Chapter 7. Life-Span Development of the Brain and Behavior
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By Helen Briggs Health editor, BBC News website More than 99% of drug trials for Alzheimer's disease during the past decade have failed, according to a study. There is an urgent need to increase the number of potential therapies being investigated, say US scientists. Only one new medicine has been approved since 2004, they report in the journal Alzheimer's Research & Therapy. The drug failure rate is troubling and higher than for other diseases such as cancer, says Alzheimer's Research UK. Dr Jeffrey Cummings, of the Cleveland Clinic Lou Ruvo Center for Brain Health, in Las Vegas, and colleagues, examined a public website that records clinical trials. Between 2002 and 2012, they found 99.6% of trials of drugs aimed at preventing, curing or improving the symptoms of Alzheimer's had failed or been discontinued. This compares with a failure rate of 81% for cancer drugs. The failure rate was "especially troubling" given the rising numbers of people with dementia, said Dr Simon Ridley, of Alzheimer's Research UK. "The authors of the study highlight a worrying decline in the number of clinical trials for Alzheimer's treatments in more recent years," he said. "There is a danger that the high failure rates of trials in the past will discourage pharmaceutical companies from investing in dementia research. BBC © 2014
Link ID: 19793 - Posted: 07.04.2014
By Smitha Mundasad Health reporter, BBC News Researchers have identified a gene that may put people at greater risk of strokes and heart attacks. Writing in PLOS ONE they say the gene fault may encourage the formation of blood clots - the ultimate cause of most heart attacks and strokes. Scientists hope gene tests may help doctors one day to pinpoint individuals more likely to suffer these conditions. But experts say lifestyle factors such as smoking and exercise have the greatest influence on risk. Around one in 10 people in the Caucasian population carries this variation of the gene, named PIA2. And researchers from King's College London reviewed more than 80 studies involving about 50,000 people - the largest analysis of this genetic fault to date. Threat to under-45s They found individuals with PIA2 were more likely to have a stroke - caused by a blood clot blocking blood supply to the brain - than those without the gene. Scientists calculate the gene increases a person's risk of having a stroke by 10-15%. But how significant this increase is depends on an individual's baseline risk - influenced by factors such as smoking, diet, weight and exercise, the scientists say. Heart attacks are caused by a blockage to the blood vessels that carry oxygen to the heart. More than 100,000 heart attacks are recorded in the UK each year And for people with two copies of the gene the risk rises by up to 70% from this baseline. In a second study published in the same journal, the scientists show PIA2 is also linked to an increased risk of heart attacks in people under 45. More research is needed to see whether this holds true for the whole population, they say. About 150,000 people have a stroke in the UK each year and more than 100,000 heart attacks are recorded annually. BBC © 2014
By GRETCHEN REYNOLDS Exercise may help to keep the brain robust in people who have an increased risk of developing Alzheimer’s disease, according to an inspiring new study. The findings suggests that even moderate amounts of physical activity may help to slow the progression of one of the most dreaded diseases of aging. For the new study, which was published in May in Frontiers in Aging Neuroscience, researchers at the Cleveland Clinic in Ohio recruited almost 100 older men and women, aged 65 to 89, many of whom had a family history of Alzheimer’s disease. Alzheimer’s disease, characterized by a gradual and then quickening loss of memory and cognitive functioning, can strike anyone. But scientists have discovered in recent years that people who harbor a specific variant of a gene, known as the APOE epsilon4 allele or the e4 gene for short, have a substantially increased risk of developing the disease. Genetic testing among the volunteers in the new study determined that about half of the group carried the e4 gene, although, at the start of the study, none showed signs of memory loss beyond what would be normal for their age. Then the scientists set out to more closely examine their volunteers’ brains. For some time, researchers have suspected that Alzheimer’s disease begins altering the structure and function of the brain years or even decades before the first symptoms appear. In particular, it’s been thought that the disease silently accelerates the atrophy of the hippocampus, a portion of the brain critical for memory processing. Brain scans of people who have Alzheimer’s show that their hippocampi are considerably more shrunken than those of people of the same age without the disease. There’s been less study, though, of possible shrinkage in the brains of cognitively normal people at risk for Alzheimer’s. One reason is that, until recently, few interventions, including drugs, had shown much promise in slowing or preventing the disease’s progression, so researchers – and patients – have been reluctant to identify markers of its potential onset. © 2014 The New York Times Company
Link ID: 19783 - Posted: 07.02.2014
Learning a second language benefits the brain in ways that can pay off later in life, suggests a deepening field of research that specializes in the relationship between bilingualism and cognition. In one large Scottish test, researchers discovered archival data on 835 native speakers of English who were born in Edinburgh in 1936. The participants had been given an intelligence test at age 11 as part of standard British educational policy and many were retested in their early 70s. Those who spoke two or more languages had significantly better cognitive abilities on certain tasks compared with what would be expected from their IQ test scores at age 11, Dr. Thomas Bak of the Centre for Cognitive Aging and Cognitive Epidemiology at the University of Edinburgh reported in the journal Annals of Neurology. "Our results suggest a protective effect of bilingualism against age-related cognitive decline," independently of IQ, Bak and his co-authors concluded. It was a watershed study in 1962 by Elizabeth Peal and Wallace Lambert at McGill University in Montreal that turned conventional thinking on bilingualism on its head and set the rationale for French immersion in Canada. Psychologists at York University in Toronto have also been studying the effect of bilingualism on the brain across the lifespan, including dementia. They’ve learned how people who speak a second language outperform those with just one on tasks that tap executive function such as attention, selection and inhibition. Those are the high-level cognitive processes we use to multitask as we drive on the highway and juggle remembering the exit and monitoring our speed without getting distracted by billboards. © CBC 2014
by Laura Sanders At the playground yesterday, Baby V commando-crawled through a tunnel with holes on the side. Every so often, I stuck my face in there with a loud “peekaboo.” She reached up longingly toward the bouncy duck. I picked her up and steadied her as she lurched back and forth. She scrambled up some low stairs and launched down a slide. I lurked near the bottom, ready to assist and yell “yay” when she didn’t face-plant. The one thing I didn’t do was sit back and leave her to her own devices, free from my helicopter-mom tendencies. But since I have the most ridiculous crush on that girl, it’s hard for me to leave her be. As a parent who works outside of the home, I treasure our time together. But as she becomes more capable and independent, I realize that I need to be more thoughtful about letting her carve out some space for herself. A recent research paper emphasized this point. The study, published June 17 in Frontiers in Psychology, finds that children who spend more time in unstructured activities may better master some important life skills. Researchers sorted kids’ activities into structured activities, which included child-initiated activities such as playing alone or with friends, singing, riding bikes and camping, and structured activities, including soccer practice, piano lessons, chores and homework. Six- and seven-year-olds who had more unstructured time scored higher on a measure of executive function, complex cognitive abilities such as seamlessly switching between tasks, resisting impulses and paying attention — all things that help people get along in this world. © Society for Science & the Public 2000 - 2013.
Keyword: Development of the Brain
Link ID: 19780 - Posted: 07.02.2014
By RICHARD A. FRIEDMAN ADOLESCENCE is practically synonymous in our culture with risk taking, emotional drama and all forms of outlandish behavior. Until very recently, the widely accepted explanation for adolescent angst has been psychological. Developmentally, teenagers face a number of social and emotional challenges, like starting to separate from their parents, getting accepted into a peer group and figuring out who they really are. It doesn’t take a psychoanalyst to realize that these are anxiety-provoking transitions. But there is a darker side to adolescence that, until now, was poorly understood: a surge during teenage years in anxiety and fearfulness. Largely because of a quirk of brain development, adolescents, on average, experience more anxiety and fear and have a harder time learning how not to be afraid than either children or adults. Different regions and circuits of the brain mature at very different rates. It turns out that the brain circuit for processing fear — the amygdala — is precocious and develops way ahead of the prefrontal cortex, the seat of reasoning and executive control. This means that adolescents have a brain that is wired with an enhanced capacity for fear and anxiety, but is relatively underdeveloped when it comes to calm reasoning. You may wonder why, if adolescents have such enhanced capacity for anxiety, they are such novelty seekers and risk takers. It would seem that the two traits are at odds. The answer, in part, is that the brain’s reward center, just like its fear circuit, matures earlier than the prefrontal cortex. That reward center drives much of teenagers’ risky behavior. This behavioral paradox also helps explain why adolescents are particularly prone to injury and trauma. The top three killers of teenagers are accidents, homicide and suicide. The brain-development lag has huge implications for how we think about anxiety and how we treat it. It suggests that anxious adolescents may not be very responsive to psychotherapy that attempts to teach them to be unafraid, like cognitive behavior therapy, which is zealously prescribed for teenagers. © 2014 The New York Times Company
Keyword: Development of the Brain
Link ID: 19775 - Posted: 07.01.2014
A toxic caffeine level was found in the system of a high school student who died unexpectedly, says a U.S. coroner who warns young people need to be educated about the dangers of taking the potent powder that is sold online. Logan Stiner, 18, was found dead at his family’s home in May. Steiner was an excellent student and a healthy young man who didn’t do drugs, Dr. Stephen Evans, a coroner in Lorain County, Ohio, said Monday. "We sent his blood out for levels, and [when] it came back it was a toxic level. Caffeine toxicity will do exactly what happened to him. It'll lead to things like cardiac arrhytmias and seizures," Evans said in an interview. Use of caffeine from coffee, tea and other beverages is so widespread that it is considered innocuous, but that’s not the case when it’s taken in an overdose amount. Powdered caffeine is sold in bulk over the internet. Problems can arise because adding a teaspoon of the caffeine powder to water is the equivalent of 30 cups of coffee. About one-sixteenth of a teaspoon of the powder is equal to about two cups of coffee. Evans said he recognizes that weightlifters will say Stiner should’ve taken the correct amount. "One-sixteenth of a teaspoon. You expect a kid to figure that out?" He suggested that regulators re-consider internet sales of a pound of powdered caffeine to young people. When Evans and his staff reviewed the pathology literature, they found 18 other cases of deaths in the U.S. from caffeine overdoses. Some were suicides and others were accidental, but he suspects the deaths are underreported since few pathologists investigating deaths from seizure and cardiac arrhytmia check caffeine levels. © CBC 2014
Emotional and behavioral problems show up even with low exposure to lead, and as blood lead levels increase in children, so do the problems, according to research funded by the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health. The results were published online June 30 in the journal JAMA Pediatrics. “This research focused on lower blood lead levels than most other studies and adds more evidence that there is no safe lead level,” explained NIEHS Health Scientist Administrator Kimberly Gray, Ph.D. “It is important to continue to study lead exposure in children around the world, and to fully understand short-term and long-term behavioral changes across developmental milestones. It is well-documented that lead exposure lowers the IQ of children.” Blood lead concentrations measured in more than 1,300 preschool children in China were associated with increased risk of behavioral and emotional problems, such as being anxious, depressed, or aggressive. The average blood lead level in the children was 6.4 micrograms per deciliter. While many studies to date have examined health effects at or above 10 micrograms per deciliter, this study focused on lower levels. The CDC now uses a reference level of 5 micrograms per deciliter, to identify children with blood lead levels that are much higher than normal, and recommends educating parents on reducing sources of lead in their environment and continued monitoring of blood lead levels.
|By Lisa Marshall Is Alzheimer's disease an acquired form of Down syndrome? When neurobiologist Huntington Potter first posed the question in 1991, Alzheimer's researchers were skeptical. They were just beginning to explore the causes of the memory-robbing neurological disease. Scientists already knew that by age 40, nearly 100 percent of patients with Down syndrome, who have an extra copy of chromosome 21, had brains full of beta-amyloid peptide—the neuron-strangling plaque that is a hallmark of Alzheimer's. They also knew that the gene that codes for that protein lives on chromosome 21, suggesting that people acquire more plaque because they get an extra dose of the peptide. Potter, though, suggested that if people with Down syndrome develop Alzheimer's because of an extra chromosome 21, healthy people may develop Alzheimer's for the same reason. A quarter of a century later mounting evidence supports the idea. “What we hypothesized in the 1990s and have begun to prove is that people with Alzheimer's begin to make molecular mistakes and generate cells with three copies of chromosome 21,” says Potter, who was recently appointed director of Alzheimer's disease research at the University of Colorado School of Medicine, with the express purpose of studying Alzheimer's through the lens of Down syndrome. He is no longer the only one exploring the link. In recent years dozens of studies have shown Alzheimer's patients possess an inordinate amount of Down syndrome–like cells. One 2009 study by Russian researchers found that up to 15 percent of the neurons in the brains of Alzheimer's patients contained an extra copy of chromosome 21. Others have shown Alzheimer's patients have 1.5 to two times as many skin and blood cells with the extra copy as healthy controls. Potter's own research in mice suggests a vicious cycle: when normal cells are exposed to the beta-amyloid peptide, they tend to make mistakes when dividing, producing more trisomy 21 cells, which, in turn, produce more plaque. In August, Potter and his team published a paper in the journal Neurobiology of Aging describing why those mistakes may occur: the inhibition of a specific enzyme. © 2014 Scientific American
Link ID: 19771 - Posted: 06.25.2014
By Gary Stix Tony Zador: The human brain has 100 billion neurons, a mouse brain has maybe 100 million. What we’d really like to understand is how we go from a bunch of neurons to thought, feelings, behavior. We think that the key is to understand how the different neurons are connected to one another. So traditionally there have been a lot of techniques for studying connectivity but at a fairly crude level. We can, for instance, tell that a bunch of neurons here tend to be connected to a bunch of neurons there. There are also techniques for looking at how single neurons are connected but only for individual links between those neurons. What we would love to be able to do is to tell how every single neuron in the brain is connected to every single other neuron in the brain. So if you wanted to navigate through the United States, one of the most useful things you could have is a roadmap. It wouldn’t tell you everything about the United States, but it would be very hard to get around without a complete roadmap of the country. We need something like that for the brain. Zador: Traditionally the way people study connectivity is as a branch of microscopy. Typically what people do is they use one method or another to label a neuron and then they observe that neuron at some level of resolution. But the challenge that’s at the core of all the microscopy techniques is that neurons can extend long distances. That might be millimeters in a mouse brain or, in fact, in a giraffe brain, there are neurons that go all the way from the brain to its foot, which can be over 15 feet. Brain cells are connected with one another at structures called synapses, which are below the resolution of light microscopy. That means that if you really want to understand how one neuron is connected to another, you need to resolve the synapse, which requires electron microscopy. You have to take incredibly thin sections of brain and then image them. © 2014 Scientific American
|By Lindsey Konkel and Environmental Health News Babies whose moms lived within a mile of crops treated with widely used pesticides were more likely to develop autism, according to new research. The study of 970 children, born in farm-rich areas of Northern California, is part of the largest project to date that is exploring links between autism and environmental exposures. The University of California, Davis research – which used women’s addresses to determine their proximity to insecticide-treated fields – is the third project to link prenatal pesticide exposures to autism and related disorders. “The weight of evidence is beginning to suggest that mothers’ exposures during pregnancy may play a role in the development of autism spectrum disorders,” said Kim Harley, an environmental health researcher at the University of California, Berkeley who was not involved in the new study. One in every 68 U.S. children has been identified with an autism spectrum disorder—a group of neurodevelopmental disorders characterized by difficulties with social interactions, according to the Centers for Disease Control and Prevention. “This study does not show that pesticides are likely to cause autism, though it suggests that exposure to farming chemicals during pregnancy is probably not a good thing,” said Dr. Bennett Leventhal, a child psychiatrist at University of California, San Francisco who studies autistic children. He did not participate in the new study. The biggest known contributor to autism risk is having a family member with it. Siblings of a child with autism are 35 times more likely to develop it than those without an autistic brother or sister, according to the National Institutes of Health. © 2014 Scientific American
|By Tori Rodriguez One of the most devastating aspects of Alzheimer's is its effect on patients' ability to recall life events. Several studies have found that music helps to strengthen these individuals' autobiographical memories, and a paper in the November 2013 Journal of Neurolinguistics builds on these findings by exploring the linguistic quality of those recollections. Researchers instructed 18 patients with Alzheimer's and 18 healthy control subjects to tell stories from their lives in a silent room or while listening to the music of their choice. Among the Alzheimer's patients, the music-cued stories contained a greater number of meaningful words, were more grammatically complex and conveyed more information per number of words. Music may enhance narrative memories because “music and language processing share a common neural basis,” explains study co-author Mohamad El Haj of Lille University in France. © 2014 Scientific American
Link ID: 19762 - Posted: 06.24.2014
By Adam Carter, CBC News Women who take antidepressants when they’re pregnant could unknowingly predispose their kids to type 2 diabetes and obesity later on in life, new research out of McMaster University suggests. The study, conducted by associate professor of obstetrics and gynecology Alison Holloway and PhD student Nicole De Long, found a link between the antidepressant fluoxetine and increased risk of obesity and diabetes in children. Holloway cautions that this is not a warning for all pregnant women to stop taking antidepressants, but rather to start a conversation about prenatal care and what works best on an individual basis. “There are a lot of women who really need antidepressants to treat depression. This is what they need,” Holloway told CBC. “We’re not saying you should necessarily take patients off antidepressants because of this — but women should have this discussion with their caregiver.” “Obesity and Type 2 diabetes in children is on the rise and there is the argument that it is related to lifestyle and availability of high calorie foods and reduced physical activity, but our study has found that maternal antidepressant use may also be a contributing factor to the obesity and diabetes epidemic.” According to a study out of Memorial University in St. John's, obesity rates in Canada have tripled between 1985 and 2011. Canada also ranks poorly when it comes to its overall number of cases of diabetes, according to international report from the Organization for Economic Co-operation and Development, released last year. © CBC 2014
By Elizabeth Norton A single dose of a century-old drug has eliminated autism symptoms in adult mice with an experimental form of the disorder. Originally developed to treat African sleeping sickness, the compound, called suramin, quells a heightened stress response in neurons that researchers believe may underlie some traits of autism. The finding raises the hope that some hallmarks of the disorder may not be permanent, but could be correctable even in adulthood. That hope is bolstered by reports from parents who describe their autistic children as being caught behind a veil. "Sometimes the veil parts, and the children are able to speak and play more normally and use words that didn't seem to be there before, if only for a short time during a fever or other stress" says Robert Naviaux, a geneticist at the University of California, San Diego, who specializes in metabolic disorders. Research also shows that the veil can be parted. In 2007, scientists found that 83% of children with autism disorders showed temporary improvement during a high fever. The timing of a fever is crucial, however: A fever in the mother can confer a higher risk for the disorder in the unborn child. As a specialist in the cell's life-sustaining metabolic processes, Naviaux was intrigued. Autism is generally thought to result from scrambled signals at synapses, the points of contact between nerve cells. But given the specific effects of something as general as a fever, Naviaux wondered if the problem lay "higher up" in the cell's metabolism. © 2014 American Association for the Advancement of Science.
Link ID: 19749 - Posted: 06.19.2014
As the popularity of soccer grows among children, doctors and researchers say the dangers of concussions need to be taken more seriously in the sport. When researchers at St. Michael's Hospital in Toronto reviewed the evidence on concussions and heading in soccer this winter, they found a higher incidence of concussions among females than males playing the world's most popular sport. Doctors warn that heading — purposely using the head to control and hit the ball — is a unique aspect of the beautiful game that needs more attention. Heading the ball isn’t necessarily going to cause an overt concussion with symptoms, but the accumulation of those impacts over time could cause difficulties with thinking, concentration and memory, said study author Monica Maher, a graduate student at the University of Toronto, and a former soccer goalkeeper. Maher doesn't want people to stop playing soccer or stop heading the ball. She does suggest limits on head exposure in younger children and padding on goal posts to prevent injury to the youngest players. Dr. David Robinson, a sports medicine physician at McMaster University in Hamilton, sees 10 to 15 concussions a week, including many related to soccer. "It's not a stretch to think that these chronic subconcussive blows may be softening the brain, injuring the brain over time," Robinson said. He calls it a step forward that balls are becoming lighter for young people. He reminds parents and coaches that if a concussion is suspected, it's best to remove an athlete from play. As for the differences in injury rates between males and females, Maher pointed to a few potential explanations: © CBC 2014
Associated Press In one of the most ambitious attempts yet to thwart Alzheimer's disease, a major study got under way Monday to see if an experimental drug can protect healthy seniors whose brains harbor silent signs that they're at risk. Scientists plan to eventually scan the brains of thousands of older volunteers in the U.S., Canada and Australia to find those with a sticky build-up believed to play a key role in development of Alzheimer's - the first time so many people without memory problems get the chance to learn the potentially troubling news. Having lots of that gunky protein called beta-amyloid doesn't guarantee someone will get sick. But the big question: Could intervening so early make a difference for those who do? "We have to get them at the stage when we can save their brains," said Dr. Reisa Sperling of Boston's Brigham and Women's Hospital and Harvard Medical School, who is leading the huge effort to find out. Researchers are just beginning to recruit volunteers, and on Monday, a Rhode Island man was hooked up for an IV infusion at Butler Hospital in Providence, the first treated. Peter Bristol, 70, of Wakefield, R.I., figured he was at risk because his mother died of Alzheimer's and his brother has it. "I felt I needed to be proactive in seeking whatever therapies might be available for myself in the coming years," said Bristol, who said he was prepared when a PET scan of his brain showed he harbored enough amyloid to qualify for the research. "Just because I have it doesn't mean I'm going to get Alzheimer's," he stressed. But Bristol and his wife are "going into the situation with our eyes wide open." He won't know until the end of what is called the A4 Study - it stands for Anti-Amyloid Treatment in Asymptomatic Alzheimer's - whether he received monthly infusions of the experimental medicine, Eli Lilly & Co.'s solanezumab, or a dummy drug. © 2014 Hearst Communications, Inc.
Link ID: 19717 - Posted: 06.10.2014
by Ashley Yeager Being put under anesthesia as an infant may make it harder for a person to recall details or events when they grow older. Previous studies on animals had shown that anesthesia impairs parts of the brain that help with recollection. But it was not clear how this type of temporary loss of consciousness affected humans. Comparing the memory of 28 children ages 6 to 11 who had undergone anesthesia as infants to 28 children similar in age who had not been put under suggests that the early treatment impairs recollection later in life, researchers report June 9 in Neuropsychopharmacology. The team reported similar results for a small study on rats and notes that early anesthesia did not appear to affect the children's familiarity with objects and events or their IQ. © Society for Science & the Public 2000 - 2013.
by Laura Sanders Transplanted cells can flourish for over a decade in the brain of a person with Parkinson’s disease, scientists write in the June 26 Cell Reports. Finding that these cells have staying power may encourage clinicians to pursue stem cell transplants, a still-experimental way to counter the brain deterioration that comes with Parkinson’s. Penelope Hallett of Harvard University and McLean Hospital in Belmont, Mass., and colleagues studied postmortem brain tissue from five people with advanced Parkinson’s. The five had received stem cell transplants between four and 14 years earlier. In all five people’s samples, neurons that originated from the transplanted cells showed signs of good health and appeared capable of sending messages with the brain chemical dopamine, a neurotransmitter that Parkinson’s depletes. Results are mixed about whether these transplanted cells are a good way to ease Parkinson’s symptoms. Some patients have shown improvements after the new cells stitched themselves into the brain, while others didn’t benefit from them. The cells can also cause unwanted side effects such as involuntary movements. P. J. Hallett et al. Long-term health of dopaminergic neuron transplants in Parkinson’s disease patients. Cell Reports. Vol. 7, June 26, 2014. doi: 10.1016/j.celrep.2014.05.027. © Society for Science & the Public 2000 - 2013
By Jenny Graves The claim that homosexual men share a “gay gene” created a furor in the 1990s. But new research two decades on supports this claim – and adds another candidate gene. To an evolutionary geneticist, the idea that a person’s genetic makeup affects their mating preference is unsurprising. We see it in the animal world all the time. There are probably many genes that affect human sexual orientation. But rather than thinking of them as “gay genes,” perhaps we should consider them “male-loving genes.” They may be common because these variant genes, in a female, predispose her to mate earlier and more often and to have more children. Likewise, it would be surprising if there were not “female-loving genes” in lesbian women that, in a male, predispose him to mate earlier and have more children. We can detect genetic variants that produce differences between people by tracking traits in families that display differences. Patterns of inheritance reveal variants of genes (called “alleles”) that affect normal differences, such as hair color, or disease states, such as sickle cell anemia. Quantitative traits, such as height, are affected by many different genes, as well as environmental factors. It’s hard to use these techniques to detect genetic variants associated with male homosexuality partly because many gay men prefer not to be open about their sexuality. It is even harder because, as twin studies have shown, shared genes are only part of the story. Hormones, birth order and environment play roles, too.
Laura Spinney One day in 1991, neurologist Warren Strittmatter asked his boss to look at some bewildering data. Strittmatter was studying amyloid-β, the main component of the molecular clumps found in the brains of people with Alzheimer's disease. He was hunting for amyloid-binding proteins in the fluid that buffers the brain and spinal cord, and had fished out one called apolipoprotein E (ApoE), which had no obvious connection with the disease. Strittmatter's boss, geneticist Allen Roses of Duke University in Durham, North Carolina, immediately realized that his colleague had stumbled across something exciting. Two years earlier, the group had identified a genetic association between Alzheimer's and a region of chromosome 19. Roses knew that the gene encoding ApoE was also on chromosome 19. “It was like a lightning bolt,” he says. “It changed my life.” In humans, there are three common variants, or alleles, of the APOE gene, numbered 2, 3 and 4. The obvious step, Roses realized, was to find out whether individual APOE alleles influence the risk of developing Alzheimer's disease. The variants can be distinguished from one another using a technique called the polymerase chain reaction (PCR). But Roses had little experience with PCR, so he asked the postdocs in his team to test samples from people with the disease and healthy controls. The postdocs refused: they were busy hunting for genes underlying Alzheimer's, and APOE seemed an unlikely candidate. The feeling in the lab, recalls Roses, was that “the chief was off on one of his crazy ideas”. Roses then talked to his wife, Ann Saunders, a mouse geneticist who was skilled at PCR. She had just given birth to their daughter and was on maternity leave, so they struck a deal. “She did the experiments while I held the baby,” he says. Within three weeks, they had collected the data that would fuel a series of landmark papers showing that the APOE4 allele is associated with a greatly increased risk of Alzheimer's disease1. © 2014 Nature Publishing Group,