Chapter 13. Memory, Learning, and Development
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
Hannah Devlin, science correspondent Scientists have raised the alert about an antibiotic routinely prescribed for chest infections, after linking it to an increased risk of epilepsy and cerebral palsy in children whose mothers took the drug during pregnancy. Children of mothers who had taken macrolide antibiotics were found to be almost twice as likely to be affected by the conditions, prompting scientists to call for a review of their use during pregnancy. The study authors urged pregnant women not to stop taking prescribed antibiotics, however. The potential adverse effects are rare and, as yet, unproven, while infections during pregnancy are a well-established cause of health problems in babies. Professor Ruth Gilbert, a clinical epidemiologist who led the research at University College London, said: “The main message is for medicines regulators and whether they need to issue a warning about these drugs. For women, if you’ve got a bacterial infection, it’s more important to get on and treat it.” The study tracked the children of nearly 65,000 women who had been prescribed a variety of antibiotics for illnesses during pregnancy, including chest and throat infections and cystitis. There was no evidence that most antibiotics (including penicillin, which made up 67% of prescriptions), led to an increased risk of the baby developing cerebral palsy or epilepsy. However, when the antibiotics were compared head-to-head, the potential adverse effect of macrolide drugs emerged. Around 10 in 1,000 children whose mothers were given the drug had developed the conditions by the age of seven, compared to 6 in 1,000 children, for those who had other types of antibiotic. © 2015 Guardian News and Media Limited
Jon Hamilton Doctors are much more likely to level with patients who have cancer than patients who have Alzheimer's, according to a report released this week by the Alzheimer's Association. The report found that just 45 percent of Medicare patients who'd been diagnosed with Alzheimer's said they were informed of the diagnosis by their doctor. By contrast, more than 90 percent of Medicare patients with cancer said they were told by their doctor. "What we found is really shocking," says Beth Kallmyer, vice president of constituent services for the Alzheimer's Association. "This is reminiscent of what happened in the 1960s and 1970s with cancer," she says. "But that's changed now, and it really needs to change for Alzheimer's as well." For years, the association's help line has been receiving complaints from family members who say that doctors are reluctant to reveal an Alzheimer's diagnosis, Kallmyer says. So the association decided to investigate by studying medical records and survey results from Medicare recipients. To make sure that Alzheimer's patients hadn't simply forgotten what a doctor said, the group also looked at Medicare survey responses from family members and other caregivers. The result wasn't much better: Just 53 percent said a doctor told them of the patient's diagnosis. © 2015 NPR
Link ID: 20721 - Posted: 03.25.2015
By Siri Carpenter “I don’t look like I have a disability, do I?” Jonas Moore asks me. I shake my head. No, I say — he does not. Bundled up in a puffy green coat, Moore, 35 and sandy-haired, doesn’t stand out in the crowd seeking refuge from the winter cold in a drafty Starbucks. His handshake is firm and his blue eyes meet mine as we talk. He comes across as intelligent and thoughtful, if perhaps a bit reserved. His disability — a form of autism — is invisible. That’s part of the problem, Moore says. Like most people with an autism spectrum disorder, he finds relationships challenging. In the past, he has been quick to anger and has had what he calls meltdowns. Those who don’t know he has autism can easily misinterpret his actions. “People think that when I do misbehave I’m somehow intentionally trying to be a jerk,” Moore says. “That’s just not the case.” His difficulty managing emotions has gotten him into some trouble, and he has had a hard time holding onto jobs — an outcome he might have avoided, he says, if his co-workers and bosses had better understood his intentions. Over time, things have gotten better. Moore has held the same job for five years, vacuuming commercial buildings on a night cleaning crew. He attributes his success to getting the right amount of medication and therapy, to time’s maturing him and to the fact that he works mostly alone. Moore is fortunate. His parents help support him financially. He has access to good mental health care where he lives in Wisconsin. And he has found a job that suits him. Many adults with autism are not so lucky.
Link ID: 20711 - Posted: 03.24.2015
By ANDREW POLLACK An experimental drug for Alzheimer’s disease sharply slowed the decline in mental function in a small clinical trial, researchers reported Friday, reviving hopes for an approach to therapy that until now has experienced repeated failures. The drug, being developed by Biogen Idec, could achieve sales of billions of dollars a year if the results from the small trial are replicated in larger trials that Biogen said it hoped to begin this year. Experts say that there are no really good drugs now to treat Alzheimer’s. Biogen’s stock has risen about 50 percent since early December, when the company first announced that the drug had slowed cognitive decline in the trial, without saying by how much. Analysts and investors had been eagerly awaiting the detailed results, some of them flying to France to hear Biogen researchers present them at a neurology meeting on Friday. The drug, called aducanumab, met and in some cases greatly exceeded Wall Street expectations in terms of how much the highest dose slowed cognitive decline. However, there was a high incidence of a particular side effect that might make it difficult to use the highest dose. Still, the net impression was positive. “Out-of-the-ballpark efficacy, acceptable safety,” Ravi Mehrotra, an analyst at Credit Suisse, wrote on Friday. Shares of Biogen rose $42.33, or 10 percent, to $475.98. Alzheimer’s specialists were impressed, but they cautioned that it was difficult to read much from a small early-stage, or Phase 1, trial that was designed to look at safety, not the effect on cognition. Also, other Alzheimer’s drugs that had looked promising in early studies ended up not working in larger trials. “It’s certainly encouraging,” said Dr. Samuel Gandy, director of the Center for Cognitive Health at Mount Sinai Hospital in New York, who was not involved in the study. He said the effect of the highest dose was “pretty impressive.” © 2015 The New York Times Company
Link ID: 20709 - Posted: 03.21.2015
by Michael Slezak What were we talking about? Oh yes, brain-training programmes may be useful for helping inattentive people focus on tasks in their daily life. At least, that's the implication of an analysis looking at one particular programme. It's the latest salvo in a field that has seen the battles lines drawn between those who believe there is no compelling scientific evidence that training the brain to do a specific task better can offer wider cognitive improvements, and those that think it can work in some cases. The party line is that brain training improves only that which it exercises, says Jared Horvath from the University of Melbourne in Australia. "What this means is, if the training programme uses a working memory game, you get better at working memory games and little else." But an analysis by Megan Spencer-Smith of Monash University in Melbourne, Australia, and Torkel Klingberg at the Karolinska Institute in Stockholm, Sweden, claims to show that there are benefits for daily life – at least for people with attention deficit hyperactivity disorder or other problems related to attentiveness. They focused on a programme called Cogmed, which Klingberg has helped develop, and combined the results of several smaller studies. Cogmed is designed to improve how much verbal or visual information you can temporarily remember and work with. © Copyright Reed Business Information Ltd.
Elie Dolgin The southern city of Guangzhou has long held the largest eye hospital in China. But about five years ago, it became clear that the Zhongshan Ophthalmic Center needed to expand. More and more children were arriving with the blurry distance vision caused by myopia, and with so many needing eye tests and glasses, the hospital was bursting at the seams. So the centre began adding new testing rooms — and to make space, it relocated some of its doctors and researchers to a local shopping mall. Now during the summer and winter school holidays, when most diagnoses are made, “thousands and thousands of children” pour in every day, says ophthalmologist Nathan Congdon, who was one of those uprooted. “You literally can't walk through the halls because of all the children.” East Asia has been gripped by an unprecedented rise in myopia, also known as short-sightedness. Sixty years ago, 10–20% of the Chinese population was short-sighted. Today, up to 90% of teenagers and young adults are. In Seoul, a whopping 96.5% of 19-year-old men are short-sighted. Other parts of the world have also seen a dramatic increase in the condition, which now affects around half of young adults in the United States and Europe — double the prevalence of half a century ago. By some estimates, one-third of the world's population — 2.5 billion people — could be affected by short-sightedness by the end of this decade. “We are going down the path of having a myopia epidemic,” says Padmaja Sankaridurg, head of the myopia programme at the Brien Holden Vision Institute in Sydney, Australia. The condition is more than an inconvenience. Glasses, contact lenses and surgery can help to correct it, but they do not address the underlying defect: a slightly elongated eyeball, which means that the lens focuses light from far objects slightly in front of the retina, rather than directly on it. © 2015 Nature Publishing Group
Michaeleen Doucleff Malaria is one of the oldest scourges of mankind. Yet it's been a mystery how the deadliest form of the disease kills children. One doctor in Michigan has dedicated her life to figuring that out. Now she and her team report their findings in this week's issue of the New England Journal of Medicine. The key to solving the mystery was looking inside the brain. Most of the time malaria causes a bad fever and body aches. But in rare cases — often in children — the parasite gets stuck in the capillaries of the brain. The child has a seizure, goes into a coma and can die. This all happens in only two or three days, says Dr. Terrie Taylor of Michigan State University. "These are bright, happy children who are suddenly felled by a disease that quickly renders them unconscious. And quickly kills them. It's a catastrophe." The sudden death of a child devastates not just the family but the whole community, Taylor says: "Imagine the ripple effects on their friends and their siblings. Suddenly their friends are gone. Just gone." Since 1986, Taylor has been treating children with severe malaria at Queen Elizabeth Central Hospital in Blantyre, Malawi. Seeing so many families deal with these huge losses, year after year, made Taylor focus her career on one goal: Figuring out why some children die from cerebral malaria but others soon recover. © 2015 NPR
Keyword: Development of the Brain
Link ID: 20702 - Posted: 03.19.2015
A long-term study has pointed to a link between breastfeeding and intelligence. The research in Brazil traced nearly 3,500 babies, from all walks of life, and found those who had been breastfed for longer went on to score higher on IQ tests as adults. Experts say the results, while not conclusive, appear to back current advice that babies should be exclusively breastfed for six months. But they say mothers should still have a choice about whether or not to do it. Regarding the findings - published in The Lancet Global Health - they stress there are many different factors other than breastfeeding that could have an impact on intelligence, although the researchers did try to rule out the main confounders, such as mother's education, family income and birth weight. Dr Bernardo Lessa Horta, from the Federal University of Pelotas in Brazil, said his study offers a unique insight because in the population he studied, breastfeeding was evenly distributed across social class - not something just practised by the rich and educated. Most of the babies, irrespective of social class, were breastfed - some for less than a month and others for more than a year. Those who were breastfed for longer scored higher on measures of intelligence as adults. They were also more likely to earn a higher wage and to have completed more schooling. Dr Horta believes breast milk may offer an advantage because it is a good source of long-chain saturated fatty acids which are essential for brain development. But experts say the study findings cannot confirm this and that much more research is needed to explore any possible link between breastfeeding and intelligence. © 2015 BBC.
By PAM BELLUCK What happens to forgotten memories — old computer passwords, friends’ previous phone numbers? Scientists have long held two different theories. One is that memories do not diminish but simply get overshadowed by new memories. The other is that older memories become weaker, that pulling to mind new passwords or phone numbers degrades old recollections so they do not interfere. The difference could be significant. If old memories stay strong and are merely papered over by new ones, they may be easier to recover. That could be positive for someone trying to remember an acquaintance’s name, but difficult for someone trying to lessen memories of abuse. It could suggest different strategies for easing traumatic memories, evaluating witness testimony about crimes, or helping students study for tests. Now, a study claims to provide evidence of memory’s weakening by showing that people’s ability to remember something and the pattern of brain activity that thing generates both appear to diminish when a competing memory gets stronger. Demonstrating sophisticated use of brain scans in memory research, authors of the study, published Monday in the journal Nature Neuroscience, appear to have identified neural fingerprints of specific memories, distinguishing brain activity patterns produced when viewing a picture of a necklace, say, from a picture of binoculars or other objects. The experiment, conducted by scientists in Birmingham and Cambridge, England, involved several stages with 24 participants first trained to associate words to two unrelated black and white pictures from lists of famous people, ordinary objects or scenes. © 2015 The New York Times Company
Keyword: Learning & Memory
Link ID: 20695 - Posted: 03.17.2015
By BENEDICT CAREY Behind all those canned compliments for older adults — spry! wily! wise! — is an appreciation for something that scientists have had a hard time characterizing: mental faculties that improve with age. Knowledge is a large part of the equation, of course. People who are middle-aged and older tend to know more than young adults, by virtue of having been around longer, and score higher on vocabulary tests, crossword puzzles and other measures of so-called crystallized intelligence. Still, young adults who consult their elders (mostly when desperate) don’t do so just to gather facts, solve crosswords or borrow a credit card. Nor, generally, are they looking for help with short-term memory or puzzle solving. Those abilities, called fluid intelligence, peak in the 20s. No, the older brain offers something more, according to a new paper in the journal Psychological Science. Elements of social judgment and short-term memory, important pieces of the cognitive puzzle, may peak later in life than previously thought. The postdoctoral fellows Joshua Hartshorne of M.I.T. and Laura Germine of Harvard and Massachusetts General Hospital analyzed a huge trove of scores on cognitive tests taken by people of all ages. The researchers found that the broad split in age-related cognition — fluid in the young, crystallized in the old — masked several important nuances. “This dichotomy between early peaks and later peaks is way too coarse,” Dr. Hartshorne said. “There are a lot more patterns going on, and we need to take those into account to fully understand the effects of age on cognition.” The new paper is hardly the first challenge to the scientific literature on age-related decline, and it won’t be the last. A year ago, German scientists argued that cognitive “deficits” in aging were caused largely by the accumulation of knowledge — that is, the brain slows down because it has to search a larger mental library of facts. That idea has stirred some debate among scientists. Experts said the new analysis raised a different question: Are there distinct, independent elements of memory and cognition that peak at varying times of life? © 2015 The New York Times Company
By John Horgan In 1990 The New York Times published a front-page article by Lawrence Altman, a reporter with a medical degree, announcing that scientists had discovered “a link between alcoholism and a specific gene.” The evidence for the "feel-good gene," which supposedly reduces anxiety, is flimsy, just like the evidence linking specific genes to high intelligence, violent aggression, homosexuality, bipolar disorder and countless other complex human traits and ailments. That was merely one in a string of reports in which the Times and other major media hyped what turned out to be erroneous claims linking complex traits and disorders—from homosexuality and high intelligence to schizophrenia and bipolar disorder—to specific genes. I thought those days were over, and that scientists and the media have learned to doubt extremely reductionist genetic accounts of complex traits and behaviors. I was wrong. Last Sunday, the “Opinion” section of the Times published an essay, “The Feel-Good Gene,” which states: “For the first time, scientists have demonstrated that a genetic variation in the brain makes some people inherently less anxious, and more able to forget fearful and unpleasant experiences. This lucky genetic mutation produces higher levels of anandamide–the so-called bliss molecule and our natural marijuana–in our brains. In short, some people are prone to be less anxious simply because they won the genetic sweepstakes and randomly got a genetic mutation that has nothing at all to do with strength of character.” This article, like the one touting the alcoholism gene 25 years ago, was written by a physician, Richard Friedman, professor of psychiatry at Weill Cornell Medical College. I emphasize this fact because scientific hype is often blamed on supposedly ignorant journalists like me rather than on physicians and other so-called experts. © 2015 Scientific American
By Maggie Fox Teenagers who use marijuana heavily grow up to have poor memories and also have brain abnormalities, a new study shows. The study cannot say which came first — the brain structure differences or the pot use. But it suggests there could be long-term effects of heavy marijuana use. A team at Northwestern University looked at 97 volunteers with and without mental illness. The dope smokers said they'd used marijuana daily starting at age 16 or 17, and said they had not used other drugs. The daily marijuana users had an abnormally shaped hippocampus and performed about 18 percent more poorly on long-term memory tasks, the researchers reported in the journal Hippocampus. The hippocampus is a part of the brain used in storing long-term memory. "The memory processes that appear to be affected by cannabis are ones that we use every day to solve common problems and to sustain our relationships with friends and family," said Dr. John Csernansky, who worked on the study. Previous research by the same Northwestern team showed heavy pot smokers had poor short-term and working memory and abnormally shaped brain structures including the striatum, globus pallidus and thalamus. "It is possible that the abnormal brain structures reveal a pre-existing vulnerability to marijuana abuse," Matthew Smith, who led the study, said in a statement.
By Emily Underwood From imaging babies to blasting apart kidney stones, ultrasound has proved to be a versatile tool for physicians. Now, several research teams aim to unleash the technology on some of the most feared brain diseases. The blood-brain barrier, a tightly packed layer of cells that lines the brain's blood vessels, protects it from infections, toxins, and other threats but makes the organ frustratingly hard to treat. A strategy that combines ultrasound with microscopic blood-borne bubbles can briefly open the barrier, in theory giving drugs or the immune system access to the brain. In the clinic and the lab, that promise is being evaluated. This month, in one of the first clinical tests, Todd Mainprize, a neurosurgeon at the University of Toronto in Canada, hopes to use ultrasound to deliver a dose of chemotherapy to a malignant brain tumor. And in some of the most dramatic evidence of the technique's potential, a research team reports this week in Science Translational Medicine that they used it to rid mice of abnormal brain clumps similar to those in Alzheimer's disease, restoring lost memory and cognitive functions. If such findings can be translated from mice to humans, “it will revolutionize the way we treat brain disease,” says biophysicist Kullervo Hynynen of the Sunnybrook Research Institute in Toronto, who originated the ultrasound method. Some scientists stress that rodent findings can be hard to translate to humans and caution that there are safety concerns about zapping the brain with even the low-intensity ultrasound used in the new study, which is similar to that used in diagnostic scans. © 2015 American Association for the Advancement of Science.
Link ID: 20685 - Posted: 03.12.2015
|By Daisy Yuhas The brain is a hotbed of electrical activity. Scientists have long known that brain cells communicate via electrical missives, created by charged atoms and molecules called ions as they travel across the membranes of those cells. But a new study suggests that in the days and weeks that lead up to a brain forming in an embryo or fetus, altering the electrical properties of these cells can dramatically change how the ensuing brain develops. Researchers at Tufts University and the University of Minnesota have investigated how the difference in charge on either side of a resting cell’s membrane—its electrical potential—helps build the brain. In previous work Tufts University developmental biologist Michael Levin found that patterns of electrical potentials in the earliest stages of an embryo’s development can direct how an animal’s body grows, and that manipulating those potentials can cause a creature to sprout extra limbs, tails or functioning eyes. Now, Levin’s group has investigated how these potentials shape the brain. Working with frog embryos the researchers first used dyes to see the patterns of electrical potentials that precede brain development. They noticed that before the development of a normal brain the cells lining the neural tube, a structure that eventually becomes the brain and spinal cord, have extreme differences in ionic charge within and outside the membrane that houses the cells. In other words, these cells are extremely polarized. © 2015 Scientific American
Keyword: Development of the Brain
Link ID: 20684 - Posted: 03.12.2015
Older people could improve or maintain their mental function through heart healthy lifestyle changes, a large randomized trial for dementia prevention shows. Researchers in Finland and Sweden designed a trial to tackle risk factors for Alzheimer's disease. The 1,260 Finns aged 60 to 77 participating in the study were all considered at risk of dementia based on standard test scores. Half were randomly assigned to receive advice from health professionals on maintaining a healthy diet, aerobic and muscle training exercises, brain training exercises and regular checks of blood pressure, height and weight for body mass index and physical exams for two years or regular health advice. Participants in the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability or FINGER study had their cognitive function measured in a battery of mental tests. "The main hypothesis was that simultaneous changes in several risk factors (even of smaller magnitude) would lead to a protective effect on cognition," Miia Kivipelto from the Karolinska Institute in Stockholm and her co-authors said in Wednesday's issue of The Lancet. Overall, test scores were 25 per cent in the diet and training group than the control group. There was no effect on memory. ©2015 CBC/Radio-Canada.
Link ID: 20683 - Posted: 03.12.2015
Mutations in the presenilin-1 gene are the most common cause of inherited, early-onset forms of Alzheimer’s disease. In a new study, published in Neuron, scientists replaced the normal mouse presenilin-1 gene with Alzheimer’s-causing forms of the human gene to discover how these genetic changes may lead to the disorder. Their surprising results may transform the way scientists design drugs that target these mutations to treat inherited or familial Alzheimer’s, a rare form of the disease that affects approximately 1 percent of people with the disorder. The study was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For decades, it has been unclear exactly how the presenilin mutations cause Alzheimer’s disease. Presenilin is a component of an important enzyme, gamma secretase, which cuts up amyloid precursor protein into two protein fragments, Abeta40 and Abeta42. Abeta42 is found in plaques, the abnormal accumulations of protein in the brain which are a hallmark of Alzheimer’s. Numerous studies suggested that presenilin-1 mutations increased activity of gamma-secretase. Investigators have developed drugs that block gamma-secretase, but they have so far failed in clinical trials to halt the disease. The study led by Raymond Kelleher, M.D., Ph.D. and Jie Shen, Ph.D., professors of neurology at Harvard Medical School, Boston, provides a plot twist in the association of presenilin-1 mutations and inherited Alzheimer’s disease. Using mice with altered forms of the presenilin gene, Drs. Kelleher and Shen discovered that the mutations may cause the disease by decreasing, rather than increasing, the activity of gamma-secretase.
|By Esther Landhuis As we age, we seem to get worse at ignoring irrelevant stimuli. It's what makes restaurant conversations challenging—having to converse while also shutting out surrounding chatter. New research bears out the aging brain's distractibility but also suggests that training may help us tune out interference. Scientists at Brown University recruited seniors and twentysomethings for a visual experiment. Presented with a sequence of letters and numbers, participants were asked to report back only the numbers—all the while disregarding a series of meaningless dots. Sometimes the dots moved randomly, but other times they traveled in a clear direction, making them harder to ignore. Older participants ended up accidentally learning the dots' patterns, based on the accuracy of their answers when asked which way the dots were moving, whereas young adults seemed able to suppress that information and focus on the numbers, the researchers reported last November in Current Biology. In a separate study published in Neuron, scientists at the University of California, San Francisco, showed they could train aging brains to become less distractible. Their regimen helped aging rats as well as older people. The researchers played three different sounds and rewarded trainees for identifying a target tone while ignoring distracter frequencies. As the subjects improved, the task grew more challenging—the distracting tone became harder to discriminate from the target. © 2015 Scientific American,
By Douglas Starr In 1906, Hugo Münsterberg, the chair of the psychology laboratory at Harvard University and the president of the American Psychological Association, wrote in the Times Magazine about a case of false confession. A woman had been found dead in Chicago, garroted with a copper wire and left in a barnyard, and the simpleminded farmer’s son who had discovered her body stood accused. The young man had an alibi, but after questioning by police he admitted to the murder. He did not simply confess, Münsterberg wrote; “he was quite willing to repeat his confession again and again. Each time it became richer in detail.” The young man’s account, he continued, was “absurd and contradictory,” a clear instance of “the involuntary elaboration of a suggestion” from his interrogators. Münsterberg cited the Salem witch trials, in which similarly vulnerable people were coerced into self-incrimination. He shared his opinion in a letter to a Chicago nerve specialist, which made the local press. A week later, the farmer’s son was hanged. Münsterberg was ahead of his time. It would be decades before the legal and psychological communities began to understand how powerfully suggestion can shape memory and, in turn, the course of justice. In the early nineteen-nineties, American society was recuperating from another panic over occult influence; Satanists had replaced witches. One case, the McMartin Preschool trial, hinged on nine young victims’ memories of molestation and ritual abuse—memories that they had supposedly forgotten and then, after being interviewed, recovered. The case fell apart, in 1990, because the prosecution could produce no persuasive evidence of the victims’ claims. A cognitive psychologist named Elizabeth Loftus, who had consulted on the case, wondered whether the children’s memories might have been fabricated—in Münsterberg’s formulation, involuntarily elaborated—rather than actually recovered.
Keyword: Learning & Memory
Link ID: 20679 - Posted: 03.12.2015
Mo Costandi Neuroscientists in France have implanted false memories into the brains of sleeping mice. Using electrodes to directly stimulate and record the activity of nerve cells, they created artificial associative memories that persisted while the animals snoozed and then influenced their behaviour when they awoke. Manipulating memories by tinkering with brain cells is becoming routine in neuroscience labs. Last year, one team of researchers used a technique called optogenetics to label the cells encoding fearful memories in the mouse brain and to switch the memories on and off, and another used it to identify the cells encoding positive and negative emotional memories, so that they could convert positive memories into negative ones, and vice versa. The new work, published today in the journal Nature Neuroscience, shows for the first time that artificial memories can be implanted into the brains of sleeping animals. It also provides more details about how populations of nerve cells encode spatial memories, and about the important role that sleep plays in making such memories stronger. Karim Benchenane of the French National Centre for Scientific Research (CNRS) in Paris and his colleagues implanted electrodes into the brains of 40 mice, targeting the medial forebrain bundle (MFB), a component of the reward circuitry, and the CA1 region of the hippocampus, which contains at least three different cell types that encode the memories needed for spatial navigation. © 2015 Guardian News and Media Limited
By Rachel Rabkin Peachman Many women with a history of depression who take antidepressants assume that once they get pregnant, they should try to wean themselves off their meds to avoid negative side effects for the baby. A new large study published in the journal Pediatrics challenges one reason behind that assumption. The research found that taking selective serotonin reuptake inhibitors (the antidepressants also known as S.S.R.I.s) while pregnant does not increase the risk of asthma in the resulting babies. What is associated with an increased risk of asthma? According to this study and other research, untreated prenatal depression. “The mechanisms underlying the association of prenatal depression and asthma are unknown,” said Dr. Xiaoqin Liu, the lead author of the Pediatrics study and an epidemiologist at Aarhus University in Denmark. An association between prenatal depression and asthma does not mean that prenatal depression causes asthma. There could be other reasons for the correlation, genetic or environmental, or both. For example, people who live in dense, polluted urban areas could be at an increased risk of both asthma and depression. The researchers used Denmark’s national registries to evaluate all singleton babies born from 1996 to 2007, and identify the mothers who had a diagnosis of depression or had used antidepressants, or both, during pregnancy or one year beforehand. Using a statistical model, the study authors found that prenatal depression — with or without the use of antidepressants — was associated with a 25 percent increased risk of asthma in children as compared with children whose mothers did not have a record of depression. © 2015 The New York Times Company