suggesting that this pathway may normally be quiescent in central axons.

Could activated B-RAF also enhance axon regeneration in the adult central nervous system? The authors found that activated B-RAF not only enabled sensory axon growth into the spinal cord after spinal injury, but also promoted regrowth of axons projecting in the optic nerve. Regeneration in the injured CNS is prevented by both the poor intrinsic regrowth capacity of axons and by inhibitory factors in the tissue environment. Importantly, the B-RAF–activated signaling growth program was insensitive to this repulsive environment.

Interestingly, the authors find that B-RAF synergizes with the PI3-kinase–mTOR pathway, which also functions downstream of growth factors. This opens the possibility that combinatorial approaches that integrate these two pathways may heighten regenerative capacity.

This in vivo study significantly advances the understanding of the role of MAP kinases in axon growth and suggests that reactivation of the B-RAF pathway may be exploited to promote axon regeneration in the injured central nervous system. An exciting future avenue will be to determine the downstream mechanisms controlled by B-RAF.

O’Donovan, K.J., et al. 2014. J. Exp. Med. doi:10.1084/jem.20131780.

http://jem.rupress.org/content/211/5/746.1.long

Using botox to treat depression

Nearly 150 years ago, Charles Darwin recognized that facial expressions not only communicate the emotions we feel but intensify them, by sending cues back to the brain. In the ensuing decades, researchers proved again and again that we can influence the way we feel by the visage we project. Smiling can help us feel happier. Frowning can make us feel angrier.

But it was only in the past few years that a dermatologist from Chevy Chase, Md., noticed that some of the patients whose brows he temporarily paralyzed with Botox, to remove wrinkles, began to feel relief from depression. That physician, Eric Finzi, took his idea to psychiatrist, Norman Rosenthal, who teaches at Georgetown Medical School and had spent many years studying how light and odors, transmitted to the brain through the nerves that connect it with the eyes and nose, affect our moods.

Now there have been three small studies that show that Botox injections can help with depression. In the latest, published in the current issue of the Journal of Psychiatric Research, Finzi and Rosenthal showed that 17 of 33 patients experienced better than 50 percent reductions in their depression symptoms after a single Botox injection, and 27 percent of the group saw their depression go into remission. The study confirms a similar one reported in 2012 by German researchers Tillmann Kroger and Axel Wollmer, who spoke of their findings at a meeting of the American Psychiatric Association in New York this past weekend.

“There are several nerves, about 12 of them, that go straight into the brain through the skull,” Rosenthal told me Tuesday. “…We’re used to thinking of them in terms of their outbound messages or signals. We’re not used to thinking of them in terms of their inbound messages.”

The idea holds promise as a supplement or alternative to anti-depressants and psychotherapy for treating depression, according to Rosenthal. Minuscule amounts of Botox — which is made from the lethal botulinum toxin — are injected into the facial muscles and don’t even enter the bloodstream. The procedure has shown no side-effects.

If the whole idea seems almost too outlandish to believe — as it did for me — Rosenthal was quick to point out that he was laughed at 30 years ago, when he proposed the idea of “seasonal affective disorder” and the notion that exposing people to bright light in the depths of winter could help with that kind of depression. “Now, it’s ubiquitous,” he said. “Then, they thought it was ridiculous.”

The treatment isn’t perfect. Botox is expensive, at about $400 per dose, wears off in about three months and isn’t covered by insurance. And as the studies showed, it doesn’t work for everyone.

But the botulinum toxin already is used to treat a wide variety of medical conditions. Perhaps depression is next.

http://www.washingtonpost.com/news/to-your-health/wp/2014/05/07/using-botox-to-treat-depression-seriously/

Psychopaths: how can you spot one?

There are a few things we take for granted in social interactions with people. We presume that we see the world in roughly the same way, that we all know certain basic facts, that words mean the same things to you as they do to me. And we assume that we have pretty similar ideas of right and wrong.

But for a small – but not that small – subset of the population, things are very different. These people lack remorse and empathy and feel emotion only shallowly. In extreme cases, they might not care whether you live or die. These people are called psychopaths. Some of them are violent criminals, murderers. But by no means all.

Professor Robert Hare is a criminal psychologist, and the creator of the PCL-R, a psychological assessment used to determine whether someone is a psychopath. For decades, he has studied people with psychopathy, and worked with them, in prisons and elsewhere. “It stuns me, as much as it did when I started 40 years ago, that it is possible to have people who are so emotionally disconnected that they can function as if other people are objects to be manipulated and destroyed without any concern,” he says.

Our understanding of the brain is still in its infancy, and it’s not so many decades since psychological disorders were seen as character failings. Slowly we are learning to think of mental illnesses as illnesses, like kidney disease or liver failure, and developmental disorders, such as autism, in a similar way. Psychopathy challenges this view. “A high-scoring psychopath views the world in a very different way,” says Hare. “It’s like colour-blind people trying to understand the colour red, but in this case ‘red’ is other people’s emotions.”

At heart, Hare’s test is simple: a list of 20 criteria, each given a score of 0 (if it doesn’t apply to the person), 1 (if it partially applies) or 2 (if it fully applies). The list in full is: glibness and superficial charm, grandiose sense of self-worth, pathological lying, cunning/manipulative, lack of remorse, emotional shallowness, callousness and lack of empathy, unwillingness to accept responsibility for actions, a tendency to boredom, a parasitic lifestyle, a lack of realistic long-term goals, impulsivity, irresponsibility, lack of behavioural control, behavioural problems in early life, juvenile delinquency, criminal versatility, a history of “revocation of conditional release” (ie broken parole), multiple marriages, and promiscuous sexual behaviour. A pure, prototypical psychopath would score 40. A score of 30 or more qualifies for a diagnosis of psychopathy. Hare says: “A friend of mine, a psychiatrist, once said: ‘Bob, when I meet someone who scores 35 or 36, I know these people really are different.’ The ones we consider to be alien are the ones at the upper end.”

But is psychopathy a disorder – or a different way of being? Anyone reading the list above will spot a few criteria familiar from people they know. On average, someone with no criminal convictions scores 5. “It’s dimensional,” says Hare. “There are people who are part-way up the scale, high enough to warrant an assessment for psychopathy, but not high enough up to cause problems. Often they’re our friends, they’re fun to be around. They might take advantage of us now and then, but usually it’s subtle and they’re able to talk their way around it.” Like autism, a condition which we think of as a spectrum, “psycho­pathy”, the diagnosis, bleeds into normalcy.

We think of psychopaths as killers, criminals, outside society. People such as Joanna Dennehy, a 31-year-old British woman who killed three men in 2013 and who the year before had been diagnosed with a psychopathic personality disorder, or Ted Bundy, the American serial killer who is believed to have murdered at least 30 people and who said of himself: “I’m the most cold-blooded son of a bitch you’ll ever meet. I just liked to kill.” But many psychopathic traits aren’t necessarily disadvantages – and might, in certain circumstances, be an advantage. For their co-authored book, “Snakes in suits: When Psychopaths go to work”, Hare and another researcher, Paul Babiak, looked at 203 corporate professionals and found about four per cent scored sufficiently highly on the PCL-R to be evaluated for psychopathy. Hare says that this wasn’t a proper random sample (claims that “10 per cent of financial executives” are psychopaths are certainly false) but it’s easy to see how a lack of moral scruples and indifference to other people’s suffering could be beneficial if you want to get ahead in business.

“There are two kinds of empathy,” says James Fallon, a neuroscientist at the University of California and author of The Psychopath Inside: A Neuroscientist’s Personal Journey into the Dark Side of the Brain. “Cognitive empathy is the ability to know what other people are feeling, and emotional empathy is the kind where you feel what they’re feeling.” Autistic people can be very empathetic – they feel other people’s pain – but are less able to recognise the cues we read easily, the smiles and frowns that tell us what someone is thinking. Psychopaths are often the opposite: they know what you’re feeling, but don’t feel it themselves. “This all gives certain psychopaths a great advantage, because they can understand what you’re thinking, it’s just that they don’t care, so they can use you against yourself.” (Chillingly, psychopaths are particularly adept at detecting vulnerability. A 2008 study that asked participants to remember virtual characters found that those who scored highly for psychopathy had a near perfect recognition for sad, unsuccessful females, but impaired memory for other characters.)

Fallon himself is a case in point. In 2005, he was looking at brain scans of psychopathic murderers, while on another study, of Alzheimer’s, he was using scans of his own family’s brains as controls. In the latter pile, he found something strange. “You can’t tell just from a brain scan whether someone’s a psychopath,” he says, “but you can make a good guess at the personality traits they’ll have.” He describes a great loop that starts in the front of the brain including the parahippocampal gyrus and the amygdala and other regions tied to emotion and impulse control and empathy. Under certain circumstances they would light up dramatically on a normal person’s MRI scan, but would be darker on a psychopath’s.

“I saw one that was extremely abnormal, and I thought this is someone who’s way off. It looked like the murderers I’d been looking at,” he says. He broke the anonymisation code in case it had been put into the wrong pile. When he did, he discovered it was his own brain. “I kind of blew it off,” he says. “But later, some psychiatrist friends of mine went through my behaviours, and they said, actually, you’re probably a borderline psychopath.”

Speaking to him is a strange experience; he barely draws breath in an hour, in which I ask perhaps three questions. He explains how he has frequently put his family in danger, exposing his brother to the deadly Marburg virus and taking his son trout-fishing in the African countryside knowing there were lions around. And in his youth, “if I was confronted by authority – if I stole a car, made pipe bombs, started fires – when we got caught by the police I showed no emotion, no anxiety”. Yet he is highly successful, driven to win. He tells me things most people would be uncomfortable saying: that his wife says she’s married to a “fun-loving, happy-go-lucky nice guy” on the one hand, and a “very dark character who she does not like” on the other. He’s pleasant, and funny, if self-absorbed, but I can’t help but think about the criteria in Hare’s PCL-R: superficial charm, lack of emotional depth, grandiose sense of self-worth. “I look like hell now, Tom,” he says – he’s 66 – “but growing up I was good-looking, six foot, 180lb, athletic, smart, funny, popular.” (Hare warns against non-professionals trying to diagnose people using his test, by the way.)

“Psychopaths do think they’re more rational than other people, that this isn’t a deficit,” says Hare. “I met one offender who was certainly a psychopath who said ‘My problem is that according to psychiatrists I think more with my head than my heart. What am I supposed to do about that? Am I supposed to get all teary-eyed?’ ” Another, asked if he had any regrets about stabbing a robbery victim, replied: “Get real! He spends a few months in hospital and I rot here. If I wanted to kill him I would have slit his throat. That’s the kind of guy I am; I gave him a break.”

And yet, as Hare points out, when you’re talking about people who aren’t criminals, who might be successful in life, it’s difficult to categorise it as a disorder. “It’d be pretty hard for me to go into high-level political or economic or academic context and pick out all the most successful people and say, ‘Look, I think you’ve got some brain deficit.’ One of my inmates said that his problem was that he’s a cat in a world of mice. If you compare the brainwave activity of a cat and a mouse, you’d find they were quite different.”

It would, says Hare, probably have been an evolutionarily successful strategy for many of our ancestors, and can be successful today; adept at manipulating people, a psychopath can enter a community, “like a church or a cultural organisation, saying, ‘I believe the same things you do’, but of course what we have is really a cat pretending to be a mouse, and suddenly all the money’s gone”. At this point he floats the name Bernie Madoff.

This brings up the issue of treatment. “Psychopathy is probably the most pleasant-feeling of all the mental disorders,” says the journalist Jon Ronson, whose book, The Psychopath Test, explored the concept of psychopathy and the mental health industry in general. “All of the things that keep you good, morally good, are painful things: guilt, remorse, empathy.” Fallon agrees: “Psychopaths can work very quickly, and can have an apparent IQ higher than it really is, because they’re not inhibited by moral concerns.”

So psychopaths often welcome their condition, and “treating” them becomes complicated. “How many psychopaths go to a psychiatrist for mental distress, unless they’re in prison? It doesn’t happen,” says Hare. The ones in prison, of course, are often required to go to “talk therapy, empathy training, or talk to the family of the victims” – but since psychopaths don’t have any empathy, it doesn’t work. “What you want to do is say, ‘Look, it’s in your own self-interest to change your behaviour, otherwise you’ll stay in prison for quite a while.’ ”

It seems Hare’s message has got through to the UK Department of Justice: in its guidelines for working with personality-disordered inmates, it advises that while “highly psychopathic individuals” are likely to be “highly treatment resistant”, the “interventions most likely to be effective are those which focus on ‘self-interest’ – what the offender wants out of life – and work with them to develop the skills to get those things in a pro-social rather than anti-social way.”

If someone’s brain lacks the moral niceties the rest of us take for granted, they obviously can’t do anything about that, any more than a colour-blind person can start seeing colour. So where does this leave the concept of moral responsibility? “The legal system traditionally asserts that all people standing in front of the judge’s bench are equal. That’s demonstrably false,” says the neuroscientist David Eagleman, author of Incognito: The Secret Lives of the Brain. He suggests that instead of thinking in terms of blameworthiness, the law should deal with the likelihood that someone will reoffend, and issue sentences accordingly, with rehabilitation for those likely to benefit and long sentences for those likely to be long-term dangers. The PCL-R is already used as part of algorithms which categorise people in terms of their recidivism risk. “Life insurance companies do exactly this sort of thing, in actuarial tables, where they ask: ‘What age do we think he’s going to die?’ No one’s pretending they know exactly when we’re going to die. But they can make rough guesses which make for an enormously more efficient system.”

What this doesn’t mean, he says, is a situation like the sci-fi film Minority Report, in which people who are likely to commit crimes are locked up before they actually do. “Here’s why,” he says. “It’s because many people in the population have high levels of psychopathy – about 1 per cent. But not all of them become criminals. In fact many of them, because of their glibness and charm and willingness to ride roughshod over the people in their way, become quite successful. They become CEOs, professional athletes, soldiers. These people are revered for their courage and their straight talk and their willingness to crush obstacles in their way. Merely having psychopathy doesn’t tell us that a person will go off and commit a crime.” It is central to the justice system, both in Britain and America, that you can’t pre-emptively punish someone. And that won’t ever change, says Eagleman, not just for moral, philosophical reasons, but for practical ones. The Minority Report scenario is a fantasy, because “it’s impossible to predict what somebody will do, even given their personality type and everything, because life is complicated and crime is conceptual. Once someone has committed a crime, once someone has stepped over a societal boundary, then there’s a lot more statistical power about what they’re likely to do in future. But until that’s happened, you can’t ever know.”

Speaking to all these experts, I notice they all talk about psychopaths as “them”, almost as a different species, although they make conscious efforts not to. There’s something uniquely troubling about a person who lacks emotion and empathy; it’s the stuff of changeling stories, the Midwich Cuckoos, Hannibal Lecter. “You know kids who use a magnifying glass to burn ants, thinking, this is interesting,” says Hare. “Translate that to an adult psychopath who treats a person that way. It is chilling.” At one stage Ronson suggests I speak to another well-known self-described psychopath, a woman, but I can’t bring myself to. I find the idea unsettling, as if he’d suggested I commune with the dead.

http://www.telegraph.co.uk/culture/books/10737827/Psychopaths-how-can-you-spot-one.html

Thanks to Steven Weihing for bringing this to the attention of the It’s Interesting community.

What I’ve Learned: Sol Snyder


Sol Snyder, Distinguished Service Professor of Neuroscience, Pharmacology and Psychiatry, School of Medicine

Growing up, I never had any strong interest in science. I did well in lots of things in high school. I liked reading philosophy and things like that, but being a philosopher is not a fit job for a nice Jewish boy.

This was in the mid-1950s, and many of my friends were going into engineering, preparatory to joining the then prominent military industrial complex. Others were going to be doctors, so I got the idea that maybe I’d be a psychiatrist. I didn’t have any special affinity for medicine or desire to cast out the lepers or heal mankind.

I was always reading things. My father valued education. He wasn’t a big advice giver, but he … had a lot of integrity. What was important to him was doing the right thing. And he had great respect for the intellectual life and science.

My father’s professional life commenced in 1935 as the 10th employee of what became the NSA. He led a team that broke one of the principal Japanese codes. At the end of World War II, computers were invented, and, if you think about it, what could be the best entity to take advantage of computers than NSA, with its mission of sorting gibberish and looking for patterns. So my father was assigned to look at these new machines and see if they would be helpful. He led the computer installations at NSA.

Summers in college I worked in the NSA. My father taught me to program computers in machine language. Computers were a big influence on me.

I learned at the NSA about keeping secrets. What is top secret, what is need-to-know—that is one of the things you learn in the business. You don’t talk to the guy at the next desk even if you’re working on the same project. If that person doesn’t need to know, you just shut up.

In medical school, I started working at the NIH in Bethesda during the summers and elective periods, largely because the only thing I really did well up to that time was play the classical guitar and one of my guitar students was an NIH researcher. In high school I thought I might go the conservatory route, but that’s even less fitting for a nice Jewish boy than being a philosopher.

It was through my contacts at NIH that I was able to get a position working with future Nobel Prize winner Julius Axelrod. Julie was a wonderful mentor who did research on drugs and neurotransmitters. Working with him was inspirational. I just adored it.

What was notable about Julie was his great creativity, always coming up with original ideas. Even though he was an eminent scientist, he didn’t have a regular office. He just had a desk in a lab. He did experiments with his own two hands every day.

Philosophically, Julie emphasized you go where the data takes you. Don’t worry that you’re an expert in enzyme X and so should focus on that. If the data point to enzyme Y, go for it. Do what’s exciting.

My very first project with Julie was studying the disposition of histamine. I thought I had found that histamine had been converted into a novel product that looked really interesting, and I was wrong. I missed the true product because we separated the chemicals on paper and discarded the radioactivity at the bottom, throwing away the real McCoy. Another lab at Yale found it, led, remarkably, by a close friend since kindergarten. My humiliation didn’t last very long. I learned not to be so sloppy, to take greater care, and, most important, to explore peculiar results.

How does one pick research directions? You can go where it’s “hot,” but there you’re competing with 300 other people, and everyone can make only incremental changes. But if you follow Julie Axelrod’s rules and you don’t worry about what’s hot, or what other people are doing—just go where your data are taking you—then you have a better chance of finding something that nobody else had found before.

With the discovery of the opiate receptor, I was fortunate to launch a new field: molecular identification of neurotransmitter receptors. Later we discovered that the gas nitrous oxide is a neurotransmitter.

I’m a klutz. I can’t hammer a nail. So for the technical side, like dissecting brains to look at different regions, I enlisted friends. I learned to collaborate, a key element in so many discoveries.

Johns Hopkins has always been a collegial place. People are just friendly and interact with each other. This tradition goes back to the founding of the medical school, permeating the school’s governance as well as research. We tend to be more productive than faculty at other schools, where one gets ahead by sticking an ice pick in the backs of colleagues.

One of my heroes was my guitar teacher, Sophocles Papas, Andrés Segovia’s best friend. Sophocles was an important influence in my life, and we stayed close until he died in his 90s. In a couple of years after commencing lessons, I was giving recitals, all thanks to him. Like Julie, Sophocles emphasized innovative short cuts to creativity.

I’ve remained involved with music. I’m the longest-serving trustee on the Baltimore Symphony Orchestra, chairing for many years its music committee. Trustees of arts organizations are typically businesspeople selected for their fundraising acumen. But the person who nominated me reportedly commented, I’d like to propose something radical: I’d like to propose a trustee who cares about music.

Most notable about psychiatry is that the major drugs—antipsychotics for schizophrenia, antidepressants, and anti-anxiety drugs—were all discovered in the mid-1950s. Subsequent tweaking has enhanced potency and diminished side effects, but there have been no major breakthroughs. No new class of drugs since 1958—rather frustrating.

As biomedical science advances, especially with the dawn of molecular biology, our power to innovate is just dazzling. Today’s students take all of this for granted, but those of us who have been doing research for several decades are daily amazed by our abilities to probe the mysteries of life.

The logic of nature is elegant and straightforward. The more we learn about how the body works, the more we are amazed by its beauty and inherent simplicity.

One of my pet peeves is that the very power of modern science leads journal and grant reviewers to expect every “i” dotted and every “t” crossed. Because of this, four years or more of work go into each scientific manuscript. Then, editors and reviewers of journals are so picayune that revising a paper consumes another year.

Now let’s consider the poor post­doctoral fellow or graduate student. To move forward in his or her career requires at least one major publication—a five-year enterprise. If you only have one shot on goal, one paper in five years, your chances of success shrivel. The duration of PhD training and postdoctoral training is getting so long that from the entry point at graduate school to the time you’re out looking for a job as an assistant professor is easily 12, 15 years. Well, that is ridiculous. If you got paid $10 million at the end of this road, that would be one thing, but scientists earn less than most other professionals. We’re deterring the young smart people from going into science.

Biomedical researchers don’t work in a vacuum. They work with grad students and postdoctoral fellows, so being a good mentor is key to being a good scientist. Keep your students well motivated and happy. Have them feel that they are good human beings, and they will do better science.

The most important thing is that you value the integrity of each person. I ask my students all the time, What do you think? And this discussion turns into minor league psychotherapy. Ah, you think that? Tell me more. Tell me more.

The “stupidest” of the students here are smarter than me. It’s a pleasure to watch them emerge.

I see my life as taking care of other people. Although I didn’t go to medical school with any intelligent motivation, once I did, I loved being a doctor and trying to help people. And I love being a psychiatrist and trying to understand people, and I try to carry that into everything I do.

In medical research, all of us want to find the causes and cures for diseases. I haven’t found the cause of any disease, although with Huntington’s disease, we are making inroads. And, of course, being a pharmacologist, my métier is discovering drugs and better treatments.

My secret? I come to work every day, and I keep my own calendar. That way I have free time to just wander around the lab and talk to the boys and girls and ask them how it’s going. That’s what makes me happy.

Sol Snyder joined Johns Hopkins in 1965 as an assistant resident in Psychiatry and would later become the youngest full professor in JHU history. In 1978, he received the Albert Lasker Basic Medical Research Award for his role in discovering the brain’s opiate receptors. In 1980, he founded the School of Medicine’s Department of Neuroscience, which in 2006 was renamed the Solomon H. Snyder Department of Neuroscience.

http://hub.jhu.edu/gazette/2014/january-february/what-ive-learned-sol-snyder

http://en.wikipedia.org/wiki/Solomon_H._Snyder

Boosting Excess Neuron Activity Builds Resilience In Mice Vulnerable To Depression

A new study has found that activating natural resilience in the brain could reduce susceptibility for stress in mice, and potentially humans.

Depressive behaviors in mice are often linked to “out-of-balance” neuron activity in the brain’s reward circuit. Suppressing or stopping this hyperactive neuron activity was typically thought to treat this susceptibility to depression or anxiety — but the new study has found quite the opposite.

“To our surprise, neurons in this circuit harbor their own self-tuning, homeostatic mechanism of natural resilience,” Ming-Hu Han of the Icahn School of Medicine at Mount Sinai in New York City, explained in a press release. What this means is that instead of suppressing this excessive neuron activity, boosting it provided a self-stabilizing response, re-establishing balance and producing an antidepressant-like effect.

The mice that were once vulnerable to being anxious, listless, depressed or withdrawn after socially stressful experiences stopped exhibiting these behaviors after their neuron activity received a boost. “As we get to the bottom of a mystery that has perplexed the field for more than a decade, the story takes an unexpected twist that may hold clues to future antidepressants that would at through this counterintuitive resilience mechanism,” Dr. Thomas Insel, NIMH Director, said in the press release.

In susceptible mice, neurons that secrete dopamine — a feel-good hormone — from a reward circuit area called the ventral tegmental area (VTA) become unusually hyperactive. This hyperaction was much higher in mice that were resilient to stress, “even though they were spared the runaway dopamine activity and depression-related behaviors,” the press release reads. Using this logic, the susceptible mice just needed a boost in activation in these neurons to produce resilience.

What is interesting about this study is that it points to the power of the body and brain’s self-correcting prowess. “Homeostatic mechanisms finely regulate other critical components of physiology required for survival — blood glucose and oxygen, body temperature, blood pressure,” Lois Winsky, chief of the NIMH Molecular, Cellular, and Genomic Neuroscience Research Branch, said in the press release. “Similar mechanisms appear to also maintain excitatory balance in brain cells. This study shows how they may regulate circuits underlying behavior.”

http://www.medicaldaily.com/boosting-excess-neuron-activity-builds-resilience-mice-vulnerable-depression-277452

New research suggests that a third of patients diagnosed as vegetative may be conscious with a chance for recovery

Imagine being confined to a bed, diagnosed as “vegetative“—the doctors think you’re completely unresponsive and unaware, but they’re wrong. As many as one-third of vegetative patients are misdiagnosed, according to a new study in The Lancet. Using brain imaging techniques, researchers found signs of minimal consciousness in 13 of 42 patients who were considered vegetative. “The consequences are huge,” lead author Dr. Steven Laureys, of the Coma Science Group at the Université de Liège, tells Maclean’s. “These patients have emotions; they may feel pain; studies have shown they have a better outcome [than vegetative patients]. Distinguishing between unconscious, and a little bit conscious, is very important.”

Detecting human consciousness following brain injury remains exceedingly difficult. Vegetative patients are typically diagnosed by a bedside clinical exam, and remain “neglected” in the health care system, Laureys says. Once diagnosed, “they might not be [re-examined] for years. Nobody questions whether or not there could be something more going on.” That’s about to change.

Laureys has collaborated previously with British neuroscientist Adrian Owen, based at Western University in London, Ont., who holds the Canada Excellence Research Chair in Cognitive Neuroscience and Imaging. (Owen’s work was featured in Maclean’s in October 2013.) Together they co-authored a now-famous paper in the journal Science, in 2006, in which a 23-year-old vegetative patient was instructed to either imagine playing tennis, or moving around her house. Using functional magnetic resonance imaging, or fMRI, they saw that the patient was activating two different parts of her brain, just like healthy volunteers did. Laureys and Owen also worked together on a 2010 follow-up study, in the New England Journal of Medicine, where the same technique was used to ask a patient to answer “yes” or “no” to various questions, presenting the stunning possibility that some vegetative patients might be able to communicate.

In the new Lancet paper, Laureys used two functional brain imaging techniques, fMRI and positron emission tomography (PET), to examine 126 patients with severe brain injury: 41 of them vegetative, four locked-in (a rare condition in which patients are fully conscious and aware, yet completely paralyzed from head-to-toe), and another 81 who were minimally conscious. After finding that 13 of 42 vegetative patients showed brain activity indicating minimal consciousness, they re-examined them a year later. By then, nine of the 13 had improved, and progressed into a minimally conscious state or higher.

The mounting evidence that some vegetative patients are conscious, even minimally so, carries ethical and legal implications. Just last year, Canada’s Supreme Court ruled that doctors couldn’t unilaterally pull the plug on Hassan Rasouli, a man in a vegetative state. This work raises the possibility that one day, some patients may be able to communicate through some kind of brain-machine interface, and maybe even weigh in on their own medical treatment. For now, doctors could make better use of functional brain imaging tests to diagnose these patients, Laureys believes. Kate Bainbridge, who was one of the first vegetative patients examined by Owen, was given a scan that showed her brain lighting up in response to images of her family. Her health later improved. “I can’t say how lucky I was to have the scan,” she said in an email to Maclean’s last year. “[It] really scares me to think what would have happened if I hadn’t had it.”

https://ca.news.yahoo.com/one-third-of-vegetative-patients-may-be-conscious–study-195412300.html

New blood test to predict who will develop Alzheimer’s disease

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In a first-of-its-kind study, researchers have developed a blood test for Alzheimer’s disease that predicts with astonishing accuracy whether a healthy person will develop the disease.

Though much work still needs to be done, it is hoped the test will someday be available in doctors’ offices, since the only methods for predicting Alzheimer’s right now, such as PET scans and spinal taps, are expensive, impractical, often unreliable and sometimes risky.

“This is a potential game-changer,” said Dr. Howard Federoff, senior author of the report and a neurologist at Georgetown University Medical Center. “My level of enthusiasm is very high.”

The study was published in Nature Medicine.

In the beginning, the researchers knew they wanted to find a blood test to detect Alzheimer’s but didn’t know what specifically to look for. Should they examine patients’ DNA? Their RNA? Or should they look for the byproducts of DNA and RNA, such as fats and proteins?

They decided to start with fats, since it was the easiest and least expensive. They drew blood from hundreds of healthy people over age 70 living near Rochester, New York, and Irvine, California. Five years later, 28 of the seniors had developed Alzheimer’s disease or the mild cognitive problems that usually precede it.

Scouring more than 100 fats, or lipids, for what might set this group apart, they found that these 28 seniors had low levels of 10 particular lipids, compared with healthy seniors.

To confirm their findings, the researchers then looked at the blood of 54 other patients who had Alzheimer’s or mild cognitive impairment. This group also had low levels of the lipids.

Overall, the blood test predicted who would get Alzheimer’s or mild cognitive impairment with over 90% accuracy.

“We were surprised,” said Mark Mapstone, a neuropsychologist at the University of Rochester Medical Center and lead author of the study. “But it turns out that it appears we were looking in the right place.”

The beauty of this test, Mapstone says, is that it caught Alzheimer’s before the patient even had symptoms, suggesting that the disease process begins long before people’s memories start failing. He says that perhaps the lipid levels started decreasing at the same time as brain cells started dying.

He and his team plan to try out this test in people in their 40s and 50s. If that works, he says, that would be the “holy grail,” because then researchers could try experimental drugs and treatments in a group that’s almost sure to get the disease. That would speed research along immensely.

Plus, people could get a heads up that they were probably destined to get Alzheimer’s. Although some people might not want to know that they’re destined for a horrible disease, others might be grateful for the warning.

Federoff said he would want to know whether he was on his way to getting the disease, even though there’s nothing he could do about it. He might want to take a family trip he’d been thinking about or might want to appoint a successor at work.

“I would make sure that things that are important to me get done,” he said.

But, Federoff added, others might not want to know they were about to get a devastating disease they were powerless to stop.

“I think it’s a very personal decision,” Federoff said. “It would have to be thought through on multiple dimensions. Patients and their families would have to be counseled.”

Other research teams are looking at other possible tests for Alzheimer’s. The need for a screening test of some kind for Alzheimer’s has never been greater: A report released last week says the disease claims the lives of perhaps a half a million Americans, making it nearly as deadly as heart disease and cancer.

If any of these tests work out — and that’s still an if — it would take years to make it to doctors’ offices, since the test would need to be validated by other labs and with larger groups of people. Thee test developed by the Georgetown and Rochester researchers, for example, was used mainly in white people, and it might not work as well with other groups.

Heather Snyder, a spokeswoman for the Alzheimer’s Association, said the study was well done but much work is still needed.

“It’s an interesting paper. It’s an intriguing study. But it is very preliminary,” she said.http://www.cnn.com/2014/03/09/health/alzheimers-blood-test/index.html?hpt=hp_t2

Mild electric current to the brain can improve math skills

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In a lab in Oxford University’s experimental psychology department, researcher Roi Cohen Kadosh is testing an intriguing treatment: He is sending low-dose electric current through the brains of adults and children as young as 8 to make them better at math.

A relatively new brain-stimulation technique called transcranial electrical stimulation may help people learn and improve their understanding of math concepts.

The electrodes are placed in a tightly fitted cap and worn around the head. The device, run off a 9-volt battery commonly used in smoke detectors, induces only a gentle current and can be targeted to specific areas of the brain or applied generally. The mild current reduces the risk of side effects, which has opened up possibilities about using it, even in individuals without a disorder, as a general cognitive enhancer. Scientists also are investigating its use to treat mood disorders and other conditions.

Dr. Cohen Kadosh’s pioneering work on learning enhancement and brain stimulation is one example of the long journey faced by scientists studying brain-stimulation and cognitive-stimulation techniques. Like other researchers in the community, he has dealt with public concerns about safety and side effects, plus skepticism from other scientists about whether these findings would hold in the wider population.

There are also ethical questions about the technique. If it truly works to enhance cognitive performance, should it be accessible to anyone who can afford to buy the device—which already is available for sale in the U.S.? Should parents be able to perform such stimulation on their kids without monitoring?

“It’s early days but that hasn’t stopped some companies from selling the device and marketing it as a learning tool,” Dr. Cohen Kadosh says. “Be very careful.”

The idea of using electric current to treat the brain of various diseases has a long and fraught history, perhaps most notably with what was called electroshock therapy, developed in 1938 to treat severe mental illness and often portrayed as a medieval treatment that rendered people zombielike in movies such as “One Flew over the Cuckoo’s Nest.”

Electroconvulsive therapy has improved dramatically over the years and is considered appropriate for use against types of major depression that don’t respond to other treatments, as well as other related, severe mood states.

A number of new brain-stimulation techniques have been developed, including deep brain stimulation, which acts like a pacemaker for the brain. With DBS, electrodes are implanted into the brain and, though a battery pack in the chest, stimulate neurons continuously. DBS devices have been approved by U.S. regulators to treat tremors in Parkinson’s disease and continue to be studied as possible treatments for chronic pain and obsessive-compulsive disorder.

Transcranial electrical stimulation, or tES, is one of the newest brain stimulation techniques. Unlike DBS, it is noninvasive.

If the technique continues to show promise, “this type of method may have a chance to be the new drug of the 21st century,” says Dr. Cohen Kadosh.

The 37-year-old father of two completed graduate school at Ben-Gurion University in Israel before coming to London to do postdoctoral work with Vincent Walsh at University College London. Now, sitting in a small, tidy office with a model brain on a shelf, the senior research fellow at Oxford speaks with cautious enthusiasm about brain stimulation and its potential to help children with math difficulties.

Up to 6% of the population is estimated to have a math-learning disability called developmental dyscalculia, similar to dyslexia but with numerals instead of letters. Many more people say they find math difficult. People with developmental dyscalculia also may have trouble with daily tasks, such as remembering phone numbers and understanding bills.

Whether transcranial electrical stimulation proves to be a useful cognitive enhancer remains to be seen. Dr. Cohen Kadosh first thought about the possibility as a university student in Israel, where he conducted an experiment using transcranial magnetic stimulation, a tool that employs magnetic coils to induce a more powerful electrical current.

He found that he could temporarily turn off regions of the brain known to be important for cognitive skills. When the parietal lobe of the brain was stimulated using that technique, he found that the basic arithmetic skills of doctoral students who were normally very good with numbers were reduced to a level similar to those with developmental dyscalculia.

That led to his next inquiry: If current could turn off regions of the brain making people temporarily math-challenged, could a different type of stimulation improve math performance? Cognitive training helps to some extent in some individuals with math difficulties. Dr. Cohen Kadosh wondered if such learning could be improved if the brain was stimulated at the same time.

But transcranial magnetic stimulation wasn’t the right tool because the current induced was too strong. Dr. Cohen Kadosh puzzled over what type of stimulation would be appropriate until a colleague who had worked with researchers in Germany returned and told him about tES, at the time a new technique. Dr. Cohen Kadosh decided tES was the way to go.

His group has since conducted a series of studies suggesting that tES appears helpful improving learning speed on various math tasks in adults who don’t have trouble in math. Now they’ve found preliminary evidence for those who struggle in math, too.

Participants typically come for 30-minute stimulation-and-training sessions daily for a week. His team is now starting to study children between 8 and 10 who receive twice-weekly training and stimulation for a month. Studies of tES, including the ones conducted by Dr. Cohen Kadosh, tend to have small sample sizes of up to several dozen participants; replication of the findings by other researchers is important.

In a small, toasty room, participants, often Oxford students, sit in front of a computer screen and complete hundreds of trials in which they learn to associate numerical values with abstract, nonnumerical symbols, figuring out which symbols are “greater” than others, in the way that people learn to know that three is greater than two.

When neurons fire, they transfer information, which could facilitate learning. The tES technique appears to work by lowering the threshold neurons need to reach before they fire, studies have shown. In addition, the stimulation appears to cause changes in neurochemicals involved in learning and memory.

However, the results so far in the field appear to differ significantly by individual. Stimulating the wrong brain region or at too high or long a current has been known to show an inhibiting effect on learning. The young and elderly, for instance, respond exactly the opposite way to the same current in the same location, Dr. Cohen Kadosh says.

He and a colleague published a paper in January in the journal Frontiers in Human Neuroscience, in which they found that one individual with developmental dyscalculia improved her performance significantly while the other study subject didn’t.

What is clear is that anyone trying the treatment would need to train as well as to stimulate the brain. Otherwise “it’s like taking steroids but sitting on a couch,” says Dr. Cohen Kadosh.

Dr. Cohen Kadosh and Beatrix Krause, a graduate student in the lab, have been examining individual differences in response. Whether a room is dark or well-lighted, if a person smokes and even where women are in their menstrual cycle can affect the brain’s response to electrical stimulation, studies have found.

Results from his lab and others have shown that even if stimulation is stopped, those who benefited are going to maintain a higher performance level than those who weren’t stimulated, up to a year afterward. If there isn’t any follow-up training, everyone’s performance declines over time, but the stimulated group still performs better than the non-stimulated group. It remains to be seen whether reintroducing stimulation would then improve learning again, Dr. Cohen Kadosh says.

http://online.wsj.com/news/articles/SB10001424052702303650204579374951187246122?mod=WSJ_article_EditorsPicks&mg=reno64-wsj&url=http%3A%2F%2Fonline.wsj.com%2Farticle%2FSB10001424052702303650204579374951187246122.html%3Fmod%3DWSJ_article_EditorsPicks

‘Jumping Genes’ Linked to Schizophrenia

sn-schizophrenia

Roaming bits of DNA that can relocate and proliferate throughout the genome, called “jumping genes,” may contribute to schizophrenia, a new study suggests. These rogue genetic elements pepper the brain tissue of deceased people with the disorder and multiply in response to stressful events, such as infection during pregnancy, which increase the risk of the disease. The study could help explain how genes and environment work together to produce the complex disorder and may even point to ways of lowering the risk of the disease, researchers say.

Schizophrenia causes hallucinations, delusions, and a host of other cognitive problems, and afflicts roughly 1% of all people. It runs in families—a person whose twin sibling has the disorder, for example, has a roughly 50-50 chance of developing it. Scientists have struggled to define which genes are most important to developing the disease, however; each individual gene associated with the disorder confers only modest risk. Environmental factors such as viral infections before birth have also been shown to increase risk of developing schizophrenia, but how and whether these exposures work together with genes to skew brain development and produce the disease is still unclear, says Tadafumi Kato, a neuroscientist at the RIKEN Brain Science Institute in Wako City, Japan and co-author of the new study.

Over the past several years, a new mechanism for genetic mutation has attracted considerable interest from researchers studying neurological disorders, Kato says. Informally called jumping genes, these bits of DNA can replicate and insert themselves into other regions of the genome, where they either lie silent, doing nothing; start churning out their own genetic products; or alter the activity of their neighboring genes. If that sounds potentially dangerous, it is: Such genes are often the culprits behind tumor-causing mutations and have been implicated in several neurological diseases. However, jumping genes also make up nearly half the current human genome, suggesting that humans owe much of our identity to their audacious leaps.

Recent research by neuroscientist Fred Gage and colleagues at the University of California (UC), San Diego, has shown that one of the most common types of jumping gene in people, called L1, is particularly abundant in human stem cells in the brain that ultimately differentiate into neurons and plays an important role in regulating neuronal development and proliferation. Although Gage and colleagues have found that increased L1 is associated with mental disorders such as Rett syndrome, a form of autism, and a neurological motor disease called Louis-Bar syndrome, “no one had looked very carefully” to see if the gene might also contribute to schizophrenia, he says.

To investigate that question, principal investigator Kazuya Iwamoto, a neuroscientist; Kato; and their team at RIKEN extracted brain tissue of deceased people who had been diagnosed with schizophrenia as well as several other mental disorders, extracted DNA from their neurons, and compared it with that of healthy people. Compared with controls, there was a 1.1-fold increase in L1 in the tissue of people with schizophrenia, as well as slightly less elevated levels in people with other mental disorders such as major depression, the team reports today in Neuron.

Next, the scientists tested whether environmental factors associated with schizophrenia could trigger a comparable increase in L1. They injected pregnant mice with a chemical that simulates viral infection and found that their offspring did, indeed, show higher levels of the gene in their brain tissue. An additional study in infant macaques, which mimicked exposure to a hormone also associated with increased schizophrenia risk, produced similar results. Finally, the group examined human neural stem cells extracted from people with schizophrenia and found that these, too, showed higher levels of L1.

The fact that it is possible to increase the number of copies of L1 in the mouse and macaque brains using established environmental triggers for schizophrenia shows that such genetic mutations in the brain may be preventable if such exposures can be avoided, Kato says. He says he hopes that the “new view” that environmental factors can trigger or deter genetic changes involved in the disease will help remove some of the disorder’s stigma.

Combined with previous studies on other disorders, the new study suggests that L1 genes are indeed more active in the brain of patients with neuropsychiatric diseases, Gage says. He cautions, however, that no one yet knows whether they are actually causing the disease. “Now that we have multiple confirmations of this occurring in humans with different diseases, the next step is to determine if possible what role, if any, they play.”

One tantalizing possibility is that as these restless bits of DNA drift throughout the genomes of human brain cells, they help create the vibrant cognitive diversity that helps humans as a species respond to changing environmental conditions, and produces extraordinary “outliers,” including innovators and geniuses such as Picasso, says UC San Diego neuroscientist Alysson Muotri. The price of such rich diversity may be that mutations contributing to mental disorders such as schizophrenia sometimes emerge. Figuring out what these jumping genes truly do in the human brain is the “next frontier” for understanding complex mental disorders, he says. “This is only the tip of the iceberg.”

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

http://news.sciencemag.org/biology/2014/01/jumping-genes-linked-schizophrenia