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

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Paula Span At first, the pills helped her feel so much better. Jessica Falstein, an artist living in the East Village in Manhattan, learned she had an anxiety disorder in 1992. It led to panic attacks, a racing pulse, sleeplessness. “Whenever there was too much stress, the anxiety would become almost intolerable, like acid in the veins,” she recalled. When a psychopharmacologist prescribed the drug Klonopin, everything brightened. “It just leveled me out,” Ms. Falstein said. “I had more energy. And it helped me sleep, which I was desperate for.” After several months, however, the horrible symptoms returned. “My body became accustomed to half a milligram, and the drug stopped working,” she said. “So then I was up to one milligram. And then two.” Her doctor kept increasing the dosage and added Ativan to the mix. Now 67, with her health and stamina in decline, Ms. Falstein has been diligently working to wean herself from both medications, part of the class called benzodiazepines that is widely prescribed for insomnia and anxiety. “They turn on you,” she said. For years, geriatricians and researchers have sounded the alarm about the use of benzodiazepines among older adults. Often called “benzos,” the problem drugs include Valium (diazepam), Klonopin (clonazepam), Xanax (alprazolam) and Ativan (lorazepam). The cautions have had scant effect: Use of the drugs has risen among older people, even though they are particularly vulnerable to the drugs’ ill effects. Like Ms. Falstein, many patients take them for years, though they’re recommended only for short periods. The chemically related “z-drugs” — Ambien, Sonata and Lunesta — present similar risks. © 2018 The New York Times Company

Keyword: Development of the Brain; Drug Abuse
Link ID: 24761 - Posted: 03.16.2018

By Anna Azvolinsky Researchers have tried to dissect the effects of an older father on kids’ longevity. One study found that kids with older dads had longer telomeres, which may indicate better health and longer lifespan, while another observed that kids with older dads have an increased risk of psychiatric disorders. So far, there have been very few experimental studies in animals that directly test whether paternal age has an affect on offspring telomere length and lifespan. Now, a team of researchers shows that bird embryos sired from old zebra finch fathers have shorter telomeres compared to those with the same moms and younger fathers. The study, published today (March 14) in Proceedings of the Royal Society B, is among the first to address whether paternal age affects telomere length of offspring using an experimental approach. “The experimental design of this study looking at the effect of paternal age on telomere length of [zebra finch] embryos is particularly strong, allowing for confidence in these results,” writes Dan Eisenberg, an anthropologist at the University of Washington who studies the effects of paternal age on telomere length in humans and chimpanzees, in an email to The Scientist. Jose Noguera, now at the University of Vigo, along with colleagues at the University of Glasgow, bred 32 middle-aged, female zebra finches first with both 16 four-month-old males and later with 16 four-year-old male birds. The team harvested the eggs, 139 in total, artificially incubated them for several days, then analyzed the telomere lengths of the embryos. © 1986-2018 The Scientist

Keyword: Development of the Brain; Sexual Behavior
Link ID: 24760 - Posted: 03.16.2018

By Abby Olena Diagnosing neurobiological disorders, such as the autism spectrum disorders, focuses on complex clinical evaluations. But a study published last week (March 6) in eLife shows that an objective measure—how the pupil varies in size while viewing an optical illusion—reveals differences in perceptual styles and correlates with a self-reported score of autistic traits. The findings suggest that tracking fluctuations in pupil size, which is called pupillometry, could be used alongside clinical assessments to help researchers and clinicians understand autism. “We used to think that the pupil was a simple light reflex or that it just indexed arousal,” says Stefan Van der Stigchel, an attention and perception researcher at Utrecht University in the Netherlands who did not participate in the work. This study shows “how the pupil can be informative of, in this situation, perceptual styles.” Previous research has shown that people with autism spectrum disorders allocate their attention differently—and therefore may perceive things differently—than people in the general population. For instance, rather than perceiving an image as a forest, they might focus on the individual trees, says coauthor David Burr of the University of Florence. It’s possible to measure what people pay attention to by having them look at images with both bright and dark areas. Their pupils are slightly larger when they attend to the dark parts and slightly smaller when they attend to the light parts. Burr, Paola Binda of the University of Pisa in Italy, and Marco Turi, a postdoc at the University of Pisa, decided to take advantage of this phenomenon and study how attention, via pupil size, tracks with autistic traits. © 1986-2018 The Scientist

Keyword: Autism; Attention
Link ID: 24755 - Posted: 03.15.2018

By SANDRA BLAKESLEE Dr. T. Berry Brazelton, America’s most celebrated baby doctor since Benjamin Spock and the pediatrician who revolutionized our understanding of how children develop psychologically, died on Tuesday at his home in Barnstable, Mass., on Cape Cod. He was 99. His daughter Christina Brazelton confirmed the death. Before Dr. Brazelton began practicing medicine in the early 1950s, the conventional wisdom about babies and child rearing was unsparingly authoritarian. It was believed that infants could not feel pain. Parents were instructed to set strict schedules, demand obedience and refrain from kissing or cuddling. Babies were to be fed every four hours, by the clock, preferably from a bottle. When children were hospitalized, parents were allowed few if any visiting hours. Dr. Brazelton, echoing Dr. Spock, whose book “The Common Sense Book of Baby and Child Care” became a best seller in 1946, rejected such beliefs and practices as being senseless, if not barbaric. “He put the baby at the center of the universe,” Dr. Barry Lester, a pediatrician and director of the Center for the Study of Children at Risk at Brown University, said in an interview for this obituary in 2009. “We take for granted all the changes he helped bring about. He more than anyone is responsible for the return to natural childbirth, breast feeding and the ability of parents to stay with a hospitalized child.” Nevertheless, Dr. Brazelton’s work never entered mainstream pediatrics and is not taught in most medical curriculums. But the public loved the charismatic Dr. Brazelton. He wrote nearly 40 books and a column in Family Circle magazine, and he was the host of an Emmy Award-winning show, “What Every Baby Knows,” which ran for 12 years on the Lifetime cable channel. He also worked with Congress to pass parental leave legislation and other parent-friendly measures. © 2018 The New York Times Company

Keyword: Development of the Brain
Link ID: 24752 - Posted: 03.15.2018

By Rachel R. Albert Parents are often their own worst critics when it comes to imparting knowledge to their children. Although helping with science fairs or homework assignments may come later on, the pressure comes early, as their infant starts to babble in increasingly word-like vocalizations. It’s easy to assume that children who can’t yet form a word are unable to understand what their parents are saying to them. But spend just a few minutes with an infant, and you quickly realize how rapidly the gears are turning. And new research by me and my colleagues Michael Goldstein and Jennifer Schwade at Cornell University, suggests these interactions are more sophisticated than we once thought. Parents’ responses to their baby’s babbling take on new significance at the age of about six months, when babies’ vocalizations start to mature. Around this age, babies become incredibly receptive to what they hear immediately after they babble. In fact, previous work from the B.A.B.Y. Lab at Cornell University suggests that if infants receive a response to their initial vocalization, they’re far more likely to vocalize again. Observations of mother-infant conversations have found that within 10 minutes of this type of exchange, children can be taught new vocalizations. For example, they can be taught to shift their consonant-vowel construction of “dada” into vowel-consonant “ada.” But what’s truly incredible about these exchanges is the level of influence babies have as actual conversation partners. © 2018 Scientific American,

Keyword: Language; Development of the Brain
Link ID: 24749 - Posted: 03.14.2018

NIH-funded researchers at Stanford University used the gene editing tool CRISPR-Cas9 to rapidly identify genes in the human genome that might modify the severity of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) caused by mutations in a gene called C9orf72. The results of the search, published in Nature Genetics, uncovered a new set of genes that may hasten neuron death during the disease. Accounting for nearly 40 percent of inherited cases of ALS and 25 percent of inherited FTD cases, disease-causing mutations in C9orf72 insert extra sequences of DNA, called hexanucleotide repeats, into the gene. These repeats produce potentially toxic RNA and protein molecules that kill neurons resulting in problems with movement and eventually paralysis for ALS patients and language and decision-making problems for FTD patients. Led by Aaron D. Gitler, Ph.D., and Michael C. Bassik, Ph.D., the researchers used CRISPR to disable each gene, one-by-one, in a line of human leukemia cells and then tested whether the cells would survive exposure to toxic proteins derived from the hexanucleotide repeats, called DPRs. Any disabled genes that caused cells to live longer or die faster than normal were considered suspects in DPR toxicity. They confirmed that genes that control the movement of molecules in and out of a cell’s nucleus may be partners. They also identified several new players, including genes that modify chromosomes and that help cells assemble proteins passing through a maze-like structure called the endoplasmic reticulum (ER). A second CRISPR search conducted on mouse brain cells confirmed the initial results. Disabling the top 200 genes identified in the leukemia cells helped neurons survive DPR exposure.

Keyword: ALS-Lou Gehrig's Disease ; Alzheimers
Link ID: 24745 - Posted: 03.13.2018

by Amy B Wang The 84-year-old man arrived in the emergency room with complaints that weren't uncommon for a patient his age. He had reported feeling unsteady over the past several months, culminating in repeated falls in recent weeks. In the three days leading up to his hospital visit, his left arm and leg had noticeably weakened. Still, there were no red flags in the man's medical history. He didn't smoke. He rarely drank. A blood test detected nothing abnormal. “There was no confusion, facial weakness, visual or speech disturbance,” doctors stated in a summary of the man's case published Feb. 27 in the medical journal BMJ Case Reports. “He was otherwise fit and well, independent with physical activities of daily living ... and lived at home with his wife and two sons.” In other words, doctors thought, there was nothing apparent that would have suggested a clear reason for his symptoms. In a way, they wouldn't be wrong. It was only after CT and MRI scans that the patient's medical team made an alarming discovery: Where much of the man's right frontal lobe of his brain should have been, there was simply a large blank space. Finlay Brown, a physician who was working in the emergency department at Causeway Hospital in Coleraine, Northern Ireland, at the time, remembers reviewing the brain-imaging scans with the rest of the staff. © 1996-2018 The Washington Post

Keyword: Development of the Brain
Link ID: 24742 - Posted: 03.13.2018

Laura Beil On the hormonal roller coaster of life, the ups and downs of childbirth are the Tower of Power. For nine long months, a woman’s body and brain absorb a slow upwelling of hormones, notably progesterone and estrogen. The ovaries and placenta produce these two chemicals in a gradual but relentless rise to support the developing fetus. With the birth of a baby, and the immediate expulsion of the placenta, hormone levels plummet. No other physiological change comes close to this kind of free fall in both speed and intensity. For most women, the brain and body make a smooth landing, but more than 1 in 10 women in the United States may have trouble coping with the sudden crash. Those new mothers are left feeling depressed, isolated or anxious at a time society expects them to be deliriously happy. This has always been so. Mental struggles following childbirth have been recognized for as long as doctors have documented the experience of pregnancy. Hippocrates described a woman’s restlessness and insomnia after giving birth. In the 19th century, some doctors declared that mothers were suffering from “insanity of pregnancy” or “insanity of lactation.” Women were sent to mental hospitals. Modern medicine recognizes psychiatric suffering in new mothers as an illness like any other, but the condition, known as postpartum depression, still bears stigma. Both depression and anxiety are thought to be woefully underdiagnosed in new mothers, given that many women are afraid to admit that a new baby is anything less than a bundle of joy. It’s not the feeling they expected when they were expecting. |© Society for Science & the Public 2000 - 2018.

Keyword: Depression; Development of the Brain
Link ID: 24741 - Posted: 03.12.2018

Researchers say they may have worked out why there is a natural loss of muscle in the legs as people age - and that it is due to a loss of nerves. In tests on 168 men, they found that nerves controlling the legs decreased by around 30% by the age of 75. This made muscles waste away, but in older fitter athletes there was a better chance of them being 'rescued' by nerves re-connecting. The scientists published their research in the Journal of Physiology. As people get older, their leg muscles become smaller and weaker, leading to problems with everyday movements such as walking up stairs or getting out of a chair. It is something that affects everyone eventually, but why it happens is not fully understood. Prof Jamie McPhee, from Manchester Metropolitan University, said young adults usually had 60-70,000 nerves controlling movement in the legs from the lumbar spine. But his research showed this changed significantly in old age. "There was a dramatic loss of nerves controlling the muscles - a 30-60% loss - which means they waste away," he said. "The muscles need to receive a proper signal from the nervous system to tell them to contract, so we can move around." The research team from Manchester Metropolitan University worked with researchers from the University of Waterloo, Ontario, and the University of Manchester. They looked at muscle tissue in detail using magnetic resonance imaging (MRI) and they recorded the electrical activity passing through the muscle to estimate the numbers and the size of surviving nerves. The good news is that healthy muscles have a form of protection: surviving nerves can send out new branches to rescue muscles and stop them wasting away. This is more likely to happen in fit people with large, healthy muscles, Prof McPhee said. © 2018 BBC.

Keyword: Movement Disorders; Development of the Brain
Link ID: 24737 - Posted: 03.12.2018

By George Musser, Satsuki Ayaya remembers finding it hard to play with other children when she was young, as if a screen separated her from them. Sometimes she felt numb, sometimes too sensitive; sometimes sounds were muted, sometimes too sharp. As a teenager, desperate to understand herself, she began keeping a journal. “I started to write my ideas in my notebooks, like: What’s happened to me? Or: What’s wrong with me? Or: Who am I?” she says, “I wrote, wrote, wrote. I filled maybe 40 notebooks.” Today, at 43, Ayaya has a better sense of who she is: She was diagnosed with autism when she was in her early 30s. As a Ph.D. student in the history and philosophy of science at the University of Tokyo, she is using the narratives from her teen years and after to generate hypotheses and suggest experiments about autism — a form of self-analysis called Tojisha-Kenkyu, introduced nearly 20 years ago by the disability-rights movement in Japan. In Ayaya’s telling, her autism involves a host of perceptual disconnects. For example, she feels in exquisite detail all the sensations that typical people readily identify as hunger, but she can’t piece them together. “It’s very hard for me to conclude I’m hungry,” she says. “I feel irritated, or I feel sad, or I feel something [is] wrong. This information is separated, not connected.” It takes her so long to realize she is hungry that she often feels faint and gets something to eat only after someone suggests it to her. © 2018 American Association for the Advancement of Science

Keyword: Autism
Link ID: 24736 - Posted: 03.10.2018

Giorgia Guglielmi Every day, the human hippocampus, a brain region involved in learning and memory, creates hundreds of new nerve cells — or so scientists thought. Now, results from a study could upend this long-standing idea. A team of researchers has found that the birth of neurons in this region seems to stop once we become adults. A few years ago, the group looked at a well-preserved adult brain sample and spotted a few young neurons in several regions, but none in the hippocampus. So they decided to analyse hippocampus samples from dozens of donors, ranging from fetuses to people in their 60s and 70s. They concluded that the number of new hippocampal neurons starts to dwindle after birth and drops to near zero in adulthood. The results1, published in Nature on 7 March, are already raising controversy. If confirmed, the findings would be a “huge blow” not only to scientists in the field, but also to people with certain brain disorders, says Ludwig Aigner, a neuroscientist at Paracelsus Medical University in Salzburg, Austria. This is because researchers had hoped to harness the brain’s ability to generate new neurons to treat neurodegenerative diseases such as Alzheimer’s and Parkinson’s, he says. But Aigner and other neuroscientists are not fully persuaded by the findings, which contradict multiple lines of evidence that the hippocampus keeps producing neurons throughout a person’s life. “I wouldn’t close the books on [that],” says neuroscientist Heather Cameron of the US National Institute of Mental Health in Bethesda, Maryland. © 2018 Macmillan Publishers Limited

Keyword: Neurogenesis; Learning & Memory
Link ID: 24733 - Posted: 03.08.2018

By Michelle Roberts Health editor, BBC News online Four dementia scientists have shared this year's 1m Euro brain prize for pivotal work that has changed our understanding of Alzheimer's disease. Profs John Hardy, Bart De Strooper, Michel Goedert, based in the UK, and Prof Christian Haass, from Germany, unpicked key protein changes that lead to this most common type of dementia. On getting the award, Prof Hardy said he hoped new treatments could be found. He is donating some of his prize money to care for Alzheimer's patients. Much of the drug discovery research that's done today builds on their pioneering work, looking for ways to stop the build-up of damaging proteins, such as amyloid and tau. Alzheimer's and other dementias affect 50 million people around the world, and none of the treatments currently available can stop the disease. Path to beating Alzheimer's Prof Hardy's work includes finding rare, faulty genes linked to Alzheimer's disease. These genetic errors implicated a build-up of amyloid as the event that kick-starts damage to nerve cells in Alzheimer's. This idea, known as the amyloid cascade hypothesis, has been central to Alzheimer's research for nearly 30 years. Together with Prof Haass, who is from the University of Munich, Prof Hardy, who's now at University College London, then discovered how amyloid production changes in people with rare inherited forms of Alzheimer's dementia. How one woman and her family transformed Alzheimer's research Prof Goedert's research at Cambridge University, meanwhile, revealed the importance of another damaging protein, called tau, while Prof De Stooper, who is the new director of the UK Dementia Research Institute at UCL, discovered how genetic errors that alter the activity of proteins called secretases can lead to Alzheimer's processes. Dr David Reynolds, Chief Scientific Officer at Alzheimer's Research UK, said: "Our congratulations go to all four of these outstanding scientists whose vital contributions have transformed our understanding of the complex causes of Alzheimer's disease. © 2018 BBC.

Keyword: Alzheimers
Link ID: 24730 - Posted: 03.08.2018

By Michael Price When you hear a B-flat music note, do you see the color blue? Do the words in this sentence look red or green? If so, you may have synesthesia, a mysterious condition in which one sense consistently mingles with another. Now, for the first time, scientists have identified a handful of genes that might predispose people to synesthesia, offering a window to better understand disorders such as autism, which is also thought to involve abnormal brain connections. “It’s very exciting,” says Romke Rouw, a cognitive psychologist who studies synesthesia at the University of Amsterdam but who wasn’t involved in the study. “It provides a fascinating suggestion of a link between particular genetic variations and hyperconnectivity in the synesthetic brain.” For decades, many psychologists and neuroscientists were reluctant to research synesthesia. Some refused to acknowledge its existence, whereas others believed the phenomenon’s individual, subjective nature made it virtually impossible to study. But increasingly sophisticated survey methods have allowed scientists to confirm that some people—it’s unclear how many—do consistently and involuntarily experience this unusual condition. Synesthesia is thought to be at least somewhat heritable, as it frequently clusters within families. But genomic investigations so far have failed to turn up individual genes that might be responsible for it. © 2018 American Association for the Advancement of Science

Keyword: Development of the Brain
Link ID: 24726 - Posted: 03.06.2018

By Katarina Zimmer Jermaine Jones’s first memory of being a “bit of a scientist” was discovering that toilet water is actually pretty clean. While conducting a science fair pro-ject during his junior year of high school in Virginia, he learned that “you get much more varied bacteria from the toilet seat as opposed to the water,” he explains. With encouragement from his aunt, who was a biologist, Jones chose to pursue a degree in science at the University of Virginia. Over the course of several undergraduate internships, he got a taste of different fields of research, from probing decision making in mice to examining the analgesic effects of rainforest plant extracts in Brazil. By the time Jones had earned his master’s degree from Old Dominion University, he was certain that investigating drug abuse would be a good fit for his two main interests, pharmacology and psychology. For his PhD, Jones moved to Washington, D.C., where he worked on elucidating the neurobiological mechanisms of cocaine’s aversive effects in rodent models with Anthony Riley, a behavioral pharmacologist at American University. At the same time, Jones examined the effects of knocking out genes encoding the neurotransmitter transporters that the drug acts upon in mice with neuroscientists George Uhl and Scott Hall at the National Institute on Drug Abuse. For his dissertation, “he was able to show, pretty unequivocally, the role of neuro-transmitter systems in the aversive effects of cocaine in these mice,” Riley recalls.1 © 1986-2018 The Scientist

Keyword: Drug Abuse; Genes & Behavior
Link ID: 24717 - Posted: 03.02.2018

Russell Bonduriansky Wouldn’t it be wonderful if we could bring back a deceased loved one? Such ideas used to be pure science fiction, but recent advances in biotechnology seem to have brought this possibility within reach (at least for the wealthy). When American singer-actress Barbra Streisand lost her beloved dog Sammie last year, she decided to have her cloned. She’s now raising Miss Scarlet and Miss Violet, both of whom are exact genetic replicas of Sammie. (You’ll be glad to know that any pet owner can do the same: for a mere US$100,000 or so, you too could have a genetic replica of your favourite cat or dog.) But Miss Scarlett and Miss Violet almost certainly won’t turn out to be identical, mini versions of Sammie. Research on cloning started in the 1960s, when British biologist John Gurdon showed that a frog egg’s nucleus (which contains the DNA) could be swapped for another nucleus extracted from an intestinal cell, and that such eggs could develop into tadpoles. This technique makes it possible to create individuals that share every single one of the thousands of genes in the original genome. By comparison, you share only about 50% of your genes with your mother. The same nucleus-swapping technique can be used with mammals. In 1996, Dolly the sheep became the first cloned mammal, and today the technology is available to clone a human being – if we wanted to. © 2010–2018, The Conversation US, Inc.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 24716 - Posted: 03.02.2018

Alice M. Gregory, Erin Leichman, Jodi Mindell Pairing the words “baby” and “sleep” can evoke strong emotions. Those who have had limited contact with little ones might interpret this word-combination as implying deep and prolonged slumber. For others, this union of words may elicit memories of prolonged periods of chaotic sleep (or what can feel like no sleep at all). Coping with the way babies sleep can be difficult. It’s not that babies don’t sleep. In fact, they sleep more than at any other stage of life. It’s more an issue of when they sleep. Newborns start by sleeping and waking around the clock. This is not always easy for parents. There is even research suggesting that in adults waking repeatedly at night can feel as bad as getting hardly any sleep in terms of attentional skills, fatigue levels and symptoms of depression. As to why infants wake at night, this is best explained by thinking about the two things that govern our sleep: the homeostatic and circadian processes. The crux of the homeostatic process is the straightforward idea that the longer we have been awake the greater our sleep drive (and the more sleepy we feel). It may take an adult an entire day to build up enough sleep drive to fall asleep at bedtime, but an infant may only need an hour or two of wakefulness before being able to drift off to sleep. The second process is circadian, which works like a clock. Adults typically feel more awake during the morning hours and sleepy at night, regardless of when we last slept. In very young babies this process is not yet developed. This means that sleep is more likely to occur at different points across the 24-hour day. © 2018 Guardian News and Media Limited

Keyword: Sleep; Development of the Brain
Link ID: 24713 - Posted: 03.01.2018

Helen Thomson In March 2015, Li-Huei Tsai set up a tiny disco for some of the mice in her laboratory. For an hour each day, she placed them in a box lit only by a flickering strobe. The mice — which had been engineered to produce plaques of the peptide amyloid-β in the brain, a hallmark of Alzheimer’s disease — crawled about curiously. When Tsai later dissected them, those that had been to the mini dance parties had significantly lower levels of plaque than mice that had spent the same time in the dark1. Tsai, a neuroscientist at Massachusetts Institute of Technology (MIT) in Cambridge, says she checked the result; then checked it again. “For the longest time, I didn’t believe it,” she says. Her team had managed to clear amyloid from part of the brain with a flickering light. The strobe was tuned to 40 hertz and was designed to manipulate the rodents’ brainwaves, triggering a host of biological effects that eliminated the plaque-forming proteins. Although promising findings in mouse models of Alzheimer’s disease have been notoriously difficult to replicate in humans, the experiment offered some tantalizing possibilities. “The result was so mind-boggling and so robust, it took a while for the idea to sink in, but we knew we needed to work out a way of trying out the same thing in humans,” Tsai says. “There’s been an explosion in brain wave research…pick your area and different people are trying to apply extra cranial stimulation.” The neuroscience that’s making waves for a wide range of conditions. © 2018 Macmillan Publishers Limited,

Keyword: Alzheimers; Learning & Memory
Link ID: 24710 - Posted: 02.28.2018

By Ashley Yeager | Human neural stem cells transplanted into the injured spines of monkeys matured into nerve cells, spurring neuronal connections and giving the animals an improved ability to grasp an orange, researchers report today (February 26) in Nature Medicine. “This type of cellular therapy, though still in its infancy, may eventually be a reasonable approach to treating central nervous system injury and possibly even neurodegenerative disease in humans,” Jonathan Glass, a neurologist at Emory University School of Medicine, tells The Scientist by email. Glass, who was not involved in the study, notes that the differentiation of stem cells over time is “impressive,” as is their ability to make connections in the monkeys’ central nervous systems, but more work needs to be done to show if the cells can grow extremely long axons to connect motor and sensory neurons after spinal injury in humans. Up to this point, most of the work on transplanting neural stem cells had been done in rats. This is the first study to show the treatment can be successfully scaled up to primates. “We definitely have more confidence to do this type of treatment in humans,” study coauthor Mark Tuszynski, a neuroscientist at the University of California, San Diego, School of Medicine, tells The Scientist. In the study, Tuszynski and his colleagues cut into a section of the spinal cord of rhesus monkeys and then two weeks later inserted a graft of human neural progenitor cells into the injury site. In the first four monkeys, the grafts did not stay in position, a finding that forced the researchers to add to the transplants more fibrinogen–thrombin, a protein-enzyme mixture the makes the graft adhere more quickly to site. The team also had to tilt the operating table to drain cerebral spinal fluid, which would wash the graft away. © 1986-2018 The Scientist

Keyword: Regeneration; Stem Cells
Link ID: 24705 - Posted: 02.27.2018

By Dina Fine Maron Millions of Americans who suffer from bipolar disorder depend on lithium. The medication has been prescribed for half a century to help stabilize patients’ moods and prevent manic or depressive episodes. Yet what it does in the brain—and why it does not work for some people—has remained largely mysterious. But last year San Diego–based researchers uncovered new details about how lithium may alter moods, thanks to an approach recently championed by a small number of scientists studying mental illness: The San Diego team used established lab techniques to reprogram patients’ skin cells into stem cells capable of becoming any other kind—and then chemically coaxed them into becoming brain cells. This process is now providing the first real stand-ins for brain cells from mentally ill humans, allowing for unprecedented direct experiments. Proponents hope studying these lab-grown neurons and related cells will eventually lead to more precise and effective treatment options for a variety of conditions. The San Diego team has already used this technique to show some bipolar cases may have more to do with protein regulation than genetic errors. And another lab discovered the activity of glial cells (a type of brain cell that supports neuron function) likely helps fuel schizophrenia—upending the theory that the disorder results mainly from faulty neurons. This new wave of research builds on Shinya Yamanaka’s Nobel-winning experiments on cellular reprogramming from a decade ago. His landmark findings about creating induced pluripotent stem cells (iPSCs) have only recently been applied to studying mental illness as the field has matured. “What’s really sparked that move now has been the ability to make patient-specific stem cells—and once you can do that, then all sorts of diseases become amenable to investigation,” says Steven Goldman, who specializes in cellular and gene therapy at the University of Rochester Medical Center. © 2018 Scientific American,

Keyword: Schizophrenia; Stem Cells
Link ID: 24703 - Posted: 02.27.2018

By Aaron E. Carroll I remember the first time my daughter discovered her hand. The look of amazement on her face was priceless. It wasn’t long before she was putting that discovery to use, trying to put everything she could find into her mouth. Babies want to feed themselves. It sometimes feels as if parents spend more time trying to stop them than encouraging them. Over the last few years, however, some people have begun to ask if we are doing the right thing. Baby-led weaning is an approach to feeding that encourages infants to take control of their eating. It’s based on the premise that infants might be better self-regulators of their food consumption. It has even been thought that baby-led weaning might lead to reductions in obesity. While babies have been spoon-fed for a long time, the explosion of commercial foods for them might be making it too easy to overfeed them, an idea that the results from a cohort study in 2015 seemed to hint at. Those weaned in a baby-led approach seemed to be more responsive to being sated and were less likely to be overweight. A case-control study from 2012 also argued that baby-led weaning was associated with a lower body mass index (B.M.I). Such trials cannot establish causality, however, and may be confounded in unmeasured ways. A recent randomized controlled trial accomplished what previous work could not. Pregnant women in New Zealand were recruited before they gave birth and randomly assigned to one of two groups. Both got standard midwifery and child care. But one group received eight more contacts, from pregnancy to the newborn’s ninth month. Five of these were with a lactation consultant, who encouraged the mothers to prolong breast-feeding and delay the introduction of solid foods until 6 months of age. The three other contacts were with research staffers who encouraged parents to read hunger and fullness cues from their infants and provide their babies (starting at 6 months) with foods that were high in energy and iron — easy to grab but hard to choke on. © 2018 The New York Times Company

Keyword: Obesity; Development of the Brain
Link ID: 24701 - Posted: 02.27.2018