Chapter 7. Life-Span Development of the Brain and Behavior

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By Kerri Smith, Cole Skinner was hanging from a wall above an abandoned quarry when he heard a car pull up. He and his friends bolted, racing along a narrow path on the quarry’s edge and hopping over a barbed-wire fence to exit the grounds. The chase is part of the fun for Skinner and his friend Alex McCallum-Toppin, both 15 and pupils at a school in Faringdon, UK. The two say that they seek out places such as construction sites and disused buildings—not to get into trouble, but to explore. There are also bragging rights to be earned. “It’s just something you can say: ‘Yeah, I’ve been in an abandoned quarry’,” says McCallum-Toppin. “You can talk about it with your friends.” Science has often looked at risk-taking among adolescents as a monolithic problem for parents and the public to manage or endure. When Eva Telzer, a neuroscientist at the University of North Carolina in Chapel Hill, asks family, friends, undergraduates or researchers in related fields about their perception of teenagers, “there’s almost never anything positive,” she says. “It’s a pervasive stereotype.” But how Alex and Cole dabble with risk—considering its social value alongside other pros and cons—is in keeping with a more complex picture emerging from neuroscience. Adolescent behaviour goes beyond impetuous rebellion or uncontrollable hormones, says Adriana Galván, a neuroscientist at the University of California, Los Angeles. “How we define risk-taking is going through a shift.” © 2018 Scientific American

Keyword: Development of the Brain; Drug Abuse
Link ID: 25350 - Posted: 08.18.2018

Decca Aitkenhead Annual media coverage of August’s exam results has traditionally conformed to an unwritten rule that all photos must show euphoric teenagers celebrating multiple A*s. This year, the images may tell a different story. Radical reforms to GCSEs are widely predicted to produce disappointment, and many teenagers are bracing themselves for the worst. Parents may be unsympathetic, however, if their 15- or 16-year-old spent the exam year ignoring all their wise advice to revise, and instead lay in bed until lunchtime and partied all night with friends. Even if the exam results turn out to be good, many will wonder why their teenager took so many risks with their future. Sarah-Jayne Blakemore looks barely older than a teenager herself. The award-winning professor of cognitive neuroscience at University College London is, in fact, 44 and has made the study of the adolescent brain her life’s work. She has been critical of the very existence of GCSEs, arguing that they impose “enormous stress” on teenagers at a time when their brains are going through huge change. “Until about 15 or 20 years ago,” she says, “we just didn’t know that the brain develops at all within the teenage years.” Until then, it was assumed that teenage behaviour was almost entirely down to hormonal changes in puberty, but brain scans and psychological experiments have now found that adolescence is a critical period of neurological change, much of which is responsible for the unique characteristics of adolescent behaviour. Far from being a defective or inferior version of an adult brain, the adolescent mind is both unique and – to Blakemore – beautiful. “Teenagers,” she says tenderly, “are brilliant.” © 2018 Guardian News and Media Limited

Keyword: Development of the Brain
Link ID: 25348 - Posted: 08.18.2018

Sara Reardon Mothers with high levels of the pesticide DDT in their blood during pregnancy are more likely to bear children who develop autism, according to a study of blood samples from more than one million pregnant women in Finland. The World Health Organization estimates that globally, one in 160 children has autism. Any case of autism is likely due to a number of factors, including genetics and other environmental exposures. Although the authors stress that the findings do not prove that autism is caused by DDT — whose use has been banned in many countries for decades over concerns about its effects on wildlife— it is the first such association using a direct measure of exposure to the pesticide. Researchers who investigate links between environment and disease say that further studies are needed to determine the mechanism, if any, by which DDT exposure could trigger autism. The study, published on 16 August in the American Journal of Psychiatry1, also examined mothers’ exposure to another set of chemicals known as polychlorinated biphenyls (PCBs), and found no association between these substances and autism. That finding deepens questions about whether or how DDT might be linked to autism. © 2018 Springer Nature Limited

Keyword: Autism; Neurotoxins
Link ID: 25346 - Posted: 08.17.2018

Alex Smith Dr. Jodi Jackson has worked for years to address infant mortality in Kansas. Often, that means she is treating newborns in a high-tech neonatal intensive care unit with sophisticated equipment whirring and beeping. That is exactly the wrong place for an infant like Lili. Lili's mother, Victoria, used heroin for the first two-thirds of her pregnancy and hated herself for it. (NPR is using her first name only, because she has used illegal drugs.) "When you are in withdrawal, you feel your baby that's in withdrawal too," says Victoria, recalling the sensations she remembers from her pregnancy. "You feel your baby uncomfortable inside of you, and you know that. And then you use and then the baby's not [uncomfortable], and that's a really awful, vulgar thought, but it's true. That's how it is. It's terrible." Though Victoria went into recovery before giving birth, Lili was born dependent on the methadone Victoria took to treat her opioid addiction. Treatment for infants like Lili has evolved, Jackson says. "What happened 10, 15 years ago, is [drug dependent] babies were immediately removed from the mom, and they were put in an ICU warmer with bright lights with nobody holding them," says Jackson, who is a neonatologist at Children's Mercy Hospital in Kansas City, Missouri. "Of course, they are going to be upset about that! And so the risk of withdrawal is much higher." © 2018 npr

Keyword: Drug Abuse; Development of the Brain
Link ID: 25344 - Posted: 08.17.2018

By Gretchen Reynolds Sitting for hours without moving can slow the flow of blood to our brains, according to a cautionary new study of office workers, a finding that could have implications for long-term brain health. But getting up and strolling for just two minutes every half-hour seems to stave off this decline in brain blood flow and may even increase it. Delivering blood to our brains is one of those automatic internal processes that most of us seldom consider, although it is essential for life and cognition. Brain cells need the oxygen and nutrients that blood contains, and several large arteries constantly shuttle blood up to our skulls. Because this flow is so necessary, the brain tightly regulates it, tracking a variety of physiological signals, including the levels of carbon dioxide in our blood, to keep the flow rate within a very narrow range. But small fluctuations do occur, both sudden and lingering, and may have repercussions. Past studies in people and animals indicate that slight, short-term drops in brain blood flow can temporarily cloud thinking and memory, while longer-term declines are linked to higher risks for some neurodegenerative diseases, including dementia. Other research has shown that uninterrupted sitting dampens blood flow to various parts of the body. Most of those studies looked at the legs, which are affected the most by our postures, upright or not. Stay seated for several hours, and blood flow within the many blood vessels of the legs can slacken. Whether a similar decline might occur in the arteries carrying blood to our brains was not known, however. So for the new study, which was published in June in the Journal of Applied Physiology, researchers at Liverpool John Moores University in England gathered 15 healthy, adult, male and female office workers. © 2018 The New York Times Company

Keyword: Alzheimers
Link ID: 25338 - Posted: 08.16.2018

by Lindsey Bever New research has shown that a common childhood vaccination given to pregnant women does not put their children at any increased risk of autism. A Kaiser Permanente study published Monday in the journal Pediatrics found no association between the prenatal Tdap (for tetanus, diphtheria and pertussis, also known as whooping cough) vaccine and autism spectrum disorder when looking at tens of thousands of children in the hospital system. It is the latest in a long line of studies showing that there is no link between vaccines and autism. Despite the abundant scientific evidence, a persistent conspiracy theory has misled some parents into fearing vaccines. “If any woman had any hesitancy, she can be reassured,” Tracy Becerra-Culqui, lead author and postdoctoral research fellow with Kaiser Permanente Southern California's department of research and evaluation, told The Washington Post. When not vaccinated, she said, “the risk of getting whooping cough is greater than any perceived risk of harm to the baby, so it should be a no-brainer to accept the vaccine.” The Centers for Disease Control and Prevention, the American College of Obstetricians and Gynecologists, and the American College of Nurse-Midwives encourage expectant mothers to get the Tdap vaccine in the third trimester of pregnancy to protect babies from bacterial infections that can be fatal for infants. © 1996-2018 The Washington Post

Keyword: Autism; Neuroimmunology
Link ID: 25332 - Posted: 08.15.2018

Philip Ball Carl Zimmer is a rarity among professional science writers in being influential among the scientists on whose work he writes and comments – to the extent that he has been appointed as professor adjunct in the department of molecular biophysics and biochemistry at Yale University. Zimmer has just published his 13th book, She Has Her Mother’s Laugh, a survey of “the power, perversions and potential of heredity”. What is the book’s main message about our attitudes to heredity? Heredity is central to our existence and how we define ourselves. But it’s not what we think it is. It’s not just genes, for example. We inherit culture too, and there may even be other channels of heredity. And the way genes enable heredity doesn’t fit our common notions. We tend to imagine that we inherit particular genes from our parents, grandparents and so on, and that these shape us in ways that are easy to understand and trace. But that’s not how heredity works. Each trait is typically influenced by hundreds or thousands of different genes, and the environment in which those genes are acting makes all the difference to how we turn out. You talk in the book about how some of these questions were brought home to you when your first daughter was born in 2001. What’s your personal journey into the story of heredity? In 2000 my wife was pregnant with our first child, and our doctor asked us to go to a genetics counsellor. I thought this was pointless. But the counsellor started asking me questions and I suddenly realised I had a really terrible grasp of my family history. I felt very ashamed and irresponsible, because here was this child who would be inheriting a lot of my genes. This was the first time heredity went from being something I learned about in class to one of the most important things in my existence. © 2018 Guardian News and Media Limited

Keyword: Genes & Behavior; Development of the Brain
Link ID: 25325 - Posted: 08.13.2018

By Jessica Wright, Boosting levels of the chemical messenger serotonin makes mice that model autism more social, according to a study published in Nature. The study suggests the approach may do the same in people with autism. It also offers an explanation for why antidepressants do not ease autism traits: They may increase serotonin levels too slowly to be effective. The researchers used a technique that rapidly increases serotonin levels in the nucleus accumbens, a brain region that mediates social reward. “Somehow, the release of serotonin in the nucleus accumbens really plays an important role in enhancing sociability,” says lead researcher Robert Malenka, professor of psychiatry and behavioral sciences at Stanford University in California. “The simple hypothesis is it makes the social interaction more reinforcing.” Decades of research have suggested a connection between serotonin and autism. About 10 years ago, this led researchers to test antidepressants, which increase serotonin levels by blocking its reabsorption into neurons, as a treatment for autism. However, in several trials, antidepressants such as fluoxetine (Prozac) proved ineffective at easing the condition’s features. The new study suggests that a drug that rapidly activates serotonin receptors would be a more effective way of treating the condition. © 2018 Scientific American

Keyword: Autism
Link ID: 25323 - Posted: 08.13.2018

There is a new study on the effect treating teens for depression has on their parents. It suggests just treating teens has benefits for parents. LULU GARCIA-NAVARRO, HOST: There are estimates that 13 percent of adolescents in the United States experience at least one episode of major depression. That depression can be treated in teens. And new research suggests that it helps not just them but also their parents. NPR's Rhitu Chatterjee reports. RHITU CHATTERJEE, BYLINE: We tend to think of depression as affecting individuals, but Myrna Weissman says... MYRNA WEISSMAN: Depression is a family affair. CHATTERJEE: Weissman is a professor of psychiatry at the College of Physicians and Surgeons at Columbia University. And she's studied depression in families for years. WEISSMAN: We know that there's high rates of depression in the offspring of depressed mothers. CHATTERJEE: Weissman's previous work has shown that when mothers are treated for depression, their children feel better, as well. That led another researcher, Kelsey Howard, to wonder, could the opposite be true? KELSEY HOWARD: So if kids get better, do parents then feel better? And we found that to be true, as well. CHATTERJEE: Howard is a graduate student at the department of Psychiatry and Behavioral Sciences at Northwestern University. To answer her question, she and her graduate adviser analyzed data from a previous study that followed more than 300 teenagers getting treatment for depression either through counseling or pills or both. Before and during the course of the study, the researchers had also surveyed one parent of each teenager for symptoms of depression. When Howard looked at that data, she found that... © 2018 npr

Keyword: Depression; Development of the Brain
Link ID: 25319 - Posted: 08.13.2018

Laurel Hamers A Nobel Prize–winning discovery — that small double-stranded RNA molecules can silence genes by interrupting the translation of DNA’s instructions into proteins — is finally delivering on its medical promise. The first drug that takes advantage of this natural biological process, called RNA interference, was approved August 10 by the U.S. Food and Drug Administration. It targets a rare hereditary disease that causes misshapen proteins to build up in patients’ nerves, tissues and organs, causing loss of sensation, organ failure and even death. Heredity transthyretin amyloidosis, or ATTR, affects about 50,000 people worldwide. This drug will help the subset of those patients who have neurological impairments. Called patisiran, the drug uses specially designed pieces of RNA to silence a mutated gene that, when active in the liver, is responsible for patients’ symptoms. In a recent 18-month clinical trial, patients who received patisiran injections every three weeks showed a slight decrease in neurological symptoms, whereas patients on the placebo worsened overall. It’s not a cure — people still have the genetic mutation — but the treatment prevents the disease from progressing. This approval is “just the beginning,” says Craig Mello of the University of Massachusetts Medical School in Worcester, who co-discovered the process of RNA interference in roundworms (SN: 10/7/06, p. 229). Many more drugs using the same approach, for diseases ranging from hemophilia to HIV, are winding through clinical trials. |© Society for Science & the Public 2000 - 2018

Keyword: Genes & Behavior
Link ID: 25316 - Posted: 08.11.2018

Tina Hesman Saey Scientists now know how long it takes for a cell to tell itself it’s time to die. Signals triggering a type of cell suicide called apoptosis move through a cell like a wave, traveling at a rate of 30 micrometers per minute, Stanford University systems biologists Xianrui Cheng and James Ferrell Jr. report in the Aug. 10 Science. These findings resolve a debate over whether these death signals spread by diffusion, with signaling molecules working their own way across a cell, or as self-regenerating trigger waves, like toppling dominoes. The apoptosis process starts with damage that causes the release of death signal chemicals. One example is cytochrome c leaking from damaged mitochondria, the cell’s power plant. Once cytochrome c concentrations get high enough, the chemicals signal proteins called caspases to go to work. Caspases trigger other proteins to poke holes in neighboring mitochondria, releasing more cytochrome c and moving the death wave across the cell. That chain reaction happens more quickly than diffusion can, Ferrell says. In an African clawed frog egg, a trigger wave takes about a half-hour to spread across the 1.2 millimeter cell, whereas diffusion would take five hours, he says. Like forest fires, trigger waves will keep going as long as there is fuel to feed them — in this case, the death signal chemicals and proteins, Ferrell says. He predicts that many other biological signals may move as trigger waves. |© Society for Science & the Public 2000 - 2018

Keyword: Apoptosis; Development of the Brain
Link ID: 25310 - Posted: 08.10.2018

by Lindsey Bever It was a solution no parent wants to hear: To get rid of a brain tumor and stop their young son's seizures, surgeons would need to cut out one-sixth of his brain. But for Tanner Collins, it was the best option. A slow-growing tumor was causing sometimes-daily seizures, and medications commonly used to treat them did not seem to be working, his father said. But removing a portion of his brain was no doubt risky. That region — the right occipital and posterior temporal lobes — is important for facial recognition, and, without it, Tanner's parents wondered if he would recognize them. Tanner, who was 6 at the time, underwent surgery at the University of Pittsburgh Medical Center's Children's Hospital. Although his brain has had to work to adapt since then, he's had no major problems. Other than some visual impairment, Tanner, now 12, said he's “perfectly fine.” “As far as I’m concerned, I’m a perfectly normal 12-year-old boy,” Tanner said. Tanner's case was published Tuesday in the scientific journal Cell Reports, explaining how the 12-year-old's brain learned to adapt after a part largely responsible for visual processing was taken out. Marlene Behrmann, a cognitive neuroscientist and lead author of the paper, said Tanner was one of the first pediatric patients studied over the past several years in her laboratory at Carnegie Mellon University to determine the extent to which a child's brain can reorganize itself after certain sections are surgically removed. In Tanner's case, she said, surgeons took out his right occipital and posterior temporal lobes, which made up about one-third of the right hemisphere of his brain. © 1996-2018 The Washington Post

Keyword: Development of the Brain; Epilepsy
Link ID: 25287 - Posted: 08.03.2018

/ By Rod McCullom Eight years ago, New York University sociologist Patrick Sharkey published a paper whose conclusions shook the worlds of criminology and adolescent psychology. Researchers had long known that children exposed to violence and crime had poorer measures of memory, attention, planning, and focus — the cognitive processes collectively known as executive function — than peers whose lives were violence-free. But what Sharkey found, using data on 6,000 Chicago homicides from 1994 to 2002, was that a killing in a child’s neighborhood could significantly lower his or her scores on standardized tests — even if the child did not witness the killing or know the victim. He proposed that post-traumatic stress caused by exposure to violence could explain about half of the “achievement gap” between black and white students — a disparity that leads to persistent inequalities in education, income, careers, housing, and more. Similar findings have been documented in more recent studies, but one question has continued to vex researchers: Why? How does even indirect violence get under a child’s skin and into the brain? Now some intriguing interdisciplinary research — by psychologists, economists, and sociologists — suggests that a large part of the answer may lie in two biological pathways: sleep and the stress hormone cortisol. Researchers at Northwestern University, DePaul University, and NYU (including Sharkey) looked at 82 adolescents aged 11 to 18 who attended public schools in a “large Midwestern city.” (The school system asked for anonymity to participate in the study.) At least half the students had at least one violent crime in their neighborhood during the participation period, according to geocoded police report data collected by the researchers. The students wore activity-tracking watches that measured sleep-wake patterns, and most of them delivered three saliva samples daily for measuring cortisol levels. Copyright 2018 Undark

Keyword: Aggression; Stress
Link ID: 25285 - Posted: 08.02.2018

Ashley Yeager Neuroscientist Gavin Clowry didn’t intend to grow a miniature human brain in a rat pup. But a few months ago, that’s essentially what happened. “We were astonished when we saw it,” recalls the faculty member at Newcastle University in the UK. Clowry and his colleagues had derived human neural stem cells from induced pluripotent stem cells, diffused them into a 3-D gel, and transplanted the gel into the young rats’ brains to test the cells’ ability to survive. A month later, much to the team’s surprise, the human cells had formed columns of tightly packed progenitor cells surrounded by immature neurons. “They looked like organoids,” says Clowry, who published the results in May. Organoids are tiny collections of tissue made from cells that self-organize into 3-D structures that mimic the anatomy of fully formed organs. Clowry attributes the unexpected development of the human brain organoids to the complex environment of the rat’s brain, where diverse cell types interact to keep neurons operating. That’s not to say cerebral organoids can’t also be grown in a dish. Scientists published the first description of lab-grown, human brain organoids in 2013. But even cultured mini-brains appear to benefit from an in vivo environment. Clowry’s study appeared in the literature just three weeks after a paper from Fred “Rusty” Gage and his colleagues at the Salk Institute for Biological Studies in La Jolla, California, described how they had transplanted lab-grown human brain organoids into the brains of mice and watched as the animals’ native blood vessels and immune cells infiltrated the organoids. Gage’s team also noted that the cells in the implanted organoids were sending and receiving signals to and from the mice’s native nerve cells. As Clowry and his colleagues would later observe in rat brains, the organoids were being integrated into the animals’ brains. © 1986 - 2018 The Scientist

Keyword: Development of the Brain; Stem Cells
Link ID: 25284 - Posted: 08.02.2018

Maria Temming Google Glass may have failed as a high-tech fashion trend, but it’s showing promise as a tool to help children with autism better navigate social situations. A new smartphone app that pairs with a Google Glass headset uses facial recognition software to give the wearer real-time updates on which emotions people are expressing. In a pilot trial, described online August 2 in npj Digital Medicine, 14 children with autism spectrum disorder used this program at home for an average of just over 10 weeks. After treatment, the kids showed improved social skills, including increased eye contact and ability to decode facial expressions. After her 9-year-old son, Alex, participated in the study, Donji Cullenbine described the Google Glass therapy as “remarkable.” She noticed within a few weeks that Alex was meeting her eyes more often — a behavior change that’s stuck since treatment ended, she says. And Alex enjoyed using the Google Glass app. Cullenbine recalls her son telling her excitedly, “Mommy, I can read minds.” Unlike most children, who naturally learn to read facial expressions by interacting with family and friends, children with autism often have to hone these skills through behavioral therapy. That typically involves a therapist leading the child through structured activities, like exercises with flash cards that depict faces wearing different expressions. But therapists are so few and far between that a child diagnosed with autism can spend 18 months on a waiting list before starting treatment. |© Society for Science & the Public 2000 - 2018

Keyword: Autism; Emotions
Link ID: 25283 - Posted: 08.02.2018

Diana Kwon Bruce Baker, a geneticist who studied gene-behavior interactions in Drosophila melanogaster, died on July 1. He was 72 years old. “Bruce had enormous respect for the details of science, not only the science in his own lab but also that of his peers,” Deborah Andrew, a biologist at Johns Hopkins and one of Baker’s former graduate students, writes in an obituary posted by the Genetics Society of America. Baker was born in Swannanoa, North Carolina in 1945. After completing his undergraduate studies at Reed College in 1966 and receiving a PhD from the University of Washington in 1971, Baker joined the faculty at the University of California, San Diego. In 1986, he became a professor at Stanford University, where he remained for more than two decades before moving to the Howard Hughes Medical Institute’s Janelia Research Campus in 2008. Over the course of his career, Baker published more than 150 papers, primarily focused on the cellular and genetic mechanisms that determine the development of sex-specific characteristics in fruit flies. He also investigated dosage compensation, the strategies used by fruit flies to deal with having one X chromosome instead of two. Among Baker’s scientific contributions is the discovery that the gene encoding the transcription factor Fruitless plays a key role in male-specific courtship behaviors. Studies led by Baker and his colleague, neurobiologist Barry Dickson, revealed that Fruitless (fru) influenced male flies’ attraction to females and, when expressed in females, led them to court other female flies. © 1986 - 2018 The Scientist.

Keyword: Genes & Behavior; Sexual Behavior
Link ID: 25276 - Posted: 08.01.2018

By Dennis Normile Researchers in Japan today announced the launch of a clinical trial to treat Parkinson’s disease with neurological material derived from induced pluripotent stem (iPS) cells, mature cells chemically manipulated to return to an early stage of development from which they can theoretically differentiate into any of the body’s specialized cells. The study team will inject dopaminergic progenitors, a cell type that develops into neurons that produce dopamine, directly into a region of the brain known to play a key role in the neural degeneration associated with Parkinson’s disease. The effort is being led by Jun Takahashi, a neurosurgeon at Kyoto University's Center for iPS Cell Research and Application (CiRA), in cooperation with Kyoto University Hospital. Parkinson’s disease results from the death of specialized cells in the brain that produce the neurotransmitter dopamine. A lack of dopamine leads to a decline in motor skills, resulting in difficulty walking and involuntary trembling. As the disease progresses it can lead to dementia. The trial strategy is to derive dopaminergic progenitors from iPS cells and inject them into the putamen, a round structure located at the base of the forebrain. Surgeons will drill two small holes through a patient’s skull and use a specialized device to inject roughly 5 million cells. © 2018 American Association for the Advancement of Science.

Keyword: Parkinsons; Stem Cells
Link ID: 25275 - Posted: 07.31.2018

By Damian Garde, In the long-running debate over just what causes Alzheimer’s disease, one side looks to have scored a victory with new results with an in-development drug. But there’s enough variation in the data to ensure that the squabbling factions of Alzheimer’s will have plenty to fight about. At issue is the so-called amyloid hypothesis, a decades-old theory claiming that Alzheimer’s gradual degradation of the brain is caused by the accumulation of sticky plaques. And the new drug is BAN2401, designed by Biogen and Eisai to prevent those amyloid plaques from clustering and attack the clumps that already have. In data presented last week, one group of patients receiving BAN2401 saw their amyloid levels plummet, a result that was tied to a significant reduction in cognitive decline compared with placebo. To the amyloid-inclined, like Dr. Howard Fillit of the Alzheimer’s Drug Discovery Foundation, that marks a clear affirmation of the linkage between plaques and mental fortitude. “I mean if you asked me five or 10 years ago if we’re going to have a drug that can remove the plaques from the brain, I would have thought this was space technology,” Fillit said. “And there was definitely a signal, in my opinion, on clinical outcomes, which is what we’ve all been looking for.” But to skeptics, the trial was laden with confounding details that make it impossible to draw conclusions. © 2018 Scientific American

Keyword: Alzheimers
Link ID: 25273 - Posted: 07.31.2018

By Katherine J. Wu Eat poorly, and your body will remember—and possibly pass the consequences onto your kids. In the past several years, mounting evidence has shown that sperm can take note of a father’s lifestyle decisions, and transfer this baggage to offspring. Today, in two complementary studies, scientists tell us how. As sperm traverse the male reproductive system, they jettison and acquire non-genetic cargo that fundamentally alters sperm before ejaculation. These modifications not only communicate the father’s current state of wellbeing, but can also have drastic consequences on the viability of future offspring. Each year, over 76,000 children are born as a result of assisted reproduction techniques, the majority of which involve some type of in vitro fertilization (IVF). These procedures unite egg and sperm outside the human body, then transfer the resulting fertilized egg—the embryo—into a woman’s uterus. Multiple variations on IVF exist, but in some cases that involve male infertility—for instance, sperm that struggle to swim—sperm must be surgically extracted from the testes or epididymis, a lengthy, convoluted duct that cradles each testis. After sperm are produced in the testes, they embark on a harrowing journey through the winding epididymis—which, in a human male, is about six meters long when unfurled—on their way to storage. Sperm wander the epididymis for about two weeks; only at the end of this path are they fully motile. Thus, while “mature” sperm can essentially be dumped on a waiting egg and be reasonably expected to achieve fertilization, sperm plucked from the testes and epididymis must be injected directly into the egg with a very fine needle. No matter the source of the sperm, these techniques have birthed healthy infants in four decades of successful procedures.

Keyword: Epigenetics
Link ID: 25268 - Posted: 07.30.2018

By Kelly Servick In the hunt for a drug to treat Alzheimer’s disease, even a whiff of success can be intoxicating. That helps explain why an experimental drug called BAN2401, which a few months ago seemed like it might join a growing heap of failed candidates, created so much buzz yesterday at the Alzheimer’s Association International Conference in Chicago, Illinois. In a phase II trial, the drug had already failed to show the level of benefit that its developers—Biogen Inc. in Cambridge, Massachusetts; and Eisai Co. Ltd. in Tokyo—set as the study’s primary endpoint. But yesterday the companies presented a series of other analyses from the same trial that suggest BAN2401 might slow the pace of cognitive decline in Alzheimer’s patients, and reverse the buildup of a brain protein thought to drive the disease’s neurodegeneration. But the subset of patients who showed those benefits was relatively small—161 people—and an unexpected change to the way the study was randomized cast some skepticism on the results. For many, the findings are too preliminary to celebrate. “If these results we saw today pan out in phase III clinical trials, then you’re looking at disease-modifying medication—the first one for Alzheimer’s disease,” says Keith Fargo, director of scientific programs & outreach at the Alzheimer’s Association in Chicago, Illinois. “But you don’t know whether they’re going to pan out until you actually do the phase III trial.” © 2018 American Association for the Advancement of Science

Keyword: Alzheimers
Link ID: 25257 - Posted: 07.27.2018