Chapter 7. Life-Span Development of the Brain and Behavior
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By Pippa Stephens Health reporter, BBC News An anti-depressant drug could be used to slow the onset of Alzheimer's disease, say scientists in the US. Research into 23 people, and transgenic mice, found citalopram hampered a protein which helps to build destructive plaques in the brains of Alzheimer's patients. Scientists said they hoped the study could help prevent the disease. Experts said the study was "interesting" and that using an approved drug could be beneficial. Alzheimer's disease is the most common cause of dementia, affecting around 496,000 people in the UK. It affects the brain through protein plaques and tangles which lead to the death of brain cells, and a shortage of chemicals important for transmitting messages. Symptoms include loss of memory, mood changes, and problems with communication and reasoning. Researchers at the University of Pennsylvania and Washington University School of Medicine carried out the study between 2012 and 2014. They bred mice with Alzheimer's disease and looked at the levels of the peptide - or protein component - amyloid beta (AB), in the brain. AB clusters in plaques which, alongside the tau protein, are thought to trigger Alzheimer's. After giving the mice citalopram, the level of AB fell by 25%, compared to the control group, with no anti-depressant. And after two months of anti-depressants, the growth of new plaques was reduced, and existing plaques did not grow any further, the study said. But it noted the drug could not cause existing plaques to shrink, or decrease in number. BBC © 2014
Bullying casts a long shadow. Children who are bullied are more prone to depression and suicidal tendencies even when they grow up; they're also more likely to get sick and have headaches and stomach troubles, researchers have discovered. A new study may have found the underlying cause: A specific indicator of illness, called C-reactive protein (CRP), is higher than normal in bullying victims, even when they get older. In contrast, the bullies, by the same gauge, seem to be healthier. The researchers focused on CRP because it's a common, easily tested marker of inflammation, the runaway immune system activity that's a feature of many chronic illnesses including cardiovascular disease, diabetes, chronic pain, and depression, explains lead author William Copeland, a psychologist and epidemiologist at Duke University Medical Center in Durham, North Carolina. To link inflammation to bullying, the researchers asked 1420 youngsters between the ages of 9 and 16 whether, and how often, they had been bullied or had bullied others. Interviewers asked participants whether they felt more teased, bullied, or treated meanly by siblings, friends, and peers than other children—and whether they had upset or hurt other people on purpose, tried to get others in trouble, or forced people to do something by threatening or hurting them. The researchers took finger stick blood tests at each assessment. Interviews took place once a year until the participants turned 16, and again when they were 19 and 21. The children interviewed were participants in the larger Great Smoky Mountains Study, in which some 12,000 children in North Carolina were assessed to track the development of psychiatric conditions. In the short term, the effect of bullying on the victims was immediate. CRP levels increased along with the number of reported bullying instances, and more than doubled in those who said they'd been bullied three times or more in the previous year, compared with kids who had never been bullied. No change was seen in bullies, or in kids who hadn't been involved with bullying one way or the other, the researchers report online today in the Proceedings of the National Academy of Sciences. © 2014 American Association for the Advancement of Science.
by Anil Ananthaswamy Children born with split brains – whereby the two hemispheres of their brains are not connected – can develop new brain wiring that helps to connect the two halves, according to brain scans of people with the condition. Such circuitry is not present in normal brains, and explains how some people with split brains can still maintain normal function. It also suggests that the developing brain is even more adaptable than previously thought. Research into people with split brains goes back to the 1960s, when neuroscientists studied people who had undergone brain surgery to treat particularly severe epilepsy. The surgery involved cutting the corpus callosum, the thick bundle of neuronal fibres that connects the brain's two halves. This disconnection prevented epileptic seizures spreading from one brain hemisphere to the other. The recipients of such split-brain surgery showed a form of disconnection syndrome whereby the two halves of their brains could not exchange information. For instance, if a patient touched an object with their left hand without seeing the object, they would be unable to name it. That is because sensory-motor signals from the left hand are processed in the right hemisphere. To put a name to the object, the tactile information from the hand has to reach the brain's left hemisphere, the seat of language. With the central connection between hemispheres severed, the object's naming information cannot be retrieved. Conversely, if that person were to touch an object with their right hand without seeing it, the sensory-motor signals from that hand would go to the left hemisphere, which hosts the brain's language centres, making naming the object easy. However, children born without a corpus callosum – and therefore whose two brain hemispheres are separated – can often pass such tactile naming tests when they are old enough to take them. Their brain hemispheres are obviously communicating, but it wasn't clear how. © Copyright Reed Business Information Ltd
By Suzanne Allard Levingston, Playing with bubble wrap is a silly activity that delights most preschoolers. But for one 21 / 2-year-old from Silver Spring, loud noises such as the pop of plastic bubbles were so upsetting that he would cover his ears and run away. Some days the sound of a vacuum cleaner would make him scream. The child so persistently avoided activities with too much noise and motion that his preschool’s administrators asked to meet with his family — and soon an assessment led to a diagnosis of sensory processing disorder, or SPD. SPD is a clinical label for people who have abnormal behavioral responses to sensory input such as sound and touch. Some children with SPD seem oversensitive to ordinary stimuli such as a shirt label’s scratching their skin. Others can be underresponsive — seemingly unaffected by the prick of a needle. A third group have motor problems that make holding a pencil or riding a bike seem impossible. Whatever the difficulty, such kids are often described as “out-of-sync,” a term popularized by Carol Stock Kranowitz’s 1998 book “The Out-of-Sync Child,” which has sold nearly 700,000 copies. As many as 16 percent of school-age kids in the United States may face sensory processing challenges. And yet there’s debate over whether these challenges constitute a discrete medical disorder. Some experts contend that SPD may be merely a symptom of some other ailment — autism, attention-deficit hyperactivity disorder, anxiety disorder or fragile X syndrome, for example — while others insist it is a separate condition that should be labeled a disorder when it interferes with daily life. The debate over how to classify SPD is not merely matter of semantics. Such discussions can affect research funding and can guide whether insurers will reimburse therapy costs. © 1996-2014 The Washington Post
Erin Allday A gene variant that scientists already knew to be associated with longer life also seems to make people smarter, and may help offset the effects of normal cognitive decline in old age, according to a team of San Francisco researchers. The findings, published Thursday in the journal Cell Reports, are encouraging news for the roughly 1 in 5 people who have the genetic trait, which is a variant of the klotho gene. Beyond that, scientists hope the findings will help them develop tools for retaining, or even boosting, intelligence in people who have suffered cognitive losses, either from disease or through the normal course of aging. 'Cognitive enhancer' "What we've discovered is a cognitive enhancer," said Dr. Dena Dubal, an assistant professor of neurology at UCSF and lead author of the study, which was done with researchers from the Gladstone Institutes. "This may represent a new way to treat problems of cognition in the brain." The name of the gene comes from Greek mythology - Klotho is one of the three sisters of fate, and she spins the thread of life. The gene is responsible for secretions of the hormone klotho, which is thought to have effects on a variety of biological systems and has been shown to disrupt some processes associated with aging. © 2014 Hearst Communications, Inc.
By DAVID L. KIRP Whenever President Obama proposes a major federal investment in early education, as he did in his two most recent State of the Union addresses, critics have a two-word riposte: Head Start. Researchers have long cast doubt on that program’s effectiveness. The most damning evidence comes from a 2012 federal evaluation that used gold-standard methodology and concluded that children who participated in Head Start were not more successful in elementary school than others. That finding was catnip to the detractors. “Head Start’s impact is no better than random,” The Wall Street Journal editorialized. Why throw good money after bad? Though the faultfinders have a point, the claim that Head Start has failed overstates the case. For one thing, it has gotten considerably better in the past few years because of tougher quality standards. For another, researchers have identified a “sleeper effect” — many Head Start youngsters begin to flourish as teenagers, maybe because the program emphasizes character and social skills as well as the three R’s. Still, few would give Head Start high marks, and the bleak conclusion of the 2012 evaluation stands in sharp contrast to the impressive results from well-devised studies of state-financed prekindergartens. Head Start, a survivor of President Lyndon B. Johnson’s war on poverty, enrolls only poor kids. That’s a big part of the problem — as the adage goes, programs for the poor often become poor programs. Whether it’s health care (compare the trajectories of Medicare, for those 65 and older of all incomes, and Medicaid, only for the poor), education or housing, the sorry truth is that “we” don’t like subsidizing “them.” Head Start is no exception. It has been perpetually underfunded, never able to enroll more than half of eligible children or pay its teachers a decent wage. If Head Start is going to realize its potential, it has to break out of the antipoverty mold. One promising but unfortunately rarely used strategy is to encourage all youngsters, not just poor kids, to enroll, with poor families paying nothing and middle-class families contributing on a sliding scale. Another is to merge Head Start with high-quality state prekindergarten. © 2014 The New York Times Company
Helen Shen For anyone fighting to save old memories, a fresh crop of brain cells may be the last thing they need. Research published today in Science suggests that newly formed neurons in the hippocampus — an area of the brain involved in memory formation — could dislodge previously learned information1. The work may provide clues as to why childhood memories are so difficult to recall. “The finding was very surprising to us initially. Most people think new neurons mean better memory,” says Sheena Josselyn, a neuroscientist who led the study together with her husband Paul Frankland at the Hospital for Sick Children in Toronto, Canada. Humans, mice and several other mammals grow new neurons in the hippocampus throughout their lives — rapidly at first, but more and more slowly with age. Researchers have previously shown that boosting neural proliferation before learning can enhance memory formation in adult mice2, 3. But the latest study shows that after information is learned, neuron growth can degrade those memories. Although seemingly counterintuitive, the disruptive role of these neurons makes some sense, says Josselyn. She notes that some theoretical models have predicted such an effect4. “More neurons increase the capacity to learn new memories in the future,” she says. “But memory is based on a circuit, so if you add to this circuit, it makes sense that it would disrupt it.” Newly added neurons could have a useful role in clearing old memories and making way for new ones, says Josselyn. Forgetting curve The researchers tested newborn and adult mice on a conditioning task, training the animals to fear an environment in which they received repeated electric shocks. All the mice learned the task quickly, but whereas infant mice remembered the negative experience for only one day after training, adult mice retained the negative memory for several weeks. © 2014 Nature Publishing Group
Scientists showed that people who have a variant of a longevity gene, called KLOTHO, have improved brain skills such as thinking, learning and memory regardless of their age, sex, or whether they have a genetic risk factor for Alzheimer’s disease. Increasing KLOTHO gene levels in mice made them smarter, possibly by increasing the strength of connections between nerve cells in the brain. The study was partly funded by the National Institutes of Health. “This could be a major step toward helping millions around the world who are suffering from Alzheimer’s disease and other dementias,” said Dena Dubal, M.D., Ph.D., an assistant professor of neurology, the David A. Coulter Endowed Chair in Aging and Neurodegeneration at the University of California San Francisco (UCSF) and the lead author of the study published in Cell Reports. “If we could boost the brain’s ability to function, we may be able to counter dementias.” As people live longer the effects of aging on the brain will become a greater health issue. This is especially true for dementias, a collection of brain disorders that can cause memory problems, impaired language skills and other symptoms. With the number of dementia cases worldwide estimated to double every 20 years from 35.6 million people in 2010 to 65.7 million in 2030 and 115.4 million in 2050, the need for treatments is growing. Klotho is the name of a Greek mythological goddess of fate, “who spins the thread of life.” People who have one copy of a variant, or form, of the KLOTHO gene, called KL-VS, tend to live longer and have lower chances of suffering a stroke whereas people who have two copies may live shorter lives and have a higher risk of stroke. In this study, the investigators found that people who had one copy of the KL-VS variant performed better on a battery of cognitive tests than subjects who did not have it, regardless of age, sex or the presence of the apolipoprotein 4 gene, the main genetic risk factor for Alzheimer’s disease.
By GRETCHEN REYNOLDS The more physically active you are at age 25, the better your thinking tends to be when you reach middle age, according to a large-scale new study. Encouragingly, the findings also suggest that if you negligently neglected to exercise when young, you can start now and still improve the health of your brain. Those of us past age 40 are generally familiar with those first glimmerings of forgetfulness and muddled thinking. We can’t easily recall people’s names, certain words, or where we left the car keys. “It’s what we scientists call having a C.R.S. problem,” said David R. Jacobs, a professor of public health at the University of Minnesota in Minneapolis and a co-author of the new study. “You can’t remember stuff.” But these slight, midlife declines in thinking skills strike some people later or less severely than others, and scientists have not known why. Genetics almost certainly play a role, most researchers agree. Yet the contribution of lifestyle, and in particular of exercise habits, has been unclear. So recently, Dr. Jacobs and colleagues from universities in the United States and overseas turned to a large trove of data collected over several decades for the Cardia study. The study, whose name is short for Coronary Artery Risk Development in Young Adults, began in the mid-1980s with the recruitment of thousands of men and women then ages 18 to 30 who underwent health testing to determine their cholesterol levels, blood pressure and other measures. Many of the volunteers also completed a treadmill run to exhaustion, during which they strode at an increasingly brisk pace until they could go no farther. The average time to exhaustion among these young adults was 10 minutes, meaning that most were moderately but not tremendously fit. © 2014 The New York Times Company
Erin Allday The game seems pretty simple. An alien-looking creature stands on a block of ice that's flowing down a river. The goal is to maneuver the ice around whales and other hurdles and periodically cause the alien to "jump" to grab green fish as they leap out of the water. The game is played on a tablet, and it looks a lot like any of hundreds of apps that can be downloaded for some mindless entertainment during an afternoon commute on BART. Here's what sets the game apart: It was designed by scientists at UCSF looking for a new way to treat serious symptoms of depression. "We're trying to see whether we can get the same effects with the game as with therapy," said Patricia Arean, a clinical psychologist at UCSF who is studying the potential mental health benefits of video game play in older adults. Arean is joining the burgeoning field of research into the use of video games as tools for promoting brain health. Video games undoubtedly have some kind of effect on our brains, but harnessing the technology and forcing a lasting - and positive - change is the challenge. So far, what little evidence does exist that video games can have a measurable impact on brain activity has been gathered almost entirely on healthy subjects. But in small clinical trials - like Arean's study of depression in older adults - the effects of games on both healthy and unhealthy people are being studied to find out whether they're useful in treating mental illness, such as autism, attention deficit and hyperactivity disorder, and post-traumatic stress disorder. Some neuroscientists say video games may also strengthen neural networks, potentially preventing or slowing down the brain deterioration associated with old age or diseases like Alzheimer's or Parkinson's. "We're in the infancy of this idea that entertaining and gaming stuff can be useful for you," said Joaquin Anguera, a UCSF neuroscientist who designs cognitive training games, including the one Arean is testing with patients. © 2014 Hearst Communications, Inc.
By Eric Niiler, Scientists studying head injuries have found something surprising: Genes may make some people more susceptible to concussion and trauma than others. A person’s genetic makeup, in fact, may play a more important role in the extent of injury than the number of blows a person sustains. While this research is still in its infancy, these scientists are working toward developing a blood test that may one day help a person decide — based on his her or her genetic predisposition — whether to try out for the football team, or perhaps take up swimming or chess instead. “Until now, all the attention has been paid to how hard and how often you get hit,” said Thomas McAllister, a professor of clinical psychiatry at the Indiana University School of Medicine. “No doubt that’s important. But it’s also becoming clear that’s it’s probably an interaction between the injury and the genetics of the person being injured.” This research is being spurred by fears that some athletes and many returning soldiers may face a lifetime of problems from head injuries. The National Football League agreed to settle a class-action concussion lawsuit by retired players last August for $765 million, although a judge rejected the agreement. In addition, the Pentagon estimates that 294,000 troops, many of whom served in Iraq and Afghanistan, suffered some kind of brain injury since 2000. “More and more we are noticing our servicemen are coming home with significant problems with brain function,” said Daniel Perl, a neuropathologist at the Center for Neuroscience and Regenerative Medicine at the Pentagon’s Uniformed Services University for Health Sciences in Bethesda. “We don’t know much about the biology of this. We need to get down to cellular level of resolution, how the brain starts to repair itself.” © 1996-2014 The Washington Post
Lida Katsimpardi Could the elixir of youth be as simple as a protein found in young blood? In recent years, researchers studying mice found that giving old animals blood from young ones can reverse some signs of aging, and last year one team identified a growth factor in the blood that they think is partly responsible for the anti-aging effect on a specific tissue--the heart. Now that group has shown this same factor can also rejuvenate muscle and the brain. "This is the first demonstration of a rejuvenation factor" that is naturally produced, declines with age, and reverses aging in multiple tissues, says Harvard stem cell researcher Amy Wagers, who led efforts to isolate and study the protein. Independently, another team has found that simply injecting plasma from young mice into old mice can boost learning. The results build on a wave of studies in the last decade in which investigators sewed together the skins of two mice, joining their circulation systems, and studied the effects on various tissues. “It’s still a bit creepy for many people. At meetings, people talk about vampires,” says Stanford University neuroscientist Tony Wyss-Coray, who led the study of learning. But he, Wagers, and others think unease will give way to excitement. The new work, he says, “opens the possibility that we can try to isolate additional factors” from blood, “and they have effects on the whole body.” Hope and hype are high in the anti-aging research arena, and other researchers caution that the work is preliminary. “These are exciting papers,” but “it’s a starting point,” says neuroscientist Sally Temple of the Neural Stem Cell Institute in Rensselaer, NY. Adds Matthew Kaeberlein, a biologist who studies aging at the University of Washington, Seattle, “The therapeutic implications are profound if this mechanism holds true in people.” But that “is the million dollar question here, and that may take some time to figure out.” © 2014 American Association for the Advancement of Science
Autism was formally described for the first time 71 years ago. The medical notes for "Case one", a 10-year-old from Mississippi, US, referred to as Donald T, describe a perplexing condition that was different from "anything reported so far". In 1943, when Donald Triplett was diagnosed, autism was considered extremely rare and treatment consisted of institutionalisation and – all too often – isolation. Today we know "autism disorder" as one of a number of autism spectrum disorders alongside Asperger's syndrome, pervasive developmental disorder and single gene disorders such as Rett syndrome. But of all neuropsychiatric conditions, autism remains one of the least understood. We now know that genetics almost certainly plays a key role, with researchers finding that if a family has one child with autism, then the likelihood of a future child having the condition is as high as 25%. But to what extent autism is defined by genes remains a mystery. "Everyone recognises that genes are part of the story but autism isn't 100% genetic," says Professor Simon Baron-Cohen of the Autism Research Centre at the University of Cambridge. "Even if you have identical twins who share all their genes, you can find that one has autism and one doesn't. That means that there must be some non-genetic factors." One of the most controversial theories about how autism develops is neuroinflammation. MRI scans of autistic patients have revealed abnormalities in the white matter – the wiring tissue responsible for connecting brains areas. Some scientists have drawn comparisons with multiple sclerosis, in which inflammatory processes attack the myelin sheath around the axons of brain cells, slowing down signalling and making it less efficient. © 2014 Guardian News and Media Limited
By Deborah Tuerkheimer Almost a decade into a 20-year prison sentence for murdering a baby in her care, 43-year-old Jennifer Del Prete was ordered freed on bond late last week. The ruling is one of a growing number that reflect skepticism on the part of judges, juries, and even prosecutors about criminal convictions based on the medical diagnosis of shaken baby syndrome. The case is also a critical turning point. The certainty that once surrounded shaken baby syndrome, or SBS, has been dissolving for years. The justice system is beginning to acknowledge this shift but should go further to re-examine and perhaps overturn more past convictions. Doctors once believed that three neurological symptoms—bleeding beneath the outer layer of membranes surrounding the brain (subdural hemorrhaging), bleeding in the retina, and brain swelling—always meant that a baby had been shaken. Because it was accepted that a baby with these three symptoms would show the effect of brain damage immediately, the “triad,” as it became known, was also used to establish the identity of the abuser—the last person with the baby. SBS was, in essence, a medical diagnosis of murder. Beginning in the 1990s, hundreds of cases were prosecuted based on this conception of SBS. The evidence of guilt was strikingly similar from case to case. This includes the Illinois prosecution of Jennifer Del Prete. In 2002, Del Prete was working at a small home day care in a Chicago suburb. One day, when she went to feed the 4-month-old baby in her care, she says she discovered the infant limp. Because the baby had the telltale triad of SBS symptoms, doctors were sure that Del Prete had shaken the baby to death. She denied it, and there were no witnesses. But based on the testimony of medical experts—primarily a pediatrician—she was convicted of murder in the first degree. © 2014 The Slate Group LLC.
By Helen Briggs BBC News A mother's diet around the time of conception can permanently influence her baby's DNA, research suggests. Animal experiments show diet in pregnancy can switch genes on or off, but this is the first human evidence. The research followed women in rural Gambia, where seasonal climate leads to big differences in diet between rainy and dry periods. It emphasises the need for a well-balanced diet before conception and in pregnancy, says a UK/US team. Scientists followed 84 pregnant women who conceived at the peak of the rainy season, and about the same number who conceived at the peak of the dry season. Nutrient levels were measured in blood samples taken from the women; while the DNA of their babies was analysed two to eight months after birth. Lead scientist Dr Branwen Hennig, from the London School of Hygiene & Tropical Medicine, said it was the first demonstration in humans that a mother's nutrition at the time of conception can change how her child's genes will be interpreted for life. She told BBC News: "Our results have shown that maternal nutrition pre-conception and in early pregnancy is important and may have implications for health outcomes of the next generation. "Women should have a well-balanced food diet prior to conception and during pregnancy." BBC © 2014
By Julie Steenhuysen CHICAGO (Reuters) - International teams of researchers using advanced gene sequencing technology have uncovered a single genetic mutation responsible for a rare brain disorder that may have stricken families in Turkey for some 400 years. The discovery of this genetic disorder, reported in two papers in the journal Cell, demonstrates the growing power of new tools to uncover the causes of diseases that previously stumped doctors. Besides bringing relief to affected families, who can now go through prenatal genetic testing in order to have children without the disorder, the discovery helps lend insight into more common neurodegenerative disorders, such as ALS, also known as Lou Gehrig's disease, the researchers said. The reports come from two independent teams of scientists, one led by researchers at Baylor College of Medicine and the Austrian Academy of Sciences, and the other by Yale University, the University of California, San Diego, and the Academic Medical Center in the Netherlands. Both focused on families in Eastern Turkey where marriage between close relatives, such as first cousins, is common. Geneticists call these consanguineous marriages. In this population, the researchers focused specifically on families whose children had unexplained neurological disorders that likely resulted from genetic defects. Both teams identified a new neurological disorder arising from a single genetic variant called CLP1. Children born with this disorder inherit two defective copies of this gene, which plays a critical role in the health of nerve cells. Babies with the disorder have small and malformed brains, they develop progressive muscle weakness, they do not speak and they are increasingly prone to seizures.
Epigenetics is one of the hottest fields in the life sciences. It’s a phenomenon with wide-ranging, powerful effects on many aspects of biology, and enormous potential in human medicine. As such, its ability to fill in some of the gaps in our scientific knowledge is mentioned everywhere from academic journals to the mainstream media to some of the less scientifically rigorous corners of the Internet. Epigenetics is essentially additional information layered on top of the sequence of letters (strings of molecules called A, C, G, and T) that makes up DNA. If you consider a DNA sequence as the text of an instruction manual that explains how to make a human body, epigenetics is as if someone's taken a pack of highlighters and used different colours to mark up different parts of the text in different ways. For example, someone might use a pink highlighter to mark parts of the text that need to be read the most carefully, and a blue highlighter to mark parts that aren't as important. There are different types of epigenetic marks, and each one tells the proteins in the cell to process those parts of the DNA in certain ways. For example, DNA can be tagged with tiny molecules called methyl groups that stick to some of its C letters. Other tags can be added to proteins called histones that are closely associated with DNA. There are proteins that specifically seek out and bind to these methylated areas, and shut it down so that the genes in that region are inactivated in that cell. So methylation is like a blue highlighter telling the cell "you don't need to know about this section right now." Methyl groups and other small molecular tags can attach to different locations on the histone proteins, each one having a different effect. Some tags in some locations loosen the attachment between the DNA and the histone, making the DNA more accessible to the proteins that are responsible for activating the genes in that region; this is like a pink highlighter telling the cell "hey, this part's important". © 2014 Guardian News and Media Limited
by Andy Coghlan HERE'S another reason to be fit and healthy. Staying free of "lifestyle diseases" and infections could put the brakes on Alzheimer's. The advice comes from teams that have pieced together how these bodily ailments create inflammation that ultimately spills over into the brain, sending its immune cells into a hyperactive, destructive state. "The idea is simple: monitoring and prompt treatment [of inflammation] could prevent the decline from Alzheimer's," said Hugh Perry of the University of Southampton, UK, as he presented the research at the Alzheimer's Research UK annual meeting in Oxford last month. As well as revealing step by step how disease and infection can aggravate and accelerate the early stages of Alzheimer's, Perry and his colleague Clive Holmes have begun a pioneering trial in 40 people to see if a drug that acts to dampen inflammation in the body can help delay the progress of the brain disease. Etanercept is already prescribed to people with rheumatoid arthritis, and works by sponging up a molecule that aggravates inflammation. According to Alzheimer's Disease International, 44 million people globally have dementia, of which Alzheimer's is the most common type. The beginnings of the disease are characterised by the appearance in the brain of plaques of amyloid proteins and tangles of tau proteins. They prompt the brain's native immune cells, the microglia, to multiply in a bid to dispose of the troublesome new debris. © Copyright Reed Business Information Ltd.
Link ID: 19536 - Posted: 04.26.2014
By Linda Carroll A college education may do a lot more than provide better job opportunities — it may also make brains more resilient to trauma, a new study suggests. The more years of education people have, the more likely they will recover from a traumatic brain injury, according to the study published Wednesday in Neurology. In fact, one year after a traumatic brain injury, people with a college education were nearly four times as likely as those who hadn’t finished high school to return to work or school with no disability. Earlier studies had shown that education might have a protective effect when it comes to degenerative brain diseases like Alzheimer’s. Scientists have theorized that education leads to greater “cognitive reserve,” which allows people to overcome or compensate for brain damage. So if there are two people with the same degree of damage from Alzheimer’s, the more highly educated one will show fewer symptoms. The assumption is that education changes and expands the brain, leaving it better able to cope with challenges. “Added capacity allows us to either work around the damaged areas or to adapt,” said Eric B. Schneider, an assistant professor of surgery at the Johns Hopkins School of Medicine. Schneider and his colleagues suspected that cognitive reserve might play an equally important role in helping people rehab from acute brain damage that results from falls, car crashes and other accidents as it does in Alzheimer’s disease.
Victoria Colliver, Erin Allday Women who gain too much or too little weight during pregnancy can greatly increase their baby's risk of being overweight or obese as a young child, according to a study by Kaiser Permanente researchers. Researchers examined the health records from 4,145 Northern California Kaiser members who filled out a health survey between 2007 and 2009 and subsequently gave birth. They found that women who exceeded the Institute of Medicine's revised 2009 guidelines for weight gain during pregnancy were 46 percent more likely than women who met the guidelines to have an obese or overweight child between the ages of 2 and 5 years old. Under the new guidelines, women who are obese - defined as those with a body mass index, or BMI, of 30 or higher - should gain 11 to 20 pounds. Overweight women - with BMIs between 25 and 29 - can gain 15 to 25 pounds. And normal-weight women are recommended to gain between 25 and 35 pounds. Those who are underweight - with BMIs under 18.5 - are to gain 28 to 40 pounds. Women who had a healthy BMI before their pregnancy but gained less weight than recommended were 63 percent more likely than those who met the guidelines to have an obese or overweight child. Meanwhile, healthy-weight women who exceeded the guidelines were 79 percent more likely to have an overweight child. Researchers suggested gaining too little or too much weight may permanently affect the body's mechanisms that manage energy balance and metabolism. The study, which is considered the largest to examine the new guidelines in relationship to childhood obesity, was published April 14 in the American Journal of Obstetrics and Gynecology. © 2014 Hearst Communications, Inc.