Chapter 13. Memory, Learning, and Development
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By Neuroskeptic According to British biochemist Donald R. Forsdyke in a new paper in Biological Theory, the existence of people who seem to be missing most of their brain tissue calls into question some of the “cherished assumptions” of neuroscience. I’m not so sure. Forsdyke discusses the disease called hydrocephalus (‘water on the brain’). Some people who suffer from this condition as children are cured thanks to prompt treatment. Remarkably, in some cases, these post-hydrocephalics turn out to have grossly abnormal brain structure: huge swathes of their brain tissue are missing, replaced by fluid. Even more remarkably, in some cases, these people have normal intelligence and display no obvious symptoms, despite their brains being mostly water. This phenomenon was first noted by a British pediatrician called John Lorber. Lorber never published his observations in a scientific journal, although a documentary was made about them. However, his work was famously discussed in Science in 1980 by Lewin in an article called “Is Your Brain Really Necessary?“. There have been a number of other more recent published cases. Forsdyke argues that such cases pose a problem for mainstream neuroscience. If a post-hydrocephalic brain can store the same amount of information as a normal brain, he says, then “brain size does not scale with information quantity”, therefore, “it would seem timely to look anew at possible ways our brains might store their information.”
The eyes may be windows to the mind, but for children with autism, the body is the better communicator. They are just as good at reading emotions in body language as those without autism. The finding challenges the commonly held notion that children with autism have difficulty reading emotions. This may have arisen from studies focusing on whether people with the condition can interpret emotions from just the face or eyes, says Candida Peterson at the University of Queensland in Australia. “Looking at a face is in itself a problem,” says Peterson. “Autistic children and adults don’t like making eye contact,” she adds, as this requires a close encounter with another person. Reading body language, by contrast, can be done from a distance. In the study, children aged 5 to 12 were shown photos of adults with blurred faces posing in ways to convey happiness, sadness, anger, fear, disgust and surprise. Those with autism were just as good as those without at recognising the emotions. But this is only part of the picture. People with autism also have difficulty changing their behaviour in response to others’ emotions, says Julie Grezes at INSERM’s Laboratory of Cognitive Neurosciences in Paris, France. When most people recognise that someone is experiencing a certain emotion, they are able to put themselves in their place to understand why they might be feeling that way. People with autism are known to struggle with this. Now we know that they can read body language, says Peterson, we can look for ways to help them link certain cues to what the other person might be thinking and feeling. She and her colleagues now plan to test how good children with autism are at reading body language cues in real-life interactions, in particular when they are faced with individuals in extremely emotional states. Journal reference: Journal of Experimental Child Psychology, doi.org/6dp © Copyright Reed Business Information Ltd.
Link ID: 21225 - Posted: 07.27.2015
By Jane E. Brody Barrett Treadway, now 3½, has never been the best of sleepers, but her sleep grew increasingly worse in the last year and a half. She gets up several times a night, often climbs into her parents’ bed and creates havoc with their nights. “We’ve known for a long time that she snores, but until a mother-daughter trip in May when we shared a bed, I didn’t realize that this was not simply snoring,” her mother, Laura, told me. “She repeatedly stopped breathing, then started again with a loud snort that often woke her up and kept me up all night.” Barrett has sleep apnea, a condition most often diagnosed in adults and usually associated with obesity. But neither of those attributes describes Barrett, who is young and lithe, although the condition is somewhat more common in overweight children. In most cases, the problem results when, during sleep, the child’s airway is temporarily obstructed by enlarged tonsils or adenoids or both — lymphoid tissues in the back of the throat — hence the name obstructive sleep apnea. When breathing stops for 10 or more seconds, the rising blood level of carbon dioxide prompts the brain to take over and restart breathing, typically accompanied by a loud snore or snort. Rarely, a child may have what is called central sleep apnea, in which the brain temporarily fails to signal the muscles that control breathing. Experts say that between 1 percent and 3 percent of children have sleep apnea that, if untreated, can disrupt far more than a family’s restful nights. Affected children simply do not get enough restorative sleep to assure normal development. If not corrected, the condition can result in hyperactivity and attention problems in school that are often mistaken for attention deficit hyperactivity disorder (A.D.H.D.) and sometimes mistreated with a stimulant that only makes matters worse. © 2015 The New York Times Company
Alexandra Sims Intelligent people are not only smarter than the average person - it seems they could also live longer as well. A study by the London School of Economics found that smarter siblings are more likely to outlive their less clever brothers and sisters, with genetics accounting for 95 per cent of the connection between intelligence and life span. The scientists examined the differences in longevity between identical twins, who share all of their genes and non-identical twins, who on average share half of their genes. Writing in the International Journal of Epidemiology, scientists noted the difference in intellect between the twins and the age at which they died. Focusing on three different twin studies from Sweden, Denmark and the United States the researchers examined sets of twins for whom both intelligence and age of death had been recorded in pairs where at least one of the twins had died. In both types of twins it was found that the smarter of the two lived longer, but this effect was far more prominent in non-identical twins. Rosalind Arden, a research associate at the LSE, told The Times that "the association between top jobs and longer lifespans is more a result of genes than having a big desk.” She added though that the research does not mean parents can "deduce your child’s likely lifespan from how he or she does in their exams this summer”.
Qazi Rahman In a recent Guardian article , Simon Copland argued that it is very unlikely people are born gay (or presumably any other sexual orientation). Scientific evidence says otherwise. It points strongly to a biological origin for our sexualities. Finding evidence for a biological basis should not scare us or undermine gay, lesbian and bisexual (LGB) rights (the studies I refer to do not include transgendered individuals, so I’ll confine my comments to lesbian, gay and bisexual people). I would argue that understanding our fundamental biological nature should make us more vigorous in promoting LGB rights. Let’s get some facts and perspective on the issue. Evidence from independent research groups who studied twins shows that genetic factors explain about 25-30% of the differences between people in sexual orientation (heterosexual, gay, lesbian, and bisexual). Twin studies are a first look into the genetics of a trait and tell us that there are such things as “genes for sexual orientation” (I hate the phrase “gay gene”). Three gene finding studies showed that gay brothers share genetic markers on the X chromosome; the most recent study also found shared markers on chromosome 8. This latest research overcomes the problems of three prior studies which did not find the same results. Gene finding efforts have issues, as Copland argues, but these are technical and not catastrophic errors in the science. For example, complex psychological traits have many causal genes (not simply “a gay gene”). But each of these genes has a small effect on the trait so do not reach traditional levels of statistical significance. In other words, lots of genes which do influence sexual orientation may fall under the radar. But scientific techniques will eventually catch up. In fact there are more pressing problems that I would like to see addressed, such as the inadequate research on female sexuality. Perhaps this is due to the stereotype that female sexuality is “too complex” or that lesbians are rarer than gay men. © 2015 Guardian News and Media Limited
Chris Woolston A study that did not find cognitive benefits of musical training for young children triggered a “media firestorm”. Researchers often complain about inaccurate science stories in the popular press, but few air their grievances in a journal. Samuel Mehr, a PhD student at Harvard University in Cambridge, Massachusetts, discussed in a Frontiers in Psychology article1 some examples of media missteps from his own field — the effects of music on cognition. The opinion piece gained widespread attention online. Arseny Khakhalin, a neuroscientist at Bard College in Annandale-on-Hudson, New York, tweeted: Mehr gained first-hand experience of the media as the first author of a 2013 study in PLoS ONE2. The study involved two randomized, controlled trials of a total of 74 four-year-olds. For children who did six weeks of music classes, there was no sign that musical activities improved scores on specific cognitive tests compared to children who did six weeks of art projects or took part in no organized activities. The authors cautioned, however, that the lack of effect of the music classes could have been a result of how they did the studies. The intervention in the trials was brief and not especially intensive — the children mainly sang songs and played with rhythm instruments — and older children might have had a different response than the four-year-olds. There are many possible benefits of musical training, Mehr said in an interview, but finding them was beyond the scope of the study. © 2015 Nature Publishing Group
Sara Reardon After years of disappointment, clinical-trial results released on 22 July suggest that antibody treatments may produce small improvements in people with Alzheimer’s disease. The drugs — Eli Lilly’s solanezumab and Biogen’s aducanumab — target the amyloid-β protein that accumulates in the brains of people with Alzheimer’s. Many researchers question whether the findings will hold up, given that antibody drugs against amyloid have failed in every previous test against the disease. Details of the results were presented at the Alzheimer's Association International Conference in Washington DC. Lilly, of Indianapolis, Indiana, says that in a trial with 440 participants, solanezumab seemed to slow the cognitive decline of people with mild Alzheimer’s by about 30%. The loss of mental acuity in these patients over 18 months was equivalent to the deterioration that participants with a similar level of Alzheimer's disease in a placebo group experienced in just 12 months. Lilly snatched this small victory from the jaws of defeat. In 2012, the company reported no difference between patients who had taken solanezumab for 18 months and those who had received a placebo. But when the company reanalyzed that trial it found a slight improvement in participants whose symptoms were mild when the trial began. Lilly continued the test for six months and began giving solanezumab to the 440-member control group, whose disease was by then more advanced. © 2015 Nature Publishing Group,
Jon Hamilton The face of Alzheimer's isn't always old. Sometimes it belongs to someone like Giedre Cohen, who is 37, yet struggles to remember her own name. Until about a year ago, Giedre was a "young, healthy, beautiful" woman just starting her life, says her husband, Tal Cohen, a real estate developer in Los Angeles. Now, he says, "her mind is slowly wasting away." People like Giedre have a rare gene mutation that causes symptoms of Alzheimer's to appear before they turn 60. Until recently, people who inherited this gene had no hope of avoiding dementia and an early death. Now there is a glimmer of hope, thanks to a project called DIAN TU that is allowing them to take part in a study of experimental Alzheimer's drugs. The project also could have a huge payoff for society, says Dr. Randall Bateman, a professor of neurology at Washington University in St. Louis. "It's highly likely," he says, that the first drug able to prevent or delay Alzheimer's will emerge from studies of people genetically destined to get the disease. Giedre Cohen enrolled in the DIAN TU study in 2013, when she still had no symptoms of Alzheimer's, her husband says. Their story began more than a decade earlier. In 2002, Tal Cohen was on a trip to Miami to attend a wedding. He met Giedre, who was born in Lithuania, and the two fell in love. © 2015 NPR
Link ID: 21211 - Posted: 07.23.2015
By Warren Cornwall The number of U.S. school children placed in special education programs due to autism more than tripled from 2000 to 2010, to nearly 420,000. But a new study argues much of that increase likely came as educators swapped one diagnosis for another. The overall percentage of kids diagnosed with a collection of brain development problems that includes autism remained unchanged, suggesting that children who used to be labeled with conditions such as “intellectual disability” were in fact autistic. “If you asked me, ‘Is there a real increase in the prevalence of autism?’ maybe there is, but probably much lower than the reported magnitude,” says Santhosh Girirajan, a geneticist at Pennsylvania State University (Penn State), University Park. In the new study, Girirajan and colleagues combed through data collected in each state for approximately 6.2 million U.S. school children with disabilities who are enrolled in special education programs. The information is collected each year under the federal Individuals with Disabilities Education Act. Based on his or her diagnosis, each child was assigned to one of 13 broader categories, ranging from autism to physical challenges such as blindness. Between 2000 and 2010, the number of children in the autism category more than tripled from 93,624 in 2000 to 419,647 a decade later. Yet nearly two-thirds of that increase was matched by a decline in the rate at which children were labeled as having an “intellectual disability.” The number of kids in that category fell from 637,270 to 457,478. © 2015 American Association for the Advancement of Science.
Link ID: 21207 - Posted: 07.23.2015
By Sandhya Somashekhar NEW WESTMINSTER, B.C. — Alanna Whitney was a weird kid. She had a strange knack for pronouncing long words. Anchovies on pizza could send her cowering under a table. Her ability to geek out on subjects such as Greek mythology and world religions could be unsettling. She drank liquids obsessively, and in her teens, her extreme water intake landed her in the hospital. Years later, she found a word that explained it all: Autistic. Instead of grieving, she felt a rush of relief. “It was the answer to every question I’d ever had,” she recalled. “It was kind of like a go-ahead to shed all of those things I could or couldn’t do and embrace myself for who I am.” So it came to be that Whitney, 24, was arranging strawberries and store-bought cookies on platters at the Queensborough Community Center for a celebration of “Autistic Pride Day,” her shoulder-length hair dyed mermaid green to match her purse and sandals. A bowl of orange earplugs sat nearby in case any of the guests found the ambient sounds overwhelming. Whitney is part of a growing movement of autistic adults who are finding a sense of community, identity and purpose in a diagnosis that most people greet with dread. These “neurodiversity” activists contend that autism — and other brain afflictions such as dyslexia and attention deficit hyperactivity disorder — ought to be treated not as a scourge to be eradicated but rather as a difference to be understood and accepted.
Link ID: 21206 - Posted: 07.23.2015
By James Gallagher Health editor, BBC News website The first hints a drug can slow the progression of Alzheimer's disease have emerged at a conference. Data from pharmaceutical company Eli Lilly suggests its solanezumab drug can cut the rate of the dementia's progression by about a third. The results are being met with cautious optimism, with a separate trial due to report next year. The death of brain cells in Alzheimer's is currently inexorable. Solanezumab may be able to keep them alive. Current medication, such as Aricept, can only manage the symptoms of dementia by helping the dying brain cells function. But solanezumab attacks the deformed proteins, called amyloid, that build up in the brain during Alzheimer's. It is thought the formation of sticky plaques of amyloid between nerve cells leads to damage and eventually brain cell death. Solanezumab has long been the great hope of dementia research, yet an 18-month trial of the drug seemingly ended in failure in 2012. But when Eli Lilly looked more closely at the data, there were hints it could be working for patients in the earliest stages of the disease. So the company asked just over 1,000 of the patients in the original trial with mild Alzheimer's to take the drug for another two years. And the results from this extension of the original trial have now been presented, at the Alzheimer's Association International Conference. Dr Eric Siemers, from the Lilly Research Laboratories, in Indiana, told the BBC: "It's another piece of evidence that solanezumab does have an effect on the underlying disease pathology. "We think there is a chance that solanezumab will be the first disease-modifying medication to be available." The company also started a completely separate trial in mild patients in 2012, and these results could prove to be the definitive moment for the drug. © 2015 BBC.
Link ID: 21203 - Posted: 07.22.2015
By BENEDICT CAREY Women who develop slight but detectable deficits in memory and mental acuity late in life tend to decline faster than men with mild impairment, researchers reported on Tuesday. Some two-thirds of the five million Americans with Alzheimer’s disease are women, in part because women live longer. Researchers have searched in vain for decades to determine other reasons for the disparity. The authors of the new study, who presented their work at the Alzheimer’s Association International Conference in Washington, said their findings indicated nothing about possible causes of gender differences and had no immediate implications for treatment. “All we can say at this point is that there appears to be a faster trajectory for women than men” toward dementia, said Dr. P. Murali Doraiswamy, a professor of psychiatry at the Duke Institute for Brain Sciences and the study’s senior author. Katherine Amy Lin, a student of Dr. Doraiswamy’s and a co-author, presented the study. Previous research had found a steeper decline in women with mild deficits over a period of about a year. The new study extends that finding to up to eight years. “It’s a very interesting finding, but it’s also still early, so we’re limited in what conclusions we can draw,” said Dr. Edward D. Huey, a geriatric psychiatrist at Columbia University, who was not involved in the study. “I think of this as an excellent hypothesis generator. It’s something we need to investigate more deeply.” In the study, the Duke researchers analyzed scores on standard cognitive tests taken by 398 men and women, most in their 70s, being followed as part of a large, continuing Alzheimer’s trial. The participants have been taking the cognitive tests — as well as other tests, like PET scans — on average for four years, and as long as eight years. Controlling for factors that influence memory and mental acuity, like age, education and genetic predisposition, the research team found that women’s scores slipped by an average of about two points a year, compared with one point for men. The team also looked at a standard measure of life quality, rating how well people functioned socially: at home, at work and with family. That, too, slipped faster for women than for men, at about the same rate. © 2015 The New York Times Company
Kashmira Gander Performing well at school and going on to have a complex job could lower the risk of dementia, scientists have found. On the contrary, loneliness, watching too much TV and a sedentary lifestyle can make a person’s cognitive abilities decline more quickly, according to new research being presented to experts at the international Alzheimer's Association International Conference in Washington DC. Researchers are also due to show attendees the results from trials Solanezumab – believed to be the first drug to halt the progression of the disease if a patient is diagnosed early enough. One study involving 7,500 people aged 65 and above in Sweden over a 20-year period showed that dementia rates were 21 per cent higher in those whose grades were in the bottom fifth of the population. Meanwhile, participants with complex jobs involving data and numbers saw their chance of developing the disease cut by 23 per cent. Read more: Why fish oil pills may not be so healthy after all Proof that dementia risk can be reduced by improving lifestyle Charity warns of a 'worrying' lack of support for dementia patients Dementia research: Drug firms despair of finding cure and withdraw funding after a catalogue of failures For separate study in Sweden, scientists followed the lives of 440 people aged 75 or over for nine years, and discovered that those in the bottom fifth for school grades were found to have a 50 per cent increase in the risk of developing dementia. © independent.co.uk
By Hanae Armitage Playing an instrument is good for your brain. Compared to nonmusicians, young children who strum a guitar or blow a trombone become better readers with better vocabularies. A new study shows that the benefits extend to teenagers as well. Neuroscientists compared two groups of high school students over 3 years: One began learning their first instrument in band class, whereas the other focused on physical fitness in Junior Reserve Officers’ Training Corps (JROTC). At the end of 3 years, those students who had played instruments were better at detecting speech sounds, like syllables and words that rhyme, than their JROTC peers, the team reports online today in the Proceedings of the National Academy of Sciences. Researchers know that as children grow up, their ability to soak up new information, especially language, starts to diminish. These findings suggest that musical training could keep that window open longer. But the benefits of music aren’t just for musicians; taking up piano could be the difference between an A and a B in Spanish class. © 2015 American Association for the Advancement of Science
Results from tests of the drug, announced this week, show that it breaks up plaques in mice affected with Alzheimer’s disease or Parkinson’s disease, and improves the memories and cognitive abilities of the animals. Other promising results in rats and monkeys mean that the drug developers, NeuroPhage Pharmaceuticals, are poised to apply for permission to start testing it in people, with trials starting perhaps as early as next year. The drug is the first that seems to target and destroy the multiple types of plaque implicated in human brain disease. Plaques are clumps of misfolded proteins that gradually accumulate into sticky, brain-clogging gunk that kills neurons and robs people of their memories and other mental faculties. Different kinds of misfolded proteins are implicated in different brain diseases, and some can be seen within the same condition (see “Proteins gone rogue”, below). One thing they share, however, is a structural kink known as a canonical amyloid fold, and it is this on which the new drug acts (Journal of Molecular Biology, DOI: 10.1016/j.jmb.2014.04.015). Animal tests show that the drug reduces levels of amyloid beta plaques and tau protein deposits implicated in Alzheimer’s disease, and the alpha-synuclein protein deposits thought to play a role in Parkinson’s disease. Tests on lab-made samples show that the drug also targets misfolded transthyretin, clumps of which can clog up the heart and kidney, and prion aggregates, the cause of CJD, another neurodegenerative condition. Because correctly folded proteins do not have the distinct “kink”, the drug has no effect on them. © Copyright Reed Business Information Ltd.
by Sarah Schwartz Brainlike cell bundles grown in a lab may expose some of the biological differences of autistic brains. Researchers chemically reprogrammed human stem cells into small bundles of functional brain cells that mimic the developing brain. These “organoids” appear to be different when built with cells from autistic patients compared with when they are built with cells from the patients’ non-autistic family members, researchers report July 16 in Cell. The brainlike structures created from cells taken from autistic children showed increased activity in genes that control brain-cell growth and development. Too much activity in one of these genes led to an overproduction of a certain type of brain cell that suppresses the activity of other brain cells. At an early stage of development, the miniature organs grown from autistic patients’ stem cells also showed faster cell division rates than those grown from the cells of non-autistic relatives. Though the study was small, using cells from only four autistic patients and eight family members, the results may indicate common factors underlying autism, the scientists say. © Society for Science & the Public 2000 - 2015.
Link ID: 21186 - Posted: 07.18.2015
by Sarah Zielinski It may not be polite to eavesdrop, but sometimes, listening in on others’ conversations can provide valuable information. And in this way, humans are like most other species in the animal world, where eavesdropping is a common way of gathering information about potential dangers. Because alarm calls can vary from species to species, scientists have assumed that eavesdropping on these calls of “danger!” requires some kind of learning. Evidence of that learning has been scant, though. The only study to look at this topic tested five golden-mantled ground squirrels and found that the animals may have learned to recognize previously unknown alarm calls. But the experiment couldn’t rule out other explanations for the squirrels’ behavior, such as that the animals had simply become more wary in general. So Robert Magrath and colleagues at Australian National University in Canberra turned to small Australian birds called superb fairy-wrens. In the wild, these birds will flee to safety when they hear unfamiliar sounds that sound like their own alarm calls, but not when they hear alarm calls that sound different from their own. There’s an exception, though: They’ll take to cover in response to the alarm calls of other species that are common where they live. That suggests the birds learn to recognize those calls. In the lab, the team played the alarm call from a thornbill or a synthetic alarm call for 10 fairy-wrens. The birds didn’t respond to the noise. Then the birds went through two days of training in which the alarm call was played as a mock predator glided overhead. Another group of birds heard the calls but there was no pretend predator. © Society for Science & the Public 2000 - 2015
By Claire Asher Even fish have role models. In a new study, researchers paired up inexperienced fathead minnows (Pimephales promelas, pictured) with two types of mentors: a minnow raised in an environment free of predators or a minnow raised in a dangerous one simulated by the odors of predatory pike and sturgeon. Fish from dangerous environments were fearful of the smell of both unknown and familiar predators, whereas fish that grew up in safety hid when they smelled a known predator but were curious about new smells. Both types of fish passed on their fears to their protégés: Minnows that spent time with fish raised in dangerous environments were scared of all smells they came across, but those that learned from fish raised in safety feared only specific predators and took new experiences in stride, the team reports online this week in the Proceedings of the Royal Society B. The authors say this is the first experiment to show that environment can influence the social transmission of fear and reveals how risk aversion can be learned. The researchers also suggest their study may shed light on how fear disorders such as post-traumatic stress disorder (PTSD) develop in humans, which research shows can be influenced by social environment; PTSD symptoms can be acquired from friends or family who have suffered trauma, for example. © 2015 American Association for the Advancement of Science
By Emily Underwood Glance at a runner's wrist or smartphone, and you'll likely find a GPS-enabled app or gadget ticking off miles and minutes as she tries to break her personal record. Long before FitBit or MapMyRun, however, the brain evolved its own system for tracking where we go. Now, scientists have discovered a key component of this ancient navigational system in rats: a group of neurons called "speed cells" that alter their firing rates with the pace at which the rodents run. The findings may help explain how the brain maintains a constantly updated map of our surroundings. In the 1970s, neuroscientist John O'Keefe, now at University College London, discovered neurons called place cells, which fire whenever a rat enters a specific location. Thirty-five years later, neuroscientists May-Britt and Edvard Moser, now at the Norwegian University of Science and Technology in Trondheim, Norway, discovered a separate group of neurons, called grid cells, which fire at regular intervals as rats traverse an open area, creating a hexagonal grid with coordinates similar to those in GPS. The Mosers and O'Keefe shared last year's Nobel Prize in Physiology and Medicine for their findings, which hint at how the brain constructs a mental map of an animal's environment. Still mysterious, however, is how grid and place cells obtain the information that every GPS system requires: the angle and speed of an object's movement relative to a known starting point, says Edvard Moser, co-author of the new study along with May-Britt Moser, his spouse and collaborator. If the brain does indeed contain a dynamic, internal map of the world, "there has to be a speed signal" that tells the network how far an animal has moved in a given period of time, he says. © 2015 American Association for the Advancement of Science.
Keyword: Learning & Memory
Link ID: 21178 - Posted: 07.16.2015
By Fredrick Kunkle A new study suggests that Alzheimer’s disease may affect the brain differently in black people compared with whites. The research, conducted by Lisa L. Barnes at the Rush University Medical Center, suggests that African Americans are less likely than Caucasians to have Alzheimer’s disease alone and more likely to have other pathologies associated with dementia. These include the presence of Lewy bodies, which are abnormal proteins found in the brain, and lesions arising from the hardening of tiny arteries in the brain, which is caused mainly by high blood pressure and other vascular conditions. The findings suggest that researchers should seek different strategies to prevent and treat Alzheimer’s disease in blacks. While many therapeutic strategies focus on removing or modifying beta amyloid – a key ingredient whose accumulation leads to the chain of event triggering the neurodegenerative disease – the study suggests that possible treatments should pursue additional targets, particularly for African Americans. But the study also points up the critical need to enroll more black people in clinical trials. Although Barnes said the research was the largest sample of its kind, she also acknowledged that the sample is still small. And that’s at least partially because blacks, for a variety of cultural and historical reasons, are less likely to participate in scientific research.
Link ID: 21176 - Posted: 07.16.2015