Chapter 13. Memory, Learning, and Development
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Roni Caryn Rabin For years experts have urged physicians to screen infants and toddlers for autism in order to begin treatment as early as possible. But now an influential panel of experts has concluded there is not enough evidence to recommend universal autism screening of young children. The findings, from a draft proposal by the U.S. Preventive Services Task Force published Monday, are already causing consternation among specialists who work with autistic children. “I was in a meeting when I read this, and I started feeling like I’d have chest pain,” said Dr. Susan E. Levy, a pediatrician who helped write the American Academy of Pediatrics guidelines urging universal screening of all babies, with standardized screening tools at both 18 and 24 months. “I would hate to see people stop screening.” Dr. David Grossman, a pediatrician and vice chairman of the U.S. Preventive Services Task Force, emphasized that the panel’s draft proposal was a call for more research and not intended to change practices. About half of all pediatricians routinely screen toddlers for autism. “This doesn’t mean ‘don’t screen.’ ” Dr. Grossman said. “It means there is not enough evidence to make a recommendation.” Dr. Grossman also noted that the panel’s conclusion applied only to routine screening of healthy children without symptoms. A child displaying symptoms associated with autism should always be evaluated, he said. “If a parent comes in and says, ‘My child isn’t looking at me,’ that’s not a screening,” Dr. Grossman said. “You hear that as a doctor and you say, ‘That needs to be looked at,’ and you embark on a series of tests.” Despite those reassurances, autism experts worry that the panel’s lack of support for early autism screening could undermine efforts to identify and treat children as early as possible. The task force is an independent panel of experts in prevention and primary care appointed by the federal Department of Health and Human Services. The task force wields enormous influence in the medical community. In 2009, the panel issued controversial screening guidelines for breast cancer, stating that routine mammograms should start at 50 rather than 40. © 2015 The New York Times Company
Link ID: 21262 - Posted: 08.04.2015
Cerebral palsy, the most common cause of physical disability in children, has long been thought to result from brain injury in the fetus. But new Canadian research is challenging that notion, finding that at least one in 10 cases likely has an underlying genetic cause. So ingrained has medical dogma been around the root causes of cerebral palsy that "when I showed the results to our clinical geneticists, initially they didn't believe it," he said. About two in every 1,000 babies born are affected by cerebral palsy. An estimated 50,000 Canadian children and adults have the condition, which leads to varying degrees of motor impairment, including muscle spasticity and involuntary movements. Symptoms can include epilepsy as well as learning, speech, hearing and visual impairments. Some with the disorder are mildly affected, while others can't walk or communicate. Traditionally, cerebral palsy was believed to be caused by a stroke or infection of the brain in the developing fetus, or by birth asphyxia — a lack of oxygen to the infant during delivery. But genetic testing of a group of affected children from across Canada found that in 10 per cent of cases, structural changes to the DNA appear to have given rise to the condition. The research team, which includes physicians at the McGill University Health Centre in Montreal, performed genome sequencing tests on 115 children with cerebral palsy and their parents. ©2015 CBC/Radio-Canada.
Steve Connor A computer game designed by neuroscientists has helped patients with schizophrenia to recover their ability to carry out everyday tasks that rely on having good memory, a study has found. Patients who played the game regularly for a month were four times better than non-players at remembering the kind of things that are critical for normal, day-to-day life, researchers said. The computer game was based on scientific principles that are known to “train” the brain in episodic memory, which helps people to remember events such as where they parked a car or placed a set of keys, said Professor Barbara Sahakian of Cambridge University, the lead author of the study. People recovering from schizophrenia suffer serious lapses in episodic memory which prevent them from returning to work or studying at university, so anything that can improve the ability of the brain to remember everyday events will help them to lead a normal life, Professor Sahakian said. Schizophrenia affects about one in every hundred people and results in hallucinations and delusions (Rex) Schizophrenia affects about one in every hundred people and results in hallucinations and delusions (Rex) “This kind of memory is essential for everyday learning and everything we do really both at home and at work. We have formulated an iPad game that could drive the neural circuitry behind episodic memory by stimulating the ability to remember where things were on the screen,” Professor Sahakian said. © independent.co.uk
Michael Sullivan It's 5:45 in the morning, and in a training field outside Siem Reap, home of Angkor Wat, Cambodia's demining rats are already hard at work. Their noses are close to the wet grass, darting from side to side, as they try to detect explosives buried just beneath the ground. Each rat is responsible for clearing a 200-square-meter (239-square-yard) patch of land. Their Cambodian supervisor, Hulsok Heng, says they're good at it. "They are very good," he says. "You see this 200 square meters? They clear in only 30 minutes or 35 minutes. If you compare that to a deminer, maybe two days or three days. The deminer will pick up all the fragmentation, the metal in the ground, but the rat picks up only the smell of TNT. Not fragmentation or metal or a nail or a piece of crap in the ground." That's right: Someone using a metal-detecting machine will take a lot longer to detect a land mine than a rat using its nose. There's plenty of work for the rats here in Cambodia. The government estimates there are 4 million to 6 million land mines or other pieces of unexploded ordnance — including bombs, shells and grenades — littering the countryside, remnants of decades of conflict. Neighboring Vietnam and Laos also have unexploded ordnance left over from the Vietnam War. Dozens of people are killed or maimed in the region every year — and there's a financial toll as well, since the presence of these potentially deadly devices decreases the amount of land available to farmers. © 2015 NPR
By Robert Gebelhoff Just in case sea snails aren't slow enough, new research has found that they get more sluggish when they grow old — and the discovery is helping us to understand how memory loss happens in humans. It turns out that the sea snail, which has a one-year lifespan, is actually a good model to study nerve cells and how the nervous system works in people. How neurons work is fundamentally identical in almost all animals, and the simplicity of the snail's body gives researchers the chance to view how different the system works more directly. "You can count the number of nerve cells that are relevant to a reflex," said Lynne Fieber, a professor at the University of Miami who leads research with the snails at the school. She and a team of researchers have been using the slimy little critters to learn how nerve cells respond to electric shock. They "taught" the snails to quickly contract their muscle tails by administering electric shocks and then poking the tails, a process called "sensitization." They then studied the responses at various ages. The scientists, whose work was published this week in the journal PlOS One, found that as the senior citizen specimens do not learn to contract from the shock very well. As the snails grow older, their tail startle reflex lessened, and then disappeared. So I guess you could say the frail snails' tails fail to avail (okay, I'll stop).
By Bret Stetka The brain is extraordinarily good at alerting us to threats. Loud noises, noxious smells, approaching predators: they all send electrical impulses buzzing down our sensory neurons, pinging our brain’s fear circuitry and, in some cases, causing us to fight or flee. The brain is also adept at knowing when an initially threatening or startling stimulus turns out to be harmless or resolved. But sometimes this system fails and unpleasant associations stick around, a malfunction thought to be at the root of post-traumatic stress disorder (PTSD). New research has identified a neuronal circuit responsible for the brain’s ability to purge bad memories, findings that could have implications for treating PTSD and other anxiety disorders. Like most emotions, fear is neurologically complicated. But previous work has consistently implicated two specific areas of the brain as contributing to and regulating fear responses. The amygdala, two small arcs of brain tissue deep beneath our temples, is involved in emotional reactions, and it flares with activity when we are scared. If a particular threat turns out to be harmless, a brain region behind the forehead called the prefrontal cortex steps in and the fright subsides. Our ability to extinguish painful memories is known to involve some sort of coordinated effort between the amygdala and the prefrontal cortex. The new study, led by Andrew Holmes at the National Institutes of Health, however, confirms that a working connection between the two brain regions is necessary to do away with fear. Normally mice that repeatedly listen to a sound previously associated with a mild foot shock will learn that on its own the tone is harmless, and they will stop being afraid. Using optogenetic stimulation technology, or controlling specific neurons and animal behavior using light, the authors found that disrupting the amygdala–prefrontal cortex connection prevents mice from overcoming the negative association with the benign tone. In neurobiology speak, memory “extinction” fails to occur. They also found that the opposite is true—that stimulating the circuit results in increased extinction of fearful memories. © 2015 Scientific American
By Ariana Eunjung Cha Think you have your hands full making sure your baby is fed and clean and gets enough sleep? Here's another thing for the list: developing your child's social skills by the way you talk. People used to think that social skills were something kids were born with, not taught. But a growing body of research shows that the environment a child grows up in as an infant and toddler can have a major impact on how they interact with others as they get older. And it turns out that a key factor may be the type of language they hear around them, even at an age when all they can do is babble. Psychologists at the University of York observed 40 mothers and their babies at 10, 12, 16 and 20 months and logged the kind of language mothers used during play. They were especially interested in "mind-related comments," which include inferences about what someone is thinking when a behavior or action happens. Elizabeth Kirk, a lecturer at the university who is the lead author of the study, published in the British Journal of Developmental Psychology on Monday, gave this as an example: If an infant has difficulty opening a door on a toy, the parent might comment that the child appears "frustrated." Then researchers revisited the children when they were 5 or 6 years of age and assessed their socio-cognitive ability. The test involved reading a story and having the children answer comprehension questions that show whether they understood the social concept -- persuasion, joke, misunderstanding, white lies, lies, and so forth -- that was represented.
Tara Haelle To tell if a baby has been injured or killed by being shaken, the courts use three hallmark symptoms: Bleeding and swelling in the brain and retinal bleeding in the eyes. Along with other evidence, those standards are used to convict caregivers of abusive head trauma, both intentional and unintentional, that can result in blindness, seizures, severe brain damage or death. But in recent years a small cadre of experts testifying for the defense in cases across the country has called into question whether those symptoms actually indicate abuse. Though they are in the minority – disputing the consensus of child abuse experts, pediatricians and an extensive evidence base – they have gained traction in the media and in courtrooms by suggesting that shaking a child cannot cause these injuries. Instead, they argue that undiagnosed medical conditions, falls or other accidents are the cause. So researchers have developed and validated a tool doctors can use to distinguish between head injuries resulting from abuse and those from accidents or medical conditions. The method, described in the journal Pediatrics Monday, asks doctors to check for six other injuries, each of which increases the likelihood that a head injury resulted from severe shaking, blunt force or both. "It is vitally important that abuse head trauma is diagnosed accurately so that the team looking after the child can ensure that they receive appropriate support and are protected from further harm," lead study author Laura Elizabeth Cowley, a PhD student at the Cardiff University School of Medicine in the U.K., said in an email. "However, it is also important that accidental head injury cases are not wrongly diagnosed as abusive," she continues, "because this can have devastating consequences for the families involved." © 2015 NPR
By Katie Free Shouting during a nightmare. Struggling to balance a checkbook. A weakened sense of smell. Hallucinations. Chronic constipation. This bizarre mix of symptoms often stumps doctors, but they are some of the telltale signs of Lewy body dementia—the second most common type (after Alzheimer's disease), affecting an estimated 1.4 million Americans. Lewy bodies are protein clumps that kill neurons. Depending on where they cluster in the brain, they can cause either Parkinson's disease or Lewy body dementia, although the two conditions tend to overlap as they progress. Lewy body dementia is more difficult to diagnose and treat, in part because the earliest warning signs have remained unknown. Now a new study finds that certain sensory and motor symptoms can help predict who will acquire the disease, paving the way for targeted studies. Researchers at the Center for Advanced Research in Sleep Medicine (which is associated with the University of Montreal) and at McGill University followed 89 patients with a history of acting out their dreams—not sleepwalking but moving or vocalizing in bed during rapid eye movement (REM) sleep. The failure to suppress such nighttime activity can be an early sign that something is going wrong in the brain; past studies have shown that up to 80 percent of patients who act out their dreams will eventually develop some form of neurodegeneration. Over 10 years the McGill researchers carefully tracked the patients' other potential symptoms of neural disease, such as mild cognitive impairment, depression and movement problems. They found a cluster of symptoms—abnormal color vision, loss of smell and motor dysfunction—that doubled the chance that a person with the REM sleep disorder would develop Parkinson's or Lewy body dementia within three years, according to the study published in February in Neurology. © 2015 Scientific American
Link ID: 21237 - Posted: 07.30.2015
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