Chapter 7. Life-Span Development of the Brain and Behavior
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Sara Reardon As a medical student in Paris in the 1980s, Eric Vilain found himself pondering the differences between men and women. What causes them to develop differently, and what happens when the process goes awry? At the time, he was encountering babies that defied simple classification as a boy or girl. Born with disorders of sex development (DSDs), many had intermediate genitalia — an overlarge clitoris, an undersized penis or features of both sexes. Then, as now, the usual practice was to operate. And the decision of whether a child would be left with male or female genitalia was often made not on scientific evidence, says Vilain, but on practicality: an oft-repeated, if insensitive, line has it that “it's easier to dig a hole than build a pole”. Vilain found the approach disturbing. “I was fascinated and shocked by how the medical team was making decisions.” Vilain has spent the better part of his career studying the ambiguities of sex. Now a paediatrician and geneticist at the University of California, Los Angeles (UCLA), he is one of the world's foremost experts on the genetic determinants of DSDs. He has worked closely with intersex advocacy groups that campaign for recognition and better medical treatment — a movement that has recently gained momentum. And in 2011, he established a major longitudinal study to track the psychological and medical well-being of hundreds of children with DSDs. © 2016 Nature Publishing Group
By PAM BELLUCK BALTIMORE — Leave it to the youngest person in the lab to think of the Big Idea. Xuyu Qian, 23, a third-year graduate student at Johns Hopkins, was chatting in late January with Hongjun Song, a neurologist. Dr. Song was wondering how to test their three-dimensional model of a brain — well, not a brain, exactly, but an “organoid,” essentially a tiny ball of brain cells, grown from stem cells and mimicking early brain development. “We need a disease,” Dr. Song said. Mr. Qian tossed out something he’d seen in the headlines: “Why don’t we check out this Zika virus?” Within a few weeks — a nanosecond compared with typical scientific research time — that suggestion led to one of the most significant findings in efforts to answer a central question: How does the Zika virus cause brain damage, including the abnormally small heads in babies born to infected mothers? The answer could spur discoveries to prevent such devastating neurological problems. And time is of the essence. One year after the virus was first confirmed in Latin America, with the raging crisis likely to reach the United States this summer, no treatment or vaccine exists. “We can’t wait,” said Dr. Song, at the university’s Institute for Cell Engineering, where he and his wife and research partner, Dr. Guo-Li Ming, provided a pipette-and-petri-dish-level tour. “To translate our work for the clinic, to the public, normally it takes years. This is a case where we can make a difference right away.” The laboratory’s initial breakthrough, published in March with researchers at two other universities, showed that the Zika virus attacked and killed so-called neural progenitor cells, which form early in fetal development and generate neurons in the brain. © 2016 The New York Times Company
By Geraldine Dawson There’s a popular saying in the autism community: “If you’ve met one person with autism, you’ve met one person with autism.” Although this phrase is meant to convey the remarkable variation in abilities and disabilities among people with autism spectrum disorder (ASD), we’re learning that it also applies to the extraordinary variability in how ASD develops. When I first began doing research on autism decades ago, we thought of it as one condition and aimed to discover its “cause.” Now we know ASD is actually a group of lifelong conditions that can arise from a complex combination of multiple genetic and environmental factors. In the same way that each person with ASD has a unique personality and profile of talents and disabilities, each also has a distinct developmental history shaped by a specific combination of genetic and environmental factors. More evidence of this extraordinary variety will be presented this week in Baltimore, where nearly 2,000 of the world’s leading autism researchers will gather for the International Meeting for Autism Research (IMFAR). As president of the International Society for Autism Research, which sponsors the conference, I am more impressed than ever with the progress we are making. New findings being presented at the conference will highlight the importance of the prenatal period in understanding how various environmental factors such as exposure to alcohol, smoking and certain chemical compounds can increase risk for ASD. The impact of many environmental factors depends, however, on an individual’s genetic background and the timing of the exposure. Other research links inflammation—detected in blood spot tests taken at birth—with a higher likelihood of an ASD diagnosis later on. Researchers suggest that certain factors such as maternal infection and other factors during pregnancy may influence an infant’s immune system and contribute to risk. As our knowledge of these risk factors grows, so do the opportunities for promoting healthy pregnancies and better outcomes. © 2016 Scientific American
Chris Woolston A story about epigenetics in the 2 May issue of The New Yorker has been sharply criticized for inaccurately describing how genes are regulated. The article by Siddhartha Mukherjee — a physician, cancer researcher and award-winning author at Columbia University in New York — examines how environmental factors can change the activity of genes without altering the DNA sequence. Jerry Coyne, an evolutionary ecologist at the University of Chicago in Illinois, posted two widely discussed blog posts calling the piece “superficial and misleading”, largely because it ignored key aspects of gene regulation. Other researchers quoted in the blog posts called the piece “horribly damaging” and “a truly painful read”. Mukherjee responded by publishing a point-by-point rebuttal online. Speaking to Nature, he says he now realizes that he erred by omitting key areas of the science, but that he didn’t mean to mislead. “I sincerely thought that I had done it justice,” he says. Mukherjee’s article, ‘Same But Different’, takes a personal view of epigenetics — a term whose definition is highly contentious in the field. The story features his mother and aunt, identical twins who have distinct personalities. Mukherjee, who won a Pulitzer Prize in 2011 for his best-selling book The Emperor of All Maladies: A Biography of Cancer (Scribner, 2010), writes that identical twins differ because: “Chance events — injuries, infections, infatuations; the haunting trill of that particular nocturne — impinge on one twin and not on the other. Genes are turned on and off in response to these events, as epigenetic marks are gradually layered above genes, etching the genome with its own scars, calluses, and freckles.” The article is drawn from a book by Mukherjee that is due out later this month, called The Gene: An Intimate History (Scribner, 2016). © 2016 Nature Publishing Group
By DAN BARRY IDIOT. Imbecile. Cretin. Feebleminded. Moron. Retarded. Offensive now but once quite acceptable, these terms figured in the research for a lengthy article I wrote in 2014 about 32 men who spent decades eviscerating turkeys in a meat-processing plant in Iowa — all for $65 a month, along with food and lodging in an ancient former schoolhouse on a hill. These were men with intellectual disability, which meant they had significant limitations in reasoning, learning and problem solving, as well as in adaptive behavior. But even though “intellectual disability” has been the preferred term for more than a decade, it gave my editors and me pause. We wondered whether readers would instantly understand what the phrase meant. What’s more, advocates and academicians were recommending that I suppress my journalistic instinct to tighten the language. I was told that it was improper to call these men “intellectually disabled,” instead of “men with intellectual disability.” Their disability does not define them; they are human beings with a disability. This linguistic preference is part of society’s long struggle to find the proper terminology for people with intellectual disability, and reflects the discomfort the subject creates among many in the so-called non-disabled world. It speaks to a continuing sense of otherness; to perceptions of what is normal, and not. “It often doesn’t matter what the word is,” said Michael Wehmeyer, the director and senior scientist at the Beach Center on Disability at the University of Kansas. “It’s that people associate that word with what their perceptions of these people are — as broken, or as defective, or as something else.” For many years, the preferred term was, simply, idiot. When Massachusetts established a commission on idiocy in the mid-1840s, it appointed Dr. Samuel G. Howe, an abolitionist and early disability rights advocate, as its chairman. The commission argued for the establishment of schools to help this segment of society, but made clear that it regarded idiocy “as an outward sign of an inward malady.” © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 22195 - Posted: 05.09.2016
By Aleszu Bajak In its May 2 issue, The New Yorker magazine published a report titled “Same But Different,” with the subhead: “How epigenetics can blur the line between nature and nurture.” The piece was written by Siddhartha Mukherjee, a physician and author of the Pulitzer prize-winning book “The Emperor of all Maladies: A Biography of Cancer.” In his New Yorker story, Mukherjee, with deft language and colorful anecdotes, examines a topic that is very much du jour in science writing: Epigenetics. Google defines epigenetics as “the study of changes in organisms caused by modification of gene expression, rather than alteration of the genetic code itself.” Merriam Webster’s definition is similar — but not exactly the same: “The study of heritable changes in gene function that do not involve changes in DNA sequence.” The slight variation in definition is telling in itself — and it’s really that “heritable” part that has sparked intense interest not just among scientists, but in the popular mind. Steven Henikoff, a molecular biologist at the Fred Hutchinson Cancer Research Center in Seattle, called Siddhartha Mukherjee’s lyrical take on epigenetics “baloney.” It’s the idea that external factors like diet, or stress or even lifestyle choices can impact not just your own genes, but the genetic information you pass down to all of your descendants. Spend your life smoking cigarettes and eating fatty foods, the thinking goes, and you’ll not just make yourself sick, you’ll predispose your offspring — and their offspring, and their offspring — to associated diseases as well. It’s heady stuff, but much of it remains speculative and poorly supported, which is where Mukherjee may have run into trouble. The publication of his story — an excerpt from his forthcoming book “The Gene: An Intimate History” — was met with swift criticism from biologists working in epigenetics and the broader field of gene regulation. They argue that Mukherjee played fast and loose with his description of epigenetic processes and misled readers by casting aside decades of research into how genes are regulated during development. Copyright 2016 Undark
Link ID: 22194 - Posted: 05.09.2016
By Jocelyn Kaiser Gene therapy is living up to its promise of halting a rare, deadly brain disease in young boys. In a new study presented in Washington, D.C., yesterday at the annual meeting of the American Society of Gene and Cell Therapy, all but one of 17 boys with adrenoleukodystrophy (ALD) remained relatively healthy for up to 2 years after having an engineered virus deliver into their cells a gene to replenish a missing protein needed by the brain. The results, which expand on an earlier pilot study, bring this ALD therapy one step closer to the clinic. About one in 21,000 boys are born with ALD, which is caused by a flaw in a gene on the X chromosome that prevents cells from making a protein that the cells need to process certain fats—females have a backup copy of the gene on their second X chromosome. Without that protein, the fats build up and gradually destroy myelin sheaths that protect nerves in the brain. In the cerebral form of ALD, which begins in childhood, patients quickly lose vision and mobility, usually dying by age 12. The disease achieved some degree of fame with the 1992 film Lorenzo’s Oil, inspired by a family’s struggle to prolong their son’s life with a homemade remedy. The only currently approved treatment for ALD is a bone marrow transplant -- white blood cells in the marrow go to the brain and turn into glial cells that produce normal ALD proteins. But bone marrow transplants carry many risks, including immune rejection, and matching donors can’t always be found. As an alternative, in the late 2000s, French researchers treated the bone cells of two boys with a modified virus carrying the ALD gene. They reported in Science in 2009 that this halted progression of the disease. © 2016 American Association for the Advancement of Science
By John Elder Robison Manipulating your brain with magnetic fields sounds like science fiction. But the technique is real, and it’s here. Called transcranial magnetic stimulation (TMS), it is approved as a therapy for depression in the US and UK. More controversially, it is being studied as a way to treat classic symptoms of autism, such as emotional disconnection. With interest and hopes rising, it’s under the spotlight at the International Meeting for Autism Research in Baltimore, Maryland, next week. I can bear witness to the power of TMS, which induces small electrical currents in neurons. As someone with Asperger’s, I tried it for medical research, and described its impact in my book Switched On. After TMS, I could see emotional cues in other people – signals I had always been blind to, but that many non-autistic people pick up with ease. That sounds great, so why the need for debate? Relieving depression isn’t controversial, because there is no question people suffer as a result of it. I too felt that I suffered – from emotional disconnection. But changing “emotional intelligence” to relieve that comes closer to changing the essence of how we think. Yes, emerging brain therapies like TMS have great potential. Several of the volunteers who went into the TMS lab at Harvard Medical School emerged with new self-awareness, and lasting changes. While I can’t speak with certainty for the others, I believe some of us have a degree of emotional insight that we didn’t have before. I certainly feel better able to fit in. As fellow participant Michael Wilcox put it, we have more emotional reactions to things we see or read. © Copyright Reed Business Information Ltd.
Link ID: 22187 - Posted: 05.07.2016
By Marta Zaraska Scientists and laypeople alike have historically attributed political beliefs to upbringing and surroundings, yet recent research shows that our political inclinations have a large genetic component. The largest recent study of political beliefs, published in 2014 in Behavior Genetics, looked at a sample of more than 12,000 twin pairs from five countries, including the U.S. Some were identical and some fraternal; all were raised together. The study reveals that the development of political attitudes depends, on average, about 60 percent on the environment in which we grow up and live and 40 percent on our genes. “We inherit some part of how we process information, how we see the world and how we perceive threats—and these are expressed in a modern society as political attitudes,” explains Peter Hatemi, who is a genetic epidemiologist at the University of Sydney and lead author of the study. The genes involved in such complex traits are difficult to pinpoint because they tend to be involved in a huge number of bodily and cognitive processes that each play a minuscule role in shaping our political attitudes. Yet a study published in 2015 in the Proceedings of the Royal Society B managed to do just that, showing that genes encoding certain receptors for the neurotransmitter dopamine are associated with where we fall on the liberal-conservative axis. Among women who were highly liberal, 62 percent were carriers of certain receptor genotypes that have previously been associated with such traits as extroversion and novelty seeking. Meanwhile, among highly conservative women, the proportion was only 37.5 percent. © 2016 Scientific American
By Karen Weintraub The four members of Asperger’s Are Us decided a long time ago that their main goal would be to amuse themselves. But after nearly a decade of laughing and writing punch lines together, Asperger’s Are Us, which is probably the only comedy troupe made up of people on the autism spectrum, is on the cusp of comedic success. A documentary about the group premiered at the SXSW conference in Austin in March and was recently sold to Netflix. The troupe is also preparing for its first national tour this summer. Comedy might be a surprising choice for someone with Asperger’s syndrome, since stereotypically, people with autism are generally regarded as socially awkward loners. But the four men in the group bonded at summer camp 11 years ago, when one was a counselor and the other three were campers, and are clearly great friends. An “Aspergers Are Us” performance from 2011. Talking recently via Skype, Noah Britton, the former counselor, settles giant black rabbit ears onto his head. Jack Hanke, another member of the troupe, dons his favorite sombrero – the black one he took with him to Oxford University during his recent junior year abroad – accessorized with a red sombrero on top. They slip into their usual banter when asked what they thought of the film, named for the group, which will be shown publicly for the first time on Friday at the Somerville Theater outside of Boston. “I liked the four weird guys in it,” Mr. Britton said. “It was better than ‘Jaws 2,’ but not as good as ‘Jaws 3,’” Mr. Hanke insisted. “I found it kind of annoying myself,” added Ethan Finlan, another member of the group. The fourth member, who changed his first name to New Michael to distinguish himself from his father, Michael Ingemi, didn’t want to join the call. © 2016 The New York Times Company
Link ID: 22169 - Posted: 05.03.2016
Patricia Neighmond Hoping to keep your mental edge as you get older? Look after your heart, a recent analysis suggests, and your brain will benefit, too. A research team led by Hannah Gardener, an epidemiologist at the University of Miami, analyzed a subset of data from the Northern Manhattan Study, a large, ongoing study of risk factors for stroke among whites, blacks and Hispanics living in the Washington Heights neighborhood of New York City. The scientists wanted to see how people in their 60s and 70s would do on repeated tests of memory and mental acuity six years later — and, specifically, what sort of subtle differences a heart-healthy lifestyle might make to the brain, beyond the prevention of strokes. Their findings appear in a recent issue of the Journal of the American Heart Association. In this particular study, the researchers started with more than a thousand people who'd had their cardiovascular health assessed using measures that the American Heart Association has dubbed Life's Simple 7. These seven factors known to benefit the heart and blood vessels include maintaining a normal body weight and good nutrition, not smoking, getting exercise regularly and keeping blood pressure, cholesterol and blood sugar levels under control. To measure thinking skills, Gardener's team used a variety of tests of memory, judgement, the ability to plan, mental quickness and other sorts of problem solving. The results were striking: Across all demographic groups, the people who had higher scores on the measures of cardiovascular health did better on the mental tests than those who scored low. © 2016 npr
Link ID: 22167 - Posted: 05.02.2016
Symptoms of depression that steadily increase over time in older age could indicate early signs of dementia, scientists have said. Other patterns of symptoms, such as chronic depression, appear not to be linked, a study found. Dutch researchers looked at different ways depression in older adults progressed over time and how this related to any risk. They concluded worsening depression may signal the condition is taking hold. The research, published in The Lancet Psychiatry, followed more than 3,000 adults aged 55 and over living in the Netherlands. All had depression but no symptoms of dementia at the start of the study. Dr M Arfan Ikram of the Erasmus University Medical Center in Rotterdam said depressive symptoms that gradually increase over time appear to be a better predictor of dementia later in life than other paths of depression. "There are a number of potential explanations, including that depression and dementia may both be symptoms of a common underlying cause, or that increasing depressive symptoms are on the starting end of a dementia continuum in older adults," he said. Only the group whose symptoms of depression increased over time were found to be at increased risk of dementia - about one in five of people (55 out of 255) in this group developed dementia. Others who had symptoms that waxed and waned or stayed the same were not at increased risk. For example, in those who experienced low but stable levels of depression, around 10% went on to develop dementia. The exact nature of depression on dementia risk remains unknown. © 2016 BBC
By n. r. kleinfield IT BEGAN WITH what she saw in the bathroom mirror. On a dull morning, Geri Taylor padded into the shiny bathroom of her Manhattan apartment. She casually checked her reflection in the mirror, doing her daily inventory. Immediately, she stiffened with fright. Huh? What? She didn’t recognize herself. She gazed saucer-eyed at her image, thinking: Oh, is this what I look like? No, that’s not me. Who’s that in my mirror? This was in late 2012. She was 69, in her early months getting familiar with retirement. For some time she had experienced the sensation of clouds coming over her, mantling thought. There had been a few hiccups at her job. She had been a nurse who climbed the rungs to health care executive. Once, she was leading a staff meeting when she had no idea what she was talking about, her mind like a stalled engine that wouldn’t turn over. “Fortunately I was the boss and I just said, ‘Enough of that; Sally, tell me what you’re up to,’” she would say of the episode. Certain mundane tasks stumped her. She told her husband, Jim Taylor, that the blind in the bedroom was broken. He showed her she was pulling the wrong cord. Kept happening. Finally, nothing else working, he scribbled on the adjacent wall which cord was which. Then there was the day she got off the subway at 14th Street and Seventh Avenue unable to figure out why she was there. So, yes, she had had inklings that something was going wrong with her mind. She held tight to these thoughts. She even hid her suspicions from Mr. Taylor, who chalked up her thinning memory to the infirmities of age. “I thought she was getting like me,” he said. “I had been forgetful for 10 years.”
Link ID: 22160 - Posted: 04.30.2016
By PAM BELLUCK Alzheimer’s disease can seem frightening, mysterious and daunting. There are still a lot of unknowns about the disease, which afflicts more than five million Americans. Here are answers to some common questions: Sometimes I forget what day it is or where I put my glasses. Is this normal aging, or am I developing Alzheimer’s? Just because you forgot an item on your grocery list doesn’t mean you are developing dementia. Most people have occasional memory lapses, which increase with age. The memory problems that characterize warning signs of Alzheimer’s are usually more frequent, and they begin to interfere with safe or competent daily functioning: forgetting to turn off the stove, leaving home without being properly dressed or forgetting important appointments. Beyond that, the disease usually involves a decline in other cognitive abilities: planning a schedule, following multistep directions, carrying out familiar logistical tasks like balancing a checkbook or cooking a meal. It can also involve mood changes, agitation, social withdrawal and feelings of confusion, and can even affect or slow a person’s gait. How is Alzheimer’s diagnosed? Diagnosing Alzheimer’s usually involves a series of assessments, including memory and cognitive tests. Clinicians will also do a thorough medical work-up to determine whether the thinking and memory problems can be explained by other diagnoses, such as another type of dementia, a physical illness or side effects from a medication. Brain scans and spinal taps may also be conducted to check for corroborating evidence like the accumulation of amyloid, the hallmark protein of Alzheimer’s, in the brain or spinal fluid. The cause is unknown for most cases. Fewer than 5 percent of cases are linked to specific, rare gene mutations. Those are usually early-onset cases that develop in middle age. © 2016 The New York Times Company
Link ID: 22159 - Posted: 04.30.2016
By Nicholas Bakalar Treating pregnant women for depression may benefit not just themselves but their babies as well. A study, in the May issue of Obstetrics & Gynecology, included 7,267 pregnant women, of whom 831 had symptoms of depression. After controlling for maternal age, race, income, body mass index and other health and behavioral characteristics, the researchers found that depressive symptoms were associated with a 27 percent increased relative risk of preterm birth (less than 37 weeks of gestation), an 82 percent increased risk of very preterm birth (less than 32 weeks of gestation), and a 28 percent increased risk of having a baby small for gestational age. They also found that among those who were treated with antidepressants for depression — about a fifth of those with the diagnosis — there was no association with increased risk for any of these problems. But they acknowledge that this group was quite small, which limits the power to draw conclusions. Still, the lead author, Dr. Kartik K. Venkatesh, a clinical fellow in obstetrics and gynecology at Harvard, said that it was important to screen mothers for depression, not only for their health but for that of their babies. “By screening early in pregnancy, you could identify those at higher risk and counsel them about the importance of treatment,” he said. “Treating these women for depression may have real benefits.” © 2016 The New York Times Company
It was December 2012 when the country learned about the massacre at Sandy Hook Elementary School, that left 20 children dead at the hands of 20-year-old shooter Adam Lanza. After the shock and the initial grief came questions about how it could have happened and why. Reports that Adam Lanza may have had some form of undiagnosed mental illness surfaced. The tragedy drove Liza Long to write a blog post on that same day, titled "I Am Adam Lanza's Mother." She wasn't Lanza's mom, but she was raising a child with a mental disorder. Her 13-year-old son had violent rages on a regular basis. He was in and out of juvenile detention. He had threatened to kill her. She detailed all this in her essay that took off online. Now, four years later, her son is speaking out too. This week on For The Record: a mother, a son and life on the edge of bipolar disorder. Eric Walton, Liza Long's son, is now a 16-year-old high school sophomore in Boise, Idaho. After a series of misdiagnoses, he's been diagnosed with bipolar disorder. But four years ago, he didn't know much about his condition. "I knew that there were times when I would have rages, didn't like them. I knew that I wanted them to stop," Walton says. Except he felt a loss of control in those moments. He describes the onset of these rages as a "blackout" of sorts. "I would start getting angry," he says. "Then it's like being trapped inside a box inside your own head. It was like a television on the wall that shows you what you're seeing. You can feel everything, but you no longer have the video game controller to control your own body." Walton's mom says when Eric would get into those states, "he would express a lot of suicidal thoughts, and hearing him just say, 'I want to die, I just want to end it.'" Then, two days before the Newtown shooting, Eric Walton had another episode. © 2016 npr
By Lisa L. Lewis On Tuesday, U.S. News and World Report released its annual public high-school rankings, with the School for the Talented and Gifted in Dallas earning the top spot for the fifth year in a row. The rankings are based on a wealth of data, including graduation rates and student performance on state proficiency tests and advanced exams, as well as other relevant factors—like the percentage of economically disadvantaged students the schools serve. But there’s one key metric that isn’t tracked despite having a proven impact on academic performance: school start times. First-period classes at the School for the Talented and Gifted start at 9:15 a.m. That’s unusually late compared to other schools but is in keeping with the best practices now recommended by public health experts. Teens require more sleep than adults and are hardwired to want to sleep in. Eight hours a night may be the goal for adults, but teens need between 8.5–9.5 hours, according to the American Academy of Pediatrics. Unfortunately, few teens meet that minimum: Studies show that two out of three high school students get less than eight hours of sleep, with high school seniors averaging less than seven hours. Sure, kids could go to bed earlier. But their bodies are set against them: Puberty makes it hard for them to fall asleep before 11 p.m. When combined with too-early start times, the result is sleep deprivation.
By Clare Wilson People who develop schizophrenia may have been born with brains with a different structure. The finding adds further support to the idea that genetics can play a key role in schizophrenia, which involves delusions and hallucinations and is often a lifelong condition once it develops. Schizophrenia has been the subject of a fierce nature-versus-nurture debate: childhood abuse is linked with a raised risk of the condition, but 108 genes have been implicated, too. Probing the biology of schizophrenia is difficult because brain tissue sampled from people with the condition is rarely available to study. Kristen Brennand of the Icahn School of Medicine at Mount Sinai in New York and her colleagues got around this by taking skin cells from 14 people with schizophrenia, and reprogramming them into stem cells and then nerve cells. They found that on average these nerve cells had lower levels of a signalling molecule called miR-9 than similar cells developed from people who do not have schizophrenia. A small string of nucleic acids, miR-9 can change the activity of certain genes and is known to play a role in how neurons develop in the fetus. In further experiments, Brennand’s team showed that miR-9 might also affect how neurons migrate from where they form, next to the fetal brain’s central cavities, out to their final resting place in the brain’s outer layers. © Copyright Reed Business Information Ltd.
By Esther Landhuis Peer inside the brain of someone with Alzheimer’s disease, and you’ll see some striking features: shriveled nerve cells and strange protein clumps. According to a leading theory, proteins called amyloid beta and tau build up in the brain and choke nerve cell communication, setting the disease in motion years before people suspect anything is wrong with their recall. Yet the Alzheimer’s brain has another curious aspect. Some of the clusters of toxic amyloid proteins are entangled with octopus-like immune cells called microglia, cells that live in the brain to clear unwanted clutter. By munching on amyloid plaques, microglia are thought to help keep the disease at bay. But these housekeeping cells have an additional role—they switch on inflammatory pathways. Inflammation is critically important when the immune system encounters infection or needs to repair tissue. If left unchecked, however, the inflammatory process churns out toxic substances that can kill surrounding cells, whose death triggers more inflammation and creates a vicious cycle. For years scientists have probed how neuroinflammation contributes to Alzheimer’s disease and other neurodegenerative ailments. Researchers face a number of immediate questions: Is neuroinflammation a driving force? Does it kick in when the disease is already underway and worsen the process? Could it be harnessed for good in the early stages? Those questions are far from settled, but research is starting to reveal a clearer picture. “It may not be the amyloid plaques themselves that directly damage neurons and the connections between them. Rather, it may be the immune reaction to the plaques that does the damage,” says Cynthia Lemere, a neuroscientist at Brigham and Women’s Hospital. Still, it is hard to say if microglia are good guys or bad, making it challenging to create therapeutics that target these cells. © 2016 Scientific American
Nicola Davis The proportion of older people suffering from dementia has fallen by a fifth over the past two decades with the most likely explanation being because men are smoking less and living healthier lives, according to new scientific research. A team from three British universities concluded that as a result the number of new cases of dementia is lower than had been predicted in the 1990s, estimated at around 210,000 a year in the UK as opposed to 250,000. The findings are potentially significant because they suggest that it is possible to take preventative action, such as stopping smoking and reducing cholesterol, that could help avoid the condition. “Physical health and brain health are clearly highly linked,” said Carol Brayne of Cambridge University, who co-authored the study. Nick Fox, professor of neurology at University College, London, who was not involved in the study, agrees: “This does suggest that our risk, in any particular age in later life, can be reduced probably by what we do 10, 20 or 30 years before.” The scientists found that new cases of dementia had dropped from 20.1 in every 1,000 people per year in the first study conducted in the early 1990s to 17.7 in the second, which looked at new cases between 2008 and 2013. When sex and age differences were taken into account, the dementia rates were found to have dropped by 20%. The trend emerges from a dramatic drop in new cases for men across all age groups. In the 1990s study, for every 1,000 men aged 70-74, 12.9 went on to develop dementia within a year. In the second study, 20 years later, that figure had dropped to only 8.7 men. For men aged 65-69 the rate of new cases had more than halved between the two studies. © 2016 Guardian News and Media Limited
Link ID: 22122 - Posted: 04.20.2016