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by Jessica Hamzelou Memories that seem to be lost forever may be lurking in the brain after all, ready to be reawakened. The finding, based on experiments in mice, could eventually give us a way to revive memories in people with Alzheimer's or amnesia. When we learn something, sets of neurons in the brain strengthen their mutual connections to lay down lasting memories. Or at least that's the theory. Susumu Tonegawa and his colleagues at the Massachusetts Institute of Technology decided to put it to the test. The team first developed a clever technique to selectively label the neurons representing what is known as a memory engram – in other words, the brain cells involved in forming a specific memory. They did this by genetically engineering mice so they had extra genes in all their neurons. As a result, when neurons fire as a memory is formed, they produce red proteins visible under a microscope, allowing the researchers to tell which cells were part of the engram. They also inserted a gene that made the neurons fire when illuminated by blue light. To mimic memory loss, some of the mice were given a drug that blocks the strengthening of connections between neurons. This made the animals forget their fear of the cage. But the telltale red proteins allowed Tonegawa's team to work out which neurons had been involved in storing the fear memory. They then attempted to reactivate just these neurons using blue light. Sure enough, after the engram had been reactivated, the mice again acted as if they were afraid of the cage. © Copyright Reed Business Information Ltd.
Keyword: Learning & Memory
Link ID: 21001 - Posted: 05.30.2015
Boer Deng The ability of the bizarre prion protein to cause an array of degenerative brain conditions may help solve a puzzle in Alzheimer's research — why the disease sometimes kills within a few years, but usually causes a slow decline that can take decades. By adopting tools used to study the prion protein, PrP, researchers have found variations in the shape of a protein involved in Alzheimer’s that may influence how much damage it causes in the brain. At the Prion 2015 meeting, held on 26–29 May in Fort Collins, Colorado, neuroscientist Lary Walker described how he has borrowed a technique from prion research to study different ‘strains’ of the amyloid-β protein, which accumulates in clumps in the brains of people with Alzheimer’s. It may be that differences between the strains account for variations in the disease’s symptoms and rate of progression. “The Alzheimer’s field has not been paying enough attention to what’s happening in the prion field,” says Walker, who is based at Emory University in Atlanta, Georgia. Similarities between rare prion diseases and common neurodegenerative diseases such as Alzheimer’s have been noted for decades: both are thought to involve proteins in the nervous system that change shape and clump together. In prion diseases, a misfolded, often foreign, protein induces cascading malformation of the native prion protein in a patient’s brain. In Alzheimer’s, proteins called tau and amyloid-β accumulate within and around nerve cells, though what triggers that process — and the role of the deposits in the disease — is unclear. © 2015 Nature Publishing Group,
Jon Hamilton Antidepressant drugs that work in hours instead of weeks could be on the market within three years, researchers say. "We're getting closer and closer to having really, truly next-generation treatments that are better and quicker than existing ones," says Dr. Carlos Zarate, a researcher at the National Institute of Mental Health. The new drugs are based on the anesthetic ketamine, which is also a popular club drug known as Special K. Unlike current antidepressants, which can take weeks to work, ketamine-like drugs have an immediate effect. They also have helped people with depression who didn't respond to other medications. The drug that is furthest along is esketamine, a chemical variant of ketamine that has been designated a potential breakthrough by the Food and Drug Administration. Esketamine is poised to begin Phase 3 trials, and the drug's maker, Johnson & Johnson, plans to seek FDA approval in 2018. Ketamine, used as a tranquilizer for animals and as an anesthetic in humans, is also being tested as a treatment for depression. Another ketamine-like drug on the horizon is rapastinel. It has completed Phase 2 studies, which showed "rapid, substantial, and sustained reductions in depressive symptoms," according to the drug's maker, Naurex. "I think it's highly probable that we'll see some version of one of these treatments being approved in the relatively near future," says Dr. Gerard Sanacora, director of the Yale Depression Research Program. "In my mind it is the most exciting development in mood disorder treatment in the last 50 years." © 2015 NPR
Link ID: 20999 - Posted: 05.30.2015
A patient tormented by suicidal thoughts gives his psychiatrist a few strands of his hair. She derives stem cells from them to grow budding brain tissue harboring the secrets of his unique illness in a petri dish. She uses the information to genetically engineer a personalized treatment to correct his brain circuit functioning. Just Sci-fi? Yes, but... An evolving “disease-in-a-dish” technology, funded by the National Institutes of Health (NIH), is bringing closer the day when such a seemingly futuristic personalized medicine scenario might not seem so far-fetched. Scientists have perfected mini cultured 3-D structures that grow and function much like the outer mantle – the key working tissue, or cortex — of the brain of the person from whom they were derived. Strikingly, these “organoids” buzz with neuronal network activity. Cells talk with each other in circuits, much as they do in our brains. Sergiu Pasca, M.D. External Web Site Policy, of Stanford University, Palo Alto, CA, and colleagues, debut what they call “human cortical spheroids,” May 25, 2015 online in the journal Nature Methods. Prior to the new study, scientists had developed a way to study neurons differentiated from stem cells derived from patients’ skin cells — using a technology called induced pluripotent stem cells (iPSCs). They had even produced primitive organoids by coaxing neurons and support cells to organize themselves, mimicking the brain’s own architecture. But these lacked the complex circuitry required to even begin to mimic the workings of our brains.
Keyword: Development of the Brain
Link ID: 20998 - Posted: 05.30.2015
by Penny Sarchet The common pet budgerigar (or parakeet) is loved for its ability to mimic its owners. But it has another special trick – it can catch yawns from other budgies, suggesting it has some kind of empathy. "Practically all vertebrates yawn," says Ramiro Joly-Mascheroni of City University, London. In 2008, he showed that dogs can catch yawns from humans. The only other species shown to yawn contagiously are humans, chimpanzees and a type of rodent called the high-yawning Sprague-Dawley rat. But Andrew Gallup of the State University of New York and his colleagues have now shown for the first time that the same happens for a species of non-mammals. To see whether budgies, a sociable parrot species, can make each other yawn, his team designed two experiments. In the first, budgies were placed in adjacent cages, either with a barrier between them, or with nothing obstructing their view of each other. They found that, when budgies could see each other, they were around three times as likely to yawn within five minutes of a yawn from their neighbour. In their second experiment, budgies were shown a video – either one that showed clips of budgies yawning, or one that had no yawning at all. Every bird that watched the yawning video also yawned, while fewer than half of the birds shown the other video yawned. "Thus far, yawning has been demonstrated to be contagious in a few highly social species," said Gallup. "To date, this is the first experimental evidence of contagious yawning in a non-mammalian species." © Copyright Reed Business Information Ltd
Link ID: 20997 - Posted: 05.30.2015
By Roberto A. Ferdman In 2007, the Food and Drug administration approved the first ever over-the-counter diet drug. Alli, as the pill was (and still is) called, could be taken by anyone, without a prescription. And it worked, so long as those who took it also maintained a healthy lifestyle. That last bit—persuading people who take diet drugs to also eat well and exercise—is the oft overlooked key with weight-loss remedies. And GlaxoSmithKline, which manufactures the drug, knew it. Marketing around the pill made it clear that Alli was not some miracle drug. But getting people to treat diet drugs for what they are—helpers, not fix alls—is actually a lot harder than it sounds. Some diet drugs have been shown to work. But a growing pool of research suggests people are prone to use them improperly. "There's a funny, kind of counterintuitive thing that happens when many people take weight-loss drugs: they gain weight," said Amit Battacharjee, an assistant professor at The Tuck School of Business, whose research focuses on consumer beliefs and well-being. "But it isn't necessarily because the drugs themselves don't work." Battacharjee has a new study titled 'The Perils of Marketing Weight-Management Remedies,' which looks closely at how the way in which weight-loss drugs are pitched to people can significantly affect the way in which people understand them.
Link ID: 20996 - Posted: 05.30.2015
John Bohannon “Slim by Chocolate!” the headlines blared. A team of German researchers had found that people on a low-carb diet lost weight 10 percent faster if they ate a chocolate bar every day. It made the front page of Bild, Europe’s largest daily newspaper, just beneath their update about the Germanwings crash. From there, it ricocheted around the internet and beyond, making news in more than 20 countries and half a dozen languages. It was discussed on television news shows. It appeared in glossy print, most recently in the June issue of Shape magazine (“Why You Must Eat Chocolate Daily”, page 128). Not only does chocolate accelerate weight loss, the study found, but it leads to healthier cholesterol levels and overall increased well-being. The Bild story quotes the study’s lead author, Johannes Bohannon, Ph.D., research director of the Institute of Diet and Health: “The best part is you can buy chocolate everywhere.” I am Johannes Bohannon, Ph.D. Well, actually my name is John, and I’m a journalist. I do have a Ph.D., but it’s in the molecular biology of bacteria, not humans. The Institute of Diet and Health? That’s nothing more than a website. Other than those fibs, the study was 100 percent authentic. My colleagues and I recruited actual human subjects in Germany. We ran an actual clinical trial, with subjects randomly assigned to different diet regimes. And the statistically significant benefits of chocolate that we reported are based on the actual data. It was, in fact, a fairly typical study for the field of diet research. Which is to say: It was terrible science. The results are meaningless, and the health claims that the media blasted out to millions of people around the world are utterly unfounded.
Link ID: 20995 - Posted: 05.28.2015
by Jessica Hamzelou IF YOU knew you were about to go through a stressful experience, would you pop a pill to protect yourself from its knock-on effects? It's an idea that has been mooted after a drug seemed to make mice immune to the negative impacts of stressful events. But could we rationalise prescribing such a drug? We all experience stress during our lives, whether it be a one-off event, such as a loved one dying, or chronic, low-level stress that results from struggling to make ends meet, for example. While most people find ways to cope, for some a particularly stressful event can trigger depression. What if there was a way to boost our stress resilience and thus shield us from depression? Rebecca Brachman at Columbia University in New York stumbled across the idea while she was giving ketamine to mice with the symptoms of depression. Even though the ketamine-taking mice had been chronically stressed, when they were dropped in a pool of water – a one-off stressful event – they were unperturbed and swam to an exit. Mice not given the drug made no attempt to escape, a classic sign of depression in rodents. There was also no change in the ketamine-taking animals' cognitive abilities or metabolism – both of which are altered in human depression. "It's really remarkable," says Brachman. "They basically look like mice that haven't been stressed." A single dose of ketamine protected mice from developing the symptoms of depression after stressful events for four weeks. But the drug only seemed to stop the symptoms of depression – some of the animals still exhibited anxiety behaviours. "It seems to protect against depression rather than anxiety," says Brachman, who controversially describes it as a depression "vaccine". The work will be published in Biological Psychiatry. © Copyright Reed Business Information Ltd
Carl Zimmer For scientists who study human evolution, the last few months have been a whirlwind. Every couple of weeks, it seems, another team pulls back the curtain on newly discovered bones or stone tools, prompting researchers to rethink what we know about early human history. On Wednesday, it happened again. Yohannes Haile-Selassie of the Cleveland Museum of Natural History and his colleagues reported finding a jaw in Ethiopia that belonged to an ancient human relative that lived some time between 3.3 and 3.5 million years. They argue that the jaw belongs to an entirely new species, which they dubbed Australopithecus deyiremeda. While some experts agree, skeptics argued that the jaw belongs to a familiar hominid species, known as Australopithecus afarensis, that existed from about 3.9 to 3 million years ago. Studies like this one are adding fresh fuel to the debate over the pace of human evolution. Some researchers now believe the human family tree bore exuberant branches early on. “I’m so excited about these discoveries, I’m driving my friends crazy,” said Carol V. Ward, a paleoanthropologist at the University of Missouri. “It makes us stop and rethink everything.” In the 1990s, the broad outlines of human evolution seemed fairly clear. Early human ancestors — known as hominids — evolved from an ancestor shared with chimpanzees about six or seven million years ago. These hominids were short, bipedal apes with small brains and arms and legs still adapted for climbing trees. Until about three million years ago, experts thought, there weren’t a lot of hominid species. In fact, some researchers argued that most hominid fossils represented just a single species. © 2015 The New York Times Company
Link ID: 20993 - Posted: 05.28.2015
by Helen Thomson Imagine a world where you think of something and it happens. For instance, what if the moment you realise you want a cup of tea, the kettle starts boiling? That reality is on the cards, now that a brain implant has been developed that can decode a person's intentions. It has already allowed a man paralysed from the neck down to control a robotic arm with unprecedented fluidity. But the implications go far beyond prosthetics. By placing an implant in the area of the brain responsible for intentions, scientists are investigating whether brain activity can give away future decisions – before a person is even aware of making them. Such a result may even alter our understanding of free will. Fluid movement "These are exciting times," says Pedro Lopes, who works at the human-computer interaction lab at Hasso Plattner Institute in Potsdam, Germany. "These developments give us a glimpse of an exciting future where devices will understand our intentions as a means of adapting to our plans." The implant was designed for Erik Sorto, who was left unable to move his limbs after a spinal cord injury 12 years ago. The idea was to give him the ability to move a stand-alone robotic arm by recording the activity in his posterior parietal cortex – a part of the brain used in planning movements. "We thought this would allow us to decode brain activity associated with the overall goal of a movement – for example, 'I want to pick up that cup'," Richard Andersen at the California Institute of Technology in Pasadena told delegates at the NeuroGaming Conference in San Francisco earlier this month. © Copyright Reed Business Information Ltd
Krishnadev Calamur Two research chimps got their day in court — though they weren't actually present in the courtroom. Steven Wise, an attorney with the Nonhuman Rights Project, told Manhattan Supreme Court Judge Barbara Jaffe that Hercules and Leo, the 8-year-old research chimps at Stony Brook University on Long Island, are "autonomous and self-determining beings" who should be granted a writ of habeas corpus, which would effectively recognize them as legal persons. The chimps, he argued, should be moved from the university to a sanctuary in Florida. But Christopher Coulston, an assistant state attorney general representing the university, called the case meritless. The Associated Press reports that he said granting chimps personhood would create, in the words of the AP, "a slippery slope regarding the rights of other animals." "The reality is these are fundamentally different species," Coulston said. "There's simply no precedent anywhere of an animal getting the same rights as a human." Jaffe, the AP adds, didn't make a ruling Wednesday but called the proceeding "extremely interesting and well argued." NPR's Hansi Lo Wang reported on the story Wednesday for our Newscast unit. He says: "Past judges have struck down this lawsuit since it was first filed in 2013. But the current judge at the Manhattan Supreme Court is ordering the university to defend why it's detaining the chimps." © 2015 NPR
Keyword: Animal Rights
Link ID: 20991 - Posted: 05.28.2015
George Yancy: You have popularized the concept of speciesism, which, I believe was first used by the animal activist Richard Ryder. Briefly, define that term and how do you see it as similar to or different from racism? Peter Singer: Speciesism is an attitude of bias against a being because of the species to which it belongs. Typically, humans show speciesism when they give less weight to the interests of nonhuman animals than they give to the similar interests of human beings. Note the requirement that the interests in question be “similar.” It’s not speciesism to say that normal humans have an interest in continuing to live that is different from the interests that nonhuman animals have. One might, for instance, argue that a being with the ability to think of itself as existing over time, and therefore to plan its life, and to work for future achievements, has a greater interest in continuing to live than a being who lacks such capacities. If we were to compare attitudes about speciesism today with past racist attitudes, we would have to say that we are back in the days in which the slave trade was still legal. On that basis, one might argue that to kill a normal human being who wants to go on living is more seriously wrong than killing a nonhuman animal. Whether this claim is or is not sound, it is not speciesist. But given that some human beings – most obviously, those with profound intellectual impairment – lack this capacity, or have it to a lower degree than some nonhuman animals, it would be speciesist to claim that it is always more seriously wrong to kill a member of the species Homo sapiens than it is to kill a nonhuman animal. © 2015 The New York Times Company
Keyword: Animal Rights
Link ID: 20990 - Posted: 05.28.2015
by Andy Coghlan A man in his mid-50s with Parkinson's disease had fetal brain cells injected into his brain last week. He is the first person in nearly 20 years to be treated this way – and could recover full control of his movements in roughly five years. "It seemed to go fine," says Roger Barker of the University of Cambridge, who is leading the international team that is reviving the procedure. The treatment was pioneered 28 years ago in Sweden, but two trials in the US reported no significant benefit within the first two years following the injections, and the procedure was abandoned in favour of deep brain stimulation treatments. What these trials overlooked is that it takes several years for fetal cells to "bed in" and connect properly to the recipient's brain. Many Swedish and North American recipients improved dramatically, around three years or more after the implants – long after the trials had finished. "In the best cases, patients who had the treatment pretty much went back to normal," says Barker. After the fetal cells were wired up properly in their brains, they started producing the brain signalling chemical dopamine – low levels of this cause the classic Parkinson's symptom of uncontrolled movements. In fact, the cells produced so much dopamine that many patients could stop taking their Parkinson's drugs. "The prospect of not having to take medications for Parkinson's is fantastic," says James Beck of the Parkinson's Disease Foundation in the US. © Copyright Reed Business Information Ltd
Children developed better fine-motor skills when the clamping of their umbilical cord at birth was delayed several minutes compared with just seconds, according to a new randomized trial. Delaying clamping allows fetal blood circulating in the placenta to be transfused to the infant, which has been shown to reduce iron deficiency at four to six months of age. Now the longer term benefits of a delay are becoming clearer. Researchers in Sweden randomly assigned 382 full-term infants born after low-risk pregnancies to be clamped at least three minutes after delivery or within 10 seconds of birth. When the children were four, a psychologist assessed them on standard tests of IQ, motor skills and behaviour. The parents also filled in questionnaires about their child's communication and social skills. "Delayed cord clamping compared with early cord clamping improved scores and reduced the number of children having low scores in fine-motor skills and social domains," the study's lead author, Dr. Ola Andersson of Uppsala University in Sweden, and his co-authors said in Tuesday's issue of JAMA Pediatrics. The fine-motor skill tests showed those in the delayed clamping group had a more mature pencil grip. There was also a difference in boys, who researchers said are generally more prone to iron deficiency than girls. Boys showed more improvements in fine-motor skills with delayed clamping. Andersson said delayed cord clamping can have quite an effect on the amount of iron in the blood, which is important for brain development just after birth. ©2015 CBC/Radio-Canada.
Keyword: Development of the Brain
Link ID: 20988 - Posted: 05.27.2015
Neurosurgeon Henry Marsh has opened heads, cut into brains and performed the most delicate and risky surgeries on the part of the body that controls everything — including breathing, movement, memory and consciousness. "What is, I think, peculiar about brain surgery is it's so dangerous," Marsh tells Fresh Air's Terry Gross. "A very small area of damage to the brain can cause catastrophic disability for the patient." Over the course of his career, Marsh, a consulting neurosurgeon at Atkinson Morley's/St. George's Hospital in London since 1987, has learned firsthand about the damage that his profession can cause. While many of the surgeries he has performed have been triumphs, there is always a risk of leaving the patient severely disabled. In the memoir Do No Harm, Marsh confesses to the fears and uncertainties he's dealt with as a surgeon, revisits his triumphs and failures and reflects on the enigmas of the brain and consciousness. Despite his decades on the job — or perhaps because of them — Marsh says that much of the brain remains beyond his grasp. He likens the mystery of the brain to that of the big-bang theory. "We're all sitting on an equally great mystery within ourselves, each of us, in this microcosm of our own consciousness, and I find that a quite nice thought," he says. You can nick the liver, you can remove bits of the lung, you can remove bits of the heart and the organ goes on working. But with the brain, although some areas can suffer some damage without terrible consequences for the patient, in general terms, it's very dangerous. Which means the decision-making is very important and ... in my experience over the years, when things have gone wrong, it's not because of [we] cut the wrong blood vessel or dropped an instrument or something like that. The mistakes made — the mistakes are in the decision-making — whether to operate or when to operate. © 2015 NPR
Link ID: 20987 - Posted: 05.27.2015
By Neuroskeptic | Neuroscientists might need to rethink much of what’s known about the amygdala, a small brain region that’s been the focus of a lot of research. That’s according to a new paper just published in Scientific Reports: fMRI measurements of amygdala activation are confounded by stimulus correlated signal fluctuation in nearby veins draining distant brain regions. The amygdala is believed to be involved in emotion, especially negative emotions such as fear. Much of the evidence for this comes from fMRI studies showing that the amygdala activates in response to stimuli such as images of scared faces. However, according to the authors of the new paper, Austrian neuroscientists Roland N. Boubela and colleagues, there’s a flaw in these fMRI studies. The problem, they say, is that the amygdala happens to be located next to a large vein, called the basal vein of Rosenthal (BVR). fMRI works by detecting blood oxygenation, so changes in the oxygen level in the blood within the BVR could produce signal changes that could be mistaken for activation in the amygdala. Because the BVR drains blood from several brain regions, some of which are themselves involved in emotion processing, the BVR could act as a proxy for emotion-related neural activation elsewhere in the brain, which is then projected onto the amygdala. Neuroscientists have long been aware of potential large vein contributions to the fMRI signal, but it hasn’t generally been seen as a serious concern. According to Boubela et al., however, the problem is serious, when it comes to the amygdala.
By Tina Hesman Saey Combatants in the age-old battle of nature versus nurture may finally be able to lay down their arms. On average, both nature and nurture contribute roughly equally to determining human traits. Researchers compiled data from half a century’s worth of studies on more than 14 million pairs of twins. The researchers measured heritability — the amount of variation in a characteristic that can be attributed to genes — for a wide variety of human traits including blood pressure, the structure of the eyeball and mental or behavioral disorders. All traits are heritable to some degree, the researchers report May 18 in Nature Genetics. Traits overall had an average heritability of 49 percent, meaning it’s a draw between genes and environment. Individual traits can be more strongly influenced by one or the other. 100% Fraction of human traits with a genetic component 49% Fraction of variability in human traits determined by genes T.J.C. Polderman et al. Meta-analysis of the heritability of human traits based on fifty years of twin studies. Nature Genetics. Published online May 18, 2015. doi:10.1038/ng.3285. © Society for Science & the Public 2000 - 2015.
By Sarah C. P. Williams Here’s an easy way to tell if a female warbler is a year-round resident of the tropics or just a visiting snowbird: Females from species that spend their lives near the equator tend to have brighter plumage more typical of male birds. In contrast, females who fly north for the summer appear drab compared with their male counterparts. In the past, researchers thought the difference was due to the shorter breeding season in the north, hypothesizing that migrating males evolved bright colors to better compete for mates. But a new study hints that northern-breeding females may have evolved to be less colorful than males in order to be less conspicuous to predators during their long migrations. Researchers at Trinity University in San Antonio, Texas, studied the coloring, migration patterns, breeding locales, and ancestry of 109 warbler species. Migration distance, not the length of the breeding season, was the best predictor of color contrasts between male and female birds, they report online today in the Proceedings of the Royal Society B. Female bay-breasted warblers (Setophaga castanea), for instance, which migrate about 7000 kilometers between their breeding grounds in North America and their wintering grounds in the Caribbean, are a dull gray and white, whereas males boast more showy yellows and browns. But both male and female slate-throated redstarts (Myioborus miniatus), like the one shown above, flaunt bright colors in their year-round tropical homes in Mexico and Central America. For migrating warblers, the researchers hypothesize that the breeding benefits of brighter male colors outweigh the threat of being spotted by a hungry predator. © 2015 American Association for the Advancement of Science.
Alison Abbott Redouan Bshary well remembers the moment he realized that fish were smarter than they are given credit for. It was 1998, and Bshary was a young behavioural ecologist with a dream project: snorkelling in Egypt's Red Sea to observe the behaviour of coral-reef fish. That day, he was watching a grumpy-looking grouper fish as it approached a giant moray eel. As two of the region's top predators, groupers and morays might be expected to compete for their food and even avoid each other — but Bshary saw them team up to hunt. First, the grouper signalled to the eel with its head, and then the two swam side by side, with the eel dipping into crevices, flushing out fish beyond the grouper's reach and getting a chance to feed alongside. Bshary was astonished by the unexpected cooperation; if he hadn't had a snorkel in his mouth, he would have gasped. This underwater observation was the first in a series of surprising discoveries that Bshary has gone on to make about the social behaviour of fish. Not only can they signal to each other and cooperate across species, but they can also cheat, deceive, console or punish one another — even show concern about their personal reputations. “I have always had a lot of respect for fish,” says Bshary. “But one after the other, these behaviours took me by surprise.” His investigations have led him to take a crash course in scuba diving, go beach camping in Egypt and build fake coral reefs in Australia. The work has also destroyed the stereotypical idea that fish are dumb creatures, capable of only the simplest behaviours — and it has presented a challenge to behavioural ecologists in a different field. Scientists who study primates have claimed that human-like behaviours such as cooperation are the sole privilege of animals such as monkeys and apes, and that they helped to drive the evolution of primates' large brains. Bshary — quiet, but afraid of neither adventure nor of contesting others' ideas — has given those scientists reason to think again. © 2015 Nature Publishing Grou
Steve Connor Having children can permanently affect the brain of women because the surge in female sex hormones during pregnancy can influence the development of key parts of the central nervous system, a series of studies has shown. The findings suggest that childbirth can affect the female brain, but they could also shed light on the controversy over whether hormone replacement therapy in menopausal women affects the risk of developing Alzheimer’s disease in later life, scientists said. The research looked at two of the oestrogen hormones used to treat the symptoms of menopausal women and found that they could have a complex effect depending on the age of the women and whether or not they had previously given birth. Although the work was mostly carried out on laboratory rats, the scientists said that the findings are more widely applicable to humans because the same hormones and brain cells are involved. The scientists found that the surge in oestrogen hormones during pregnancy, where levels can soar to several hundred times normal levels, can alter “neuroplasticity” or the re-growth of nerve cells in a part of the brain called the hippocampus, which is responsible for aspects of memory and spatial awareness. “Our most recent research show that previous motherhood alters cognition and neuroplasticity in response to hormone therapy, demonstrating that motherhood permanently alters the brain,” said Liisa Galea of the University of British Columbia in Vancouver, Canada.