TIME Addiction

Gamblers Get Less Of a Buzz From Pleasure, Study Finds

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New research presented at the European College of Neuropsychopharmacology Congress in Berlin sheds light on what happens in the brains of gamblers.

Pathological gambling is a difficult condition to classify. Though the Diagnostic and Statistical Manual of Mental Disorders (DSM) formerly classified it as an impulse control disorder, the most recent version, the DSM-5, made the switch to defining it as an addictive disorder because of the growing research finding that “gambling disorder is similar to substance-related disorders in clinical expression, brain origin, comorbidity, physiology, and treatment,” the DSM website says.

But this new small study shows that it might be unique in some neurologic ways, too. Researchers performed Positron Emission Tomography (PET) scans on 14 male pathological gamblers and 15 non-gambling volunteers to measure their levels of opioid receptors, the parts of the brain activated by pleasure-inducing endorphins. People with addictions like alcoholism or drug addiction have been found to have more opioid receptors. In problem gamblers, however, the researchers saw no difference from healthy volunteers, a finding that surprised them.

Then, participants took an amphetamine capsule, which unleashes endorphins with similar effects to the rush you get from exercise or alcohol, the study says. An additional PET scan revealed that pathological gamblers responded differently to the drug. They released fewer endorphins than those who didn’t gamble, and they also reported lower levels of euphoria on a questionnaire afterward. This might help explain the addictive part of pathological gambling: to get pleasure from the act, problem gamblers might need more of it or to work harder for it.

These findings suggest the involvement of the opioid system in pathological gambling and that it may differ from addiction to substances such as alcohol,” says lead researcher Dr. Inge Mick of the Imperial College London in a press release. “We hope that in the long run this can help us to develop new approaches to treat pathological gambling.”

TIME Health Care

Terminally Ill Woman Explains Her Decision to Die

"I don't want to die"

A 29-year-old terminally-ill woman in Oregon defended in a new interview Tuesday her decision to forgo aggressive cancer treatment in favor of physician-assisted suicide.

“I don’t want to die,” Brittany Maynard said on CBS.”If anyone wants to hand me, like, a magical cure and save my life so that I can have children with my husband, you know, I will take them up on it.”

In the interview, Maynard’s husband and mother explain how they came to terms with Brittany’s decision.

“The idea of wanting my wife at my side forever—that was the original plan, right?” said Dan Diaz, Maynard’s husband “But the reality that I guess that feeds into the argument of quality of life versus just quantity.”

Maynard said her goal is to make it to Nov. 1 before allowing herself to die. She moved to Oregon because it allows certain types of physician assisted-suicide.

[CBS]

TIME Research

Ann Romney Launches Center, Says Family ‘Done’ With Campaigning

“Not only Mitt and I are done, but the kids are done. Done. Done. Done”

As the political world speculates about a potential third Mitt Romney bid for president, Ann Romney has other things on her mind. On Tuesday, she launched a center at the Brigham and Women’s Hospital in Boston aimed at solving some of the world’s most devastating neurological diseases.

Ann Romney also laid to rest any rumors that her husband might run again, the Los Angeles Times reported. “Not only Mitt and I are done, but the kids are done. Done. Done. Done,” she said.

“By combining Brigham and Women’s Hospital’s unique assets with the world’s most advanced resources and minds, the center will accelerate life-giving breakthroughs,” the hospital’s president Betsy Nabel said in a press release.

Ann Romney said her personal experience with multiple sclerosis (MS) and the work of the doctors at Brigham and Women’s inspired the center.

“I know firsthand how terrifying and devastating these neurologic diseases can be, and I want to do everything in my power to help change outcomes for future generations,” she said in a press release. “The team at Brigham and Women’s Hospital gave me the gift of enduring hope and that is what this center is about.”

The center, planned to open in 2016, will focus on preventing and curing MS, Alzheimer’s disease, Parkinson’s disease, brain tumors and Lou Gehrig’s disease.

Read next: The Pros and Cons of ‘President Grandma’

TIME neuroscience

This Alzheimer’s Breakthrough Could Be a Game Changer

Scientists recreated what goes on in the brains of Alzheimer’s patients in a 3D culture dish that could speed development of new drugs for the disease

Researchers have overcome a major barrier in the study of Alzheimer’s that could pave the way for breakthroughs in our understanding of the disease, a new report shows—and that new understanding could, in turn, pave the way for drugs that treat or interrupt the progression of the neurodegenerative condition.

For decades, animals have been the stand-ins for studying human disease, and for good reason. Their shorter lifespans mean they can model human conditions in weeks or months, and their cells can be useful for testing promising new drug treatments.

But they haven’t been so helpful in studying Alzheimer’s disease. Two factors contribute to the neurodegenerative condition — the buildup of sticky plaques of the protein amyloid, and the toxic web of another protein, tau, which strangles healthy nerve cells and leaves behind a tangled mess of dead and dying neurons. Despite attempts by scientists to engineer mice who exhibit both factors, they haven’t been able to generate the tau tangles that contribute to the disease.

Now, Dr. Rudolph Tanzi and Dr. Doo Kim at the Mass General Institute for Neurodegenerative Diseases at Massachusetts General Hospital, have devised a work-around that doesn’t involve animals. They have developed a way to watch the disease progress in a lab dish.

“In this new system that we call ‘Alzheimer’s-in-a-dish,’ we’ve been able to show for the first time that amyloid deposition is sufficient to lead to tangles and subsequent cell death,” said Tanzi in a statement.

MORE: Blood Test for Alzheimer’s

While autopsies showed evidence of both amyloid and tau in the brain, Alzheimer’s experts have been debating for years which came first — do amyloid plaques trigger the formation of tau tangles, or does the presence of tau cause amyloid to get stickier and bunch together in the brain? Tanzi and his colleagues showed definitively for the first time that amyloid is the first step in the Alzheimer’s process, followed by tau tangles. When he blocked the formation of amyloid in the culture with a known amyloid inhibitor, tau tangles never formed.

The disease-in-a-dish model is an emerging way of understanding conditions that either can’t be recapitulated accurately in animals, or diseases that make it difficult to study and test in human patients. In recent years, for example, scientists have successfully recreated the process behind amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, using stem cells from patients and allowing them to develop into the motor neurons that are affected by the disease. The technique led to a breakthrough in understanding that a certain population of nerve cells known as glial cells poison the motor neurons and impede their normal function. Now experts are focusing on finding ways to control the glial cell activity as possible treatment for ALS.

MORE: How Moodiness and Jealousy May Lead to Alzheimer’s

Tanzi and his team are hoping that something similar will come from their model of Alzheimer’s.

While the genes responsible for the inherited form of Alzheimer’s differ slightly from those involved in the more common form that affects people as they age, the end result — the build up of amyloid plaques and tau tangles — are the same. So now that they can see both the clumps of amyloid and the tau tangles, form, they can start to tease apart the processes that link the two processes together.

That will open the way toward finding drugs or other ways of interrupting the process more quickly than they could working with animals. It took six to eight weeks for the cells in the dish to form plaques and then tangles, compared to a year or so in mice. “We can now screen hundreds of thousands of drugs in this system that recapitulates both plaques and tangles…in a matter of months,” Tanzi said. “This was not possible in mouse models.” The system also makes it possible to test these drug compounds at one-tenth the cost of evaluating them in mice, he said. And that means that finding a way to prevent Alzheimer’s may come both faster and cheaper than scientists had expected.

TIME review

Steven Pinker’s Ultimate Writing Guide

Class is in session—and it's one you'll enjoy
Class is in session—and it's one you'll enjoy

You wouldn't ordinarily take literary advice from a neuroscientist—but Pinker's new book will make you think otherwise

Sometime during middle school, I showed my father something I’d written for a class assignment. About halfway through reading, he stopped, pointed and said “that’s grammatically incorrect. You wrote ‘I will now describe.’ The correct wording is ‘I shall describe.'” The word “will”, he told me, implies defiance and determination. But if your sentence starts with the pronouns he, she, we, you or they, the rule is reversed.

It sounded nutty, to say nothing of pointlessly precise, but that was evidently what he’d learned in grade school back in the 1930’s. As far as he was concerned, that made it an eternal truth. For decades now, I’ve just assumed that the rule had gone out of style—but on reading Steven Pinker’s charming and erudite new book The Sense of Style: The Thinking Person’s Guide to Writing in the 21st Century, I’ve learned that there never was such a rule, in the sense of something that was universally agreed on by language experts.

If anyone should know, it’s Pinker. Not only is he an extraordinarily stylish and prolific writer himself—he’s written on the history of violence, why words don’t mean what they mean, the mystery of consciousness, the role of genes in shaping character, how the mind works and more—but he’s also got the intellectual chops to back up what he says, what with his being a psycholinguist and neuroscientist at Harvard and all.

With that backing him up, it’s no surprise that while The Sense of Style is very much a practical guide to clear and compelling writing, it’s also far more. Pinker dives deep into the neuroscience of language to explain why some writing is clear, some murky and some sublime.

Style has all the fun stuff that makes usage guides so popular. For example, he lambastes the language scolds who wag their fingers over such evils as split infinitives—absurdly, Pinker says, because the rule against them is based on the fact that infinitives such as “to go” are single, unsplittable words in Latin and other languages that arose from it. Our two-word infinitives should not be governed by the old one-word rule—meaning that Captain Kirk was just fine, when he said “to boldly go.” Pinker pooh-poohs the idea that words must always stick to their original meaning: “decimate” means “to cut by ten percent” in Latin; now people use it to mean “more or less destroy,” and that’s fine with him.

Sometimes Pinker works a little too hard at this debunking campaign. He informs us that while “ain’t” is generally incorrect, it’s fine when used in expressions like as “it ain’t over till it’s over.” But since nobody has thought otherwise since the Herbert Hoover administration, it’s a point that hardly needs to be made.

Pinker then steps back from talking about excessively fussy rules to talk about something he calls “classic style”—a concept he attributes to the scholars Mark Turner and Francis-Noël Thomas. The basic rule here is “write clearly,” and Pinker’s advice on how to do so is pretty standard, albeit written with great clarity.

Among his suggestions: read your prose out loud to yourself in order to pick up on awkwardnesses that might not be evident when you’re reading silently; avoid jargon; keep your sentences short; jettison superfluous and unnecessary words—like, say, using both “superfluous” and “unnecessary” when just one will do. In one of the many tables of good versus bad that appear in the book he shows how phrases such as “for the purpose of” or “in view of the fact that” can be replaced simply by “to” or “since” with no loss of meaning.

Finally, Pinker plunges into what really sets this book apart: the neuroscientific underpinnings of what makes some writing good and some bad, based on how our brains process language. Classic style or not, this bit takes a fair amount of work to get through. Pinker acknowledges that many very good writers get by purely on intuition, but, he says:

Just below the surface of these inchoate intuitions, I believe, is a tacit awareness that the writer’s goal is to encode a web of ideas into a string of words using a tree of phrases. Aspiring wordsmiths would do well to cultivate this awareness.”

Well, maybe. But the chapter that covers these ideas is filled with sentence diagrams and technical language that runs the risk of making aspiring wordsmiths run screaming from the room. Here’s a passage in which Pinker tries to move the awareness-cultivation process along, talking about a set of words he calls “determiners.”

A determiner answers the question “Which one?” or “How Many?” Here [i.e., in a passage about a play by Sophocles] the determiner role is filled by what is traditionally called a possessive noun (though it is really a noun marked for genitive case, as I will explain).

There’s lots more of this sort of thing, which Pinker thinks “can take the fear and boredom out of grammar.” I’m not entirely sure about that. For experienced writers, however, it’s pretty fascinating stuff—the unconscious mechanics that underlie the instincts they’ve developed through experience.

In the end, Pinker’s formula for good writing is pretty basic: write clearly, try to follow the rules most of the time—but only the when they make sense. It’s neither rocket science nor brain surgery. But the wit and insight and clarity he brings to that simple formula is what makes this book such a gem.

TIME Ideas hosts the world's leading voices, providing commentary and expertise on the most compelling events in news, society, and culture. We welcome outside contributions. To submit a piece, email ideas@time.com.

TIME neuroscience

How A Girl’s Brain Changes After a Traumatic Brain Injury

Close up of teenage girls eyelashes
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Concussions may influence girls differently than boys

Girls who suffer traumatic brain injuries (TBIs) may be more susceptible to behavioral problems like psychological distress and smoking compared to boys, according to a new study.

Each year, TBIs cause 2.5 million emergency room visits, and so far research has consistently shown that they’re more common among boys than girls. Girls still get them, though, and often in sports like soccer, basketball and cheerleading. A new study published in the journal PLOS ONE that surveyed 9,288 Ontario students in grades 7 through 12 reports that girls who suffered brain injuries—in sports, most commonly—were more likely to report having contemplated suicide, experienced psychological distress, been the target of bullying and having smoked cigarettes.

Overall, the new study reports that one in five adolescents had sustained a TBI that resulted in their loss of consciousness for at least five minutes or hospitalization at some point in their lifetime. Boys experienced them 6% more than girls. These young people who had experienced a lifetime TBI also reported behaviors in the last year like daily smoking, binge drinking, using marijuana, cyberbullying and poor grades.

MORE: The Tragic Risks of American Football

Since the results were self-reported, the researchers could not determine causation, nor could they provide a definitive explanation for the gender differences. In the study, they speculate that it could have to do with a variety of factors that include hormonal differences, treatment differences, differences in cognitive abilities or some combination.

Dr. Geoffrey Manley, vice chairman of neurological surgery at the University of California, San Francisco, was not involved in the study but has another theory. According to his own research, women tend to be more forthcoming about their concussion symptoms than men. “Currently, we don’t have a clear idea of what exactly a concussion is,” he says. “We are really limited to self-reporting, and women are more honest about their symptoms than boys.”

Girls get TBIs most often playing soccer and basketball, but other sports—cheerleading, in particular—have very high risk for injuries. The American Academy of Pediatrics has called for more safety regulations for the cheerleading, even though it tends to not be included in national high school sports injury research.

There’s still a lot we don’t know about TBIs and concussions, including the best way to diagnose them. So far there is not a reliable imaging or biomarker test. But understanding who is at a risk, and for which reasons, helps bolster the collective knowledge of the issue. “No matter how you slice this, a subset of these folks are going to go on and have long-term disability,” says Manley. “We can try to predict who these people are going to be, and gender may be part of this.”

TIME neuroscience

This Curry Spice Might Help the Brain Heal Itself

A chemical commonly found in turmeric was shown to encourage nerve-cell growth in rats

A spice commonly used to make curry could help the brain heal itself by encouraging the growth of nerve cells, according to a new study.

Researchers at the Institute of Neuroscience and Medicine in Julich, Germany, found that rats injected with aromatic-turmerone, a compound found naturally in turmeric, showed increased activity in parts of the brain associated with nerve-cell growth.

The compound could encourage the proliferation of brain cells, researchers said — though it was unclear whether it could be used to help stall or reverse the symptoms of degenerative-brain diseases like Alzheimer’s or dementia in human beings.

A separate trial by the same research group found that rodent neural stem cells grew when they were bathed in a solution of aromatic-turmerone. The cells bathed in the turmeric compound also appeared to specialize into certain types of brain cells more rapidly.

“It is interesting that it might be possible to boost the effectiveness of the stem cells with aromatic-turmerone,” Maria Adele Rueger, a researcher on the team, told the BBC. “And it is possible this in turn can help boost repair in the brain.”

An outside researcher said it was unclear whether the findings would be applicable to people, and whether it could help people with Alzheimer’s.

Turmeric was already known for its potential health-giving properties. One 2009 study found that one of its component chemicals — curcumin — killed off cancer cells.

TIME Mental Health/Psychology

One Dose of Antidepressant Changes the Brain, Study Finds

One dose of antidepressant is all it takes to change the brain, finds a small new study published in the journal Current Biology.

The study authors took brain scans of 22 healthy people who weren’t depressed and who had never before taken antidepressants. Some were randomized to take a dose of the most common kind of antidepressant, an SSRI (selective serotonin reuptake inhibitors).

After another brain scan three hours later, researchers saw a dramatic change: a widespread drop in connectivity throughout the brain, except where it was enhanced in two brain regions, the cerebellum and thalamus.

The results suggest that antidepressants may alter brain connections much faster than previously thought. “We were surprised,” says study author Julia Sacher, of the Max Planck Institute for Human Cognitive and Brain Sciences, in an email to TIME. “We were not expecting the SSRI to have such a prominent effect on such a short time-scale and the resulting signal to encompass the entire brain.”

Antidepressants are generally thought to take several weeks to kick in. “It is possible that these connectivity changes are the first step in remodeling the brain, as there is evidence from other experiments that such functional connectivity changes can reflect neuroplastic change,” Sacher says.

“However, much work remains before we understand how different antidepressants affect the brains of people with and without depression, not only after the first dose, but also over the longer term. The hope that we have for future studies is to uncover distinct differences in brain connectivity between depression patients who ultimately respond to an antidepressant and those who do not.”

TIME Developmental Disorders

3 in 10 Former NFL Players Will Get Alzheimer’s, Dementia

Percy Harvin
Seattle Seahawks wide receiver Percy Harvin (11) reacts after taking a big hit during an NFL Divisional Playoff game against the New Orleans Saints on Jan. 11, 2014. Kevin Terrell—AP

That's at least twice the rate at which the general population experiences the same diseases

Nearly 30 percent of former NFL players will develop brain conditions like Alzheimer’s or a less debilitating form of dementia, according to a report released Friday by the NFL and the NFL Players’ Association.

The data in the report was used to calculate the size of a $675 million pool that will be provided to former NFL players who suffer from brain problems as a consequence of their time as professional athletes. The information was provided to the federal judge overseeing a lawsuit against the NFL on behalf of former players.

The report said that the rate of brain conditions for former players were “materially higher than those expected in the general population” and diagnosis occurred at an earlier age, according to an Associated Press report.

The terms of the settlement provide $675 million for treatment of former players, $75 million for neurological testing and $10 million for research. The judge overseeing the case expressed concern that the funds might not be sufficient to cover the estimated 6,000 former players who may suffer from brain disorders.

[AP]

TIME neuroscience

Alzheimer’s Linked to Sleeping Pills and Anti-Anxiety Drugs

New research suggests that people who take benzodiazepines may have a higher risk of developing Alzheimer’s

About 9 million Americans rely on sleeping pills or some sort of sedative to doze off at night, and 11% of middle-aged women take anti-anxiety medications. The most common of these include benzodiazapines, and now scientists say the drugs are associated with a higher risk of Alzheimer’s.

In a report published Wednesday in The BMJ, researchers say that among 1,796 people with Alzheimer’s disease and 7,184 controls, those who have used benzodiazepines showed a 51% higher risk of the neurodegenerative disorder. Among people who took the drugs more than 180 days, the risk escalated to about two-fold higher.

Previous studies have linked the drugs to memory and cognitive problems, but primarily in those taking them short term. But in the current study, in which the scientists, led by Sophie Billioti de Gage, a PhD student at INSERM, University of Bordeaux, followed the participants for six years, the connection to dementia appeared strong. The interaction remained even after the scientists adjusted for potential confounding effect on Alzheimer’s rates such as blood pressure, heart disease, depression and insomnia.

In order to rule out the possibility that it was happening the other way around—that Alzheimer’s was causing a rise in insomnia and anxiety—the authors focused on people who had been prescribed sleeping and anxiety meds more than five years before they were diagnosed with Alzheimer’s. “We believe that the likelihood that the results are mainly driven by reverse causation is low,” de Gage said in an email discussion about the results.

It’s not clear why the drugs might increase the risk of Alzheimer’s, although de Gage speculates that the short-term effects on memory and cognitive functions may deplete reserve capacities that might help to offset reduce nerve functions as the disease’s hallmark protein plaques start to build up.

She also said that the study did not find an effect among those who used benzodiazepines for less than three months. That’s how most of the medications are prescribed, so people shouldn’t stop using them to treat anxiety disorders, social phobias and insomnia. But, she added, “It seems crucial to encourage physicians to carefully balance the benefits and risks when initiating or renewing a treatment [with benzodiazepines].”

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