Chapter 15. Emotions, Aggression, and Stress
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By Rebecca Brewer, Jennifer Murphy, There is a persistent stereotype that people with autism are individuals who lack empathy and cannot understand emotion. It’s true that many people with autism don’t show emotion in ways that people without the condition would recognize. But the notion that people with autism generally lack empathy and cannot recognize feelings is wrong. Holding such a view can distort our perception of these individuals and possibly delay effective treatments. We became skeptical of this notion several years ago. In the course of our studies of social and emotional skills, some of our research volunteers with autism and their families mentioned to us that people with autism do display empathy. Many of these individuals said they experience typical, or even excessive, empathy at times. One of our volunteers, for example, described in detail his intense empathic reaction to his sister’s distress at a family funeral. Yet some of our volunteers with autism agreed that emotions and empathy are difficult for them. We were not willing to brush off this discrepancy with the ever-ready explanation that people with autism differ from one another. We wanted to explain the difference, rather than just recognize it. So we looked into the overlap between autism and alexithymia, a condition defined by a difficulty understanding and identifying one’s own emotions. People with high levels of alexithymia (which we assess with questionnaires) might suspect they are experiencing an emotion, but are unsure which emotion it is. They could be sad, angry, anxious or maybe just overheated. About 10 percent of the population at large — and about 50 percent of people with autism — has alexithymia. © 2016 Scientific American
By Bret Stetka Beloved crank and Seinfeld co-creator Larry David once told an interviewer that he tolerates people like he tolerates lactose — which is to say, I'm assuming, not well. David's particular degree of grumpiness might be extreme, and perhaps embellished in the interest his shtick, but his social misgivings echo those of many in their dotage who’d rather spend time with old friends than deal with the sweat and small talk required to go out and make new ones. Humans may not be alone here. According to new research, our primate cousins also become more socially selective with age, preferring the companionship of their “friends” to monkeys that are less familiar (or maybe just a drag at parties). The findings also hint at a possible evolutionary explanation for why our social preferences change over the years. The work, conducted primarily by researchers from the German Primate Center in Göttingen, Germany, was recently published in the journal Current Biology and entailed observing the behaviors of over 100 Barbary macaque monkeys, an out-going, some might say "screechy," species hailing from North Africa. To get a sense of how interest in non-social vs social stimulation changes over the course of their lifetimes, monkeys of varying ages were observed in the presence of both inanimate objects and other monkeys. They were first presented with three novel objects: animal toys, a see-through cube filled with glitter in a viscous liquid, and a tube baited with food. Those that had reached early adulthood were not interested in the objects without a reward. The younger ones were intrigued by all three. © 2016 Scientific American
Laura Sanders Feeling good may help the body fight germs, experiments on mice suggest. When activated, nerve cells that help signal reward also boost the mice’s immune systems, scientists report July 4 in Nature Medicine. The study links positive feelings to a supercharged immune system, results that may partially explain the placebo effect. Scientists artificially dialed up the activity of nerve cells in the ventral tegmental area — a part of the brain thought to help dole out rewarding feelings. This activation had a big effect on the mice’s immune systems, Tamar Ben-Shaanan of Technion-Israel Institute of Technology in Haifa and colleagues found. A day after the nerve cells in the ventral tegmental area were activated, mice were infected with E. coli bacteria. Later tests revealed that mice with artificially activated nerve cells had less E. coli in their bodies than mice without the nerve cell activation. Certain immune cells seemed to be ramped up, too. Monocytes and macrophages were more powerful E. coli killers after the nerve cell activation. If a similar effect is found in people, the results may offer a biological explanation for how positive thinking can influence health. |© Society for Science & the Public 2000 - 2016
By Maya Smith Bonobos (pictured) are known as the peaceful ape. They’re less aggressive than their chimpanzee cousins, and when they have disagreements they’re more likely to make love, not war. Now, a new study reveals one way females keep the peace. In most primate societies, female genitals swell to advertise that they’re ready to mate, leading to fighting among males as they jostle for a partner. But in bonobos, the swellings only indicate fertility half the time, according to a study in the wild published this week in BMC Evolutionary Biology. The findings confirm what scientists have observed in captivity. The researchers behind the new study hypothesize females may have evolved the behavior to gain the upper hand in mating. Because males cannot look to sexual swellings as a reliable indicator of fertility, the females are free to choose their mates. And that helps everyone get along. © 2016 American Association for the Advancement of Science.
by Bethany Brookshire There’s an osprey nest just outside Jeffrey Brodeur’s office at the Woods Hole Oceanographic Institution in Massachusetts. “I literally turn to my left and they’re right there,” says Brodeur, the organization’s communications and outreach specialist. WHOI started live-streaming the osprey nest in 2005. For the first few years, few people really noticed. All that changed in 2014. An osprey pair had taken up residence and produced two chicks. But the mother began to attack her own offspring. Brodeur began getting e-mails complaining about “momzilla.” And that was just the beginning. “We became this trainwreck of an osprey nest,” he says. In the summer of 2015, the osprey family tried again. This time, they suffered food shortages. The camera received an avalanche of attention, complaints and e-mails protesting the institute’s lack of intervention. One scolded, “it is absolutely disgusting that you will not take those chicks away from that demented witch of a parent!!!!! Instead you let them be constantly abused and go without [sic] food. Yes this is nature but you have a choice to help or not. This is totally unacceptable. She should be done away with so not to abuse again.” By mid-2015, Brodeur began to receive threats. “People were saying ‘we’re gonna come help them if you don’t,’” he recalls. The osprey cam was turned off, and remains off to this day. Brodeur says he’s always wondered why people had such strong feelings about a bird’s parenting skills. Why do people spend so much time and emotion attempting to apply their own moral sense to an animal’s actions? The answer lies in the human capacity for empathy — one of the qualities that helps us along as a social species. © Society for Science & the Public 2000 - 2016.
By Gary Stix Bullies often like being bullies—and an entire line of research links aggressive behaviors to brain areas tied to sensations of reward—sites deep below the organ’s surface with names like the ventromedial hypothalamus and the extended amygdala. One lingering puzzle is what precedes the aggressive act. What makes a person—or, in this case, a mouse—lash out? A new study, published June 29 in Nature, shows that the thought of being the aggressor simply feels good to certain animals. I had a fascinating talk this week with Scott Russo from the Icahn School of Medicine at Mount Sinai, the paper’s senior author, who described the significance of these findings. What did your study find? We discovered a brain circuit—connecting the basal forebrain and lateral habenula—that appears to control the motivation of a male mouse to be aggressive and subordinate another male mouse. The significance of these findings is that the circuit seems to be telling an animal that subordinating, or “bullying,” another animal is a rewarding behavior. To test this, we adapted a conditioned place preference protocol—often used to measure the rewarding properties of addictive drugs, whereby mice were allowed to attack an intruder mouse within one of two environmental contexts: When asked which of the two environmental contexts they preferred, aggressive mice chose the environment in which they were allowed to attack the intruder mouse over the environment in which they had no access to the intruder mouse. Interestingly, the basal forebrain and lateral habenula have been previously shown to support conditioned place preference to drugs of abuse, such as nicotine and cocaine, suggesting that similar neural processes mediate rewarding aspects of aggression and addictive substances. © 2016 Scientific American
Link ID: 22380 - Posted: 06.30.2016
Susan Gaidos By age 25, Patrick Schnur had cycled through a series of treatment programs, trying different medications to kick his heroin habit. But the drugs posed problems too: Vivitrol injections were painful and created intense heroin cravings as the drug wore off. Suboxone left him drowsy, depressed and unable to study or go running like he wanted to. Determined to resume the life he had before his addiction, Schnur decided to hunker down and get clean on his own. In December 2015, he had been sober for two years and had just finished his first semester of college, with a 4.0 grade point average. Yet, just before the holidays, he gave in to the cravings. Settling into his dorm room he stuck a needle in his vein. It was his last shot. Scientists are searching for a different kind of shot to prevent such tragedies: a vaccine to counter addiction to heroin and other opioids, such as the prescription painkiller fentanyl and similar knockoff drugs. In some ways, the vaccines work like traditional vaccines for infectious diseases such as measles, priming the immune system to attack foreign molecules. But instead of targeting viruses, the vaccines zero in on addictive chemicals, training the immune system to usher the drugs out of the body before they can reach the brain. Such a vaccine may have helped Schnur, a onetime computer whiz who grew up in the Midwest, far removed from the hard edges of the drug world. His overdose death reflects a growing heroin epidemic and alarming trend. In the 1960s, heroin was seen as a hard-core street drug abused mostly in inner cities. Now heroin is a problem in many suburban and rural towns across America, where it is used primarily by young, white adults — male and female, according to research published by psychiatrist Theodore Cicero of Washington University in St. Louis and colleagues in 2014 in JAMA Psychiatry. © Society for Science & the Public 2000 - 201
By Perri Klass, M.D. In the 1990s, in my first month in practice as a pediatrician, I asked the mother of a 4-year-old about discipline and she told me that her son was often out of line and wild, and spanking was the only thing that worked, though she was sure I was going to tell her not to, just as her previous pediatrician had done. Around the same time, my colleague in the same clinic walked into an exam room to find a cranky toddler who was acting out, and a frustrated father who was taking off his belt and threatening punishment. In each case, and in many others, we had to decide how to talk to the parents, and whether to bring up the issue of child abuse — which is definitely an issue when a child is being struck, or threatened, with a belt. Corporal punishment, also known as “physical discipline,” has become illegal in recent decades in many countries, starting with Sweden in 1979. The United States is not one of those countries, and pediatricians regularly find ourselves talking with parents about why hitting children is a bad idea. The American Academy of Pediatrics officially recommends against physical discipline, saying that evidence shows it is ineffective and puts children at risk for abuse; pediatricians are mandated reporters, responsible for notifying the authorities if we think there is a possibility of abuse, though the boundaries are not clearly defined by law. But many parents continue to spank, even when they don’t think it does much good. In a recent report by the nonprofit organization Zero to Three of a national sample of 2,200 parents of children birth to age 5, parents were asked which discipline strategies they used a few times a week or more. Twenty-six percent said they “pop or swat” their child, 21 percent spank, and 17 percent reported hitting with an object like a belt or a wooden spoon. (Parents could respond that they used more than one strategy.) Zero to Three reported that even those who used these strategies frequently did not rate them as effective, and 30 percent agreed with the statement, “I spank even though I don’t feel O.K. about it.” © 2016 The New York Times Company
Annie Murphy Paul Twelve years ago, I tried to drive a stake into the heart of the personality-testing industry. Personality tests are neither valid nor reliable, I argued, and we should stop using them — especially for making decisions that affect the course of people's lives, like workplace hiring and promotion. But if I thought that my book, The Cult of Personality Testing, would lead to change in the world, I was keenly mistaken. Personality tests appear to be more popular than ever. I say "appear" because — today as when I wrote the book — verifiable numbers on the use of such tests are hard to come by. Personality testing is an industry the way astrology or dream analysis is an industry: slippery, often underground, hard to monitor or measure. There are the personality tests administered to job applicants "to determine if you're a good fit for the company;" there are the personality tests imposed on people who are already employed, "in order to facilitate teamwork;" there are the personality tests we take voluntarily, in career counseling offices and on self-improvement retreats and in the back pages of magazines (or, increasingly, online.) I know these tests are popular because after the book was published, most of the people I heard from were personality-test enthusiasts, eager to rebut my critique of the tests that had, they said, changed their lives. © 2016 npr
Link ID: 22359 - Posted: 06.25.2016
Ian Sample Science editor Brain scans have highlighted “striking” differences between the brains of young men with antisocial behavioural problems and those of their better-behaved peers. The structural changes, seen as variations in the thickness of the brain’s cortex or outer layer of neural tissue, may result from abnormal development in early life, scientists at Cambridge University claim. But while the images show how the two groups of brains differ on average, the scans cannot be used to identify individuals with behavioural issues, nor pinpoint specific developmental glitches that underpin antisocial behaviour. Led by Luca Passamonti, a neurologist at Cambridge, the researchers scanned the brains of 58 young men aged 16 to 21 who had been diagnosed with conduct disorder, defined by persistent problems that ranged from aggressive and destructive behaviour, to lying and stealing, carrying weapons or staying out all night. When compared with brain scans from 25 healthy men of the same age, the scientists noticed clear differences. Those diagnosed with conduct disorder before the age of 10 had similar variations in the thickness of the brain’s cortex. “It may be that problems they experience in childhood affect and delay the way the cortex is developing,” said Passamonti. But the brains of men diagnosed with behavioural problems in adolescence differed in another way. Scans on them showed fewer similarities in cortical thickness than were seen in the healthy men. That, Passamonti speculates, may arise when normal brain maturation, such as the “pruning” of neurons and the connections between them, goes awry. © 2016 Guardian News and Media Limited
Aggressive chemotherapy followed by a stem cell transplant can halt the progression of multiple sclerosis (MS), a small study has suggested. The research, published in The Lancet, looked at 24 patients aged between 18 and 50 from three hospitals in Canada. For 23 patients the treatment greatly reduced the onset of the disease, but in one case a person died. An MS Society spokeswoman said this type of treatment does "offer hope" but also comes with "significant risks". Around 100,000 people in the UK have MS, which is an incurable neurological disease. 'No relapses' The condition causes the immune system to attack the lining of nerves in the brain and spinal cord. Most patients are diagnosed in their 20s and 30s. One existing treatment is for the immune system to be suppressed with chemotherapy and then stem cells are introduced to the patient's bloodstream - this procedure is known as an autologous haematopoietic stem cell transplant (HSCT). But in this study, Canadian researchers went further - not just suppressing the immune system, but destroying it altogether. It is then rebuilt with stem cells harvested from the patient's own blood which are at such an early stage, they have not developed the flaws that trigger MS. The authors said that among the survivors, over a period of up to 13 years, there were no relapses and no new detectable disease activity. All the patients who took part in the trial had a "poor prognosis" and had previously undergone standard immunosuppressive therapy which had not controlled the MS - which affects around two million people worldwide. © 2016 BBC.
By ROBERT F. WORTH In early 2012, a neuropathologist named Daniel Perl was examining a slide of human brain tissue when he saw something odd and unfamiliar in the wormlike squiggles and folds. It looked like brown dust; a distinctive pattern of tiny scars. Perl was intrigued. At 69, he had examined 20,000 brains over a four-decade career, focusing mostly on Alzheimer’s and other degenerative disorders. He had peered through his microscope at countless malformed proteins and twisted axons. He knew as much about the biology of brain disease as just about anyone on earth. But he had never seen anything like this. The brain under Perl’s microscope belonged to an American soldier who had been five feet away when a suicide bomber detonated his belt of explosives in 2009. The soldier survived the blast, thanks to his body armor, but died two years later of an apparent drug overdose after suffering symptoms that have become the hallmark of the recent wars in Iraq and Afghanistan: memory loss, cognitive problems, inability to sleep and profound, often suicidal depression. Nearly 350,000 service members have been given a diagnosis of traumatic brain injury over the past 15 years, many of them from blast exposure. The real number is likely to be much higher, because so many who have enlisted are too proud to report a wound that remains invisible. For years, many scientists have assumed that explosive blasts affect the brain in much the same way as concussions from football or car accidents. Perl himself was a leading researcher on chronic traumatic encephalopathy, or C.T.E., which has caused dementia in N.F.L. players. Several veterans who died after suffering blast wounds have in fact developed C.T.E. But those veterans had other, nonblast injuries too. No one had done a systematic post-mortem study of blast-injured troops. That was exactly what the Pentagon asked Perl to do in 2010, offering him access to the brains they had gathered for research. It was a rare opportunity, and Perl left his post as director of neuropathology at the medical school at Mount Sinai to come to Washington. © 2016 The New York Times Company
By Rita Celli, This is what Jennifer Molson remembers doctors saying to her about the high-stakes procedure she would undergo in 2002 as part of an Ottawa study that has yielded some promising results in multiple sclerosis patients. The 41-year-old Ottawa woman was in a wheelchair before the treatment. She now walks, runs and works full time. "I had no feeling from my chest down. I could barely cut my food," Molson remembers. Molson was diagnosed with MS when she was 21, and within five years she needed full-time care. "It was scary. [The procedure] was my last shot at living." MS is among the most common chronic inflammatory diseases of the central nervous system, affecting an estimated two million people worldwide. New Canadian research led by two Ottawa doctors and published in The Lancet medical journal on Thursday suggests the high-risk therapy may stop the disease from progressing. "This is the first treatment to produce this level of disease control or neurological recovery" from MS, said The Lancet in a news release. But The Lancet also highlights the high mortality rate associated with the procedure — one patient out of 24 involved in the clinical trial died from liver failure. "Treatment related risks limit [the therapy's] widespread use," The Lancet concludes. Results 'impressive' Nevertheless, in the journal's accompanying editorial a German doctor calls the results "impressive." ©2016 CBC/Radio-Canada.
By JAMES GORMAN This summer’s science horror blockbuster is a remake: Return of the Leaping Electric Eel! If you have any kind of phobia of slimy, snakelike creatures that can rise from the water and use their bodies like Tasers, this story — and the accompanying video — may not be for you. The original tale (there was, alas, no video) dates to 1800 when the great explorer Alexander von Humboldt was in South America and enlisted local fishermen to catch some of these eels for the new (at the time) study of electricity. He wrote that the men herded horses and mules into a shallow pond and let the eels attack by pressing themselves against the horses. The horses and mules tried to escape, but the fishermen kept them in the water until the eels used up their power. Two horses died, probably from falling and drowning. Or so Humboldt said. Though the story was widely retold, no other report of this kind of fishing-with-horses phenomenon surfaced for more than 200 years, according to Kenneth Catania, a scientist with a passion for studying the eel species in question, electrophorus electricus. In 2014, he reported on how the eels freeze their prey. They use rapid pulses of more than 600 volts generated by modified muscle cells and sent through the water. These volleys of shocks cause the muscles of prey to tense at once, stopping all movement. The eels’ bodies function like Tasers, Dr. Catania wrote. But they can also project high-voltage pulses in the water in isolated couplets rather than full volleys for a different effect. The pairs of shocks don’t freeze the prey, but cause their bodies to twitch. That movement reveals the prey’s location, and then the eels send out a rapid volley to immobilize then swallow it. Dr. Catania noticed another kind of behavior, however. He was using a metal-handled net — wearing rubber gloves — while working with eels in an aquarium, and the eels would fling themselves up the handle of the net, pressing themselves to the metal and generating rapid electric shocks. © 2016 The New York Times Company
By LISA FELDMAN BARRETT WHEN the world gets you down, do you feel just generally “bad”? Or do you have more precise emotional experiences, such as grief or despair or gloom? In psychology, people with finely tuned feelings are said to exhibit “emotional granularity.” When reading about the abuses of the Islamic State, for example, you might experience creeping horror or fury, rather than general awfulness. When learning about climate change, you could feel alarm tinged with sorrow and regret for species facing extinction. Confronted with this year’s presidential campaign, you might feel astonished, exasperated or even embarrassed on behalf of the candidates — an emotion known in Mexico as “pena ajena.” Emotional granularity isn’t just about having a rich vocabulary; it’s about experiencing the world, and yourself, more precisely. This can make a difference in your life. In fact, there is growing scientific evidence that precisely tailored emotional experiences are good for you, even if those experiences are negative. According to a collection of studies, finely grained, unpleasant feelings allow people to be more agile at regulating their emotions, less likely to drink excessively when stressed and less likely to retaliate aggressively against someone who has hurt them. Perhaps surprisingly, the benefits of high emotional granularity are not only psychological. People who achieve it are also likely to have longer, healthier lives. They go to the doctor and use medication less frequently, and spend fewer days hospitalized for illness. Cancer patients, for example, have lower levels of harmful inflammation when they more frequently categorize, label and understand their emotions. © 2016 The New York Times Company
Link ID: 22285 - Posted: 06.06.2016
By Ann Griswold, Women who develop infections during pregnancy run an increased risk of having a child with autism. Most data indicate that an overactive maternal immune response underlies the risk. But a new analysis runs contrary to this view: It ties high levels of an inflammatory protein in pregnant women to a low risk of autism in their children, suggesting that a strong immune response is protective. Researchers looked at 1,315 mother-child pairs, including 500 children with autism and 235 with developmental delay. They found that healthy pregnant women with high levels of C-reactive protein (CRP), a marker of inflammation, are less likely to have a child with autism than are women with typical levels of the protein. The findings contradict a 2013 report from a large Finnish cohort that tied high CRP levels during pregnancy to an increased risk of having a child with autism. “It was the opposite of what we expected to find,” says senior researcher Lisa Croen, director of the Autism Research Program at Kaiser Permanente in Oakland, California. The work appeared in April in Translational Psychiatry. The results suggest that the strength of a woman’s immune system, rather than its response to infection, is the important factor in determining autism risk. Moderate or low baseline levels of CRP might indicate a relatively weak ability to fight off infection. And a less vigorous immune response might boost the risk in some women, the researchers say. © 2016 Scientific American,
By Anil Ananthaswamy and Alice Klein Our brain’s defence against invading microbes could cause Alzheimer’s disease – which suggests that vaccination could prevent the condition. Alzheimer’s disease has long been linked to the accumulation of sticky plaques of beta-amyloid proteins in the brain, but the function of plaques has remained unclear. “Does it play a role in the brain, or is it just garbage that accumulates,” asks Rudolph Tanzi of Harvard Medical School. Now he has shown that these plaques could be defences for trapping invading pathogens. Working with Robert Moir at the Massachusetts General Hospital in Boston, Tanzi’s team has shown that beta-amyloid can act as an anti-microbial compound, and may form part of our immune system. .. To test whether beta-amyloid defends us against microbes that manage to get into the brain, the team injected bacteria into the brains of mice that had been bred to develop plaques like humans do. Plaques formed straight away. “When you look in the plaques, each one had a single bacterium in it,” says Tanzi. “A single bacterium can induce an entire plaque overnight.” Double-edged sword This suggests that infections could be triggering the formation of plaques. These sticky plaques may trap and kill bacteria, viruses or other pathogens, but if they aren’t cleared away fast enough, they may lead to inflammation and tangles of another protein, called tau, causing neurons to die and the progression towards © Copyright Reed Business Information Ltd.
By Jordana Cepelewicz General consensus among Alzheimer’s researchers has it that the disease’s main culprit, a protein called amyloid beta, is an unfortunate waste product that is not known to play any useful role in the body—and one that can have devastating consequences. When not properly cleared from the brain it builds up into plaques that destroy synapses, the junctions between nerve cells, resulting in cognitive decline and memory loss. The protein has thus become a major drug target in the search for a cure to Alzheimer’s. Now a team of researchers at Harvard Medical School and Massachusetts General Hospital are proposing a very different story. In a study published this week in Science Translational Medicine, neurologists Rudolph Tanzi and Robert Moir report evidence that amyloid beta serves a crucial purpose: protecting the brain from invading microbes. “The original idea goes back to 2010 or so when Rob had a few too many Coronas,” Tanzi jokes. Moir had come across surprising similarities between amyloid beta and LL37, a protein that acts as a foot soldier in the brain’s innate immune system, killing potentially harmful bugs and alerting other cells to their presence. “These types of proteins, although small, are very sophisticated in what they do,” Moir says. “And they’re very ancient, going back to the dawn of multicellular life.” © 2016 Scientific American,
By GINA KOLATA Could it be that Alzheimer’s disease stems from the toxic remnants of the brain’s attempt to fight off infection? Provocative new research by a team of investigators at Harvard leads to this startling hypothesis, which could explain the origins of plaque, the mysterious hard little balls that pockmark the brains of people with Alzheimer’s. It is still early days, but Alzheimer’s experts not associated with the work are captivated by the idea that infections, including ones that are too mild to elicit symptoms, may produce a fierce reaction that leaves debris in the brain, causing Alzheimer’s. The idea is surprising, but it makes sense, and the Harvard group’s data, published Wednesday in the journal Science Translational Medicine, supports it. If it holds up, the hypothesis has major implications for preventing and treating this degenerative brain disease. The Harvard researchers report a scenario seemingly out of science fiction. A virus, fungus or bacterium gets into the brain, passing through a membrane — the blood-brain barrier — that becomes leaky as people age. The brain’s defense system rushes in to stop the invader by making a sticky cage out of proteins, called beta amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage and dies. What is left behind is the cage — a plaque that is the hallmark of Alzheimer’s. So far, the group has confirmed this hypothesis in neurons growing in petri dishes as well as in yeast, roundworms, fruit flies and mice. There is much more work to be done to determine if a similar sequence happens in humans, but plans — and funding — are in place to start those studies, involving a multicenter project that will examine human brains. “It’s interesting and provocative,” said Dr. Michael W. Weiner, a radiology professor at the University of California, San Francisco, and a principal investigator of the Alzheimer’s Disease Neuroimaging Initiative, a large national effort to track the progression of the disease and look for biomarkers like blood proteins and brain imaging to signal the disease’s presence. © 2016 The New York Times Company
Ronald Crystal The goal of antiaddiction vaccines is to prevent addictive molecules from reaching the brain, where they produce their effects and can create chemical dependencies. Vaccines can accomplish this task, in theory, by generating antibodies—proteins produced by the immune system—that bind to addictive particles and essentially stop them in their tracks. But challenges remain. Among them, addictive molecules are often too small to be spotted by the human immune system. Thus, they can circulate in the body undetected. Researchers have developed two basic strategies for overcoming this problem. One invokes so-called active immunity by tethering an addictive molecule to a larger molecule, such as the proteins that encase a common cold virus. This viral shell does not make people sick but does prompt the immune system to produce high levels of antibodies against it and whatever is attached to it. In our laboratory, we have tested this method in animal models and successfully blocked chemical forms of cocaine or nicotine from reaching the brain. Another approach researchers are testing generates what is known as passive immunity against addictive molecules in the body. They have cultured monoclonal antibodies that can bind selectively to addictive molecules. The hurdle with this particular method is that monoclonal antibodies are expensive to produce and need to be administrated frequently to be effective. © 2016 Scientific American