Chapter 7. Life-Span Development of the Brain and Behavior
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Hannah Devlin Rambling and long-winded anecdotes could be an early sign of Alzheimer’s disease, according to research that suggests subtle changes in speech style occur years before the more serious mental decline takes hold. The scientists behind the work said it may be possible to detect these changes and predict if someone is at risk more than a decade before meeting the threshold for an Alzheimer’s diagnosis. Janet Cohen Sherman, clinical director of the Psychology Assessment Center at Massachusetts General Hospital, said: “One of the greatest challenges right now in terms of Alzheimer’s disease is to detect changes very early on when they are still very subtle and to distinguish them from changes we know occur with normal ageing.” Speaking at the American Association for the Advancement of Science in Boston, Sherman outlined new findings that revealed distinctive language deficits in people with mild cognitive impairment (MCI), a precursor to dementia. “Many of the studies to date have looked at changes in memory, but we also know changes occur in language,” she said. “I’d hope in the next five years we’d have a new linguistic test.” Sherman cites studies of the vocabulary in Iris Murdoch’s later works, which showed signs of Alzheimer’s years before her diagnosis, and the increasingly repetitive and vague phrasing in Agatha Christie’s final novels – although the crime writer was never diagnosed with dementia. Another study, based on White House press conference transcripts, found striking changes in Ronald Reagan’s speech over the course of his presidency, while George HW Bush, who was a similar age when president, showed no such decline.
By WINNIE HU Ruth Brunn finally said yes to marijuana. She is 98. She pops a green pill filled with cannabis oil into her mouth with a sip of vitamin water. Then Ms. Brunn, who has neuropathy, settles back in her wheelchair and waits for the jabbing pain in her shoulders, arms and hands to ebb. “I don’t feel high or stoned,” she said. “All I know is I feel better when I take this.” Ms. Brunn will soon have company. The nursing home in New York City where she lives, the Hebrew Home at Riverdale, is taking the unusual step of helping its residents use medical marijuana under a new program to treat various illnesses with an alternative to prescription drugs. While the staff will not store or administer pot, residents are allowed to buy it from a dispensary, keep it in locked boxes in their rooms and take it on their own. From retirement communities to nursing homes, older Americans are increasingly turning to marijuana for relief from aches and pains. Many have embraced it as an alternative to powerful drugs like morphine, saying that marijuana is less addictive, with fewer side effects. For some people, it is a last resort when nothing else helps. Marijuana, which is banned by federal law, has been approved for medical use in 29 states, including New York, and the District of Columbia. Accumulating scientific evidence has shown its effectiveness in treating certain medical conditions. Among them: neuropathic pain, severe muscle spasms associated with multiple sclerosis, unintentional weight loss, and vomiting and nausea from chemotherapy. There have also been reports that pot has helped people with Alzheimer’s disease and other types of dementia as well as Parkinson’s disease. © 2017 The New York Times Company
By JANE E. BRODY “Feeling My Way Into Blindness,” an essay published in The New York Times in November by Edward Hoagland, an 84-year-old nature and travel writer and novelist, expressed common fears about the effects of vision loss on quality of life. Mr. Hoagland, who became blind about four years ago, projected deep-seated sadness in describing the challenges he faces of pouring coffee, not missing the toilet, locating a phone number, finding the food on his plate, and knowing to whom he is speaking, not to mention shopping and traveling, when he often must depend on the kindness of strangers. And, of course, he sorely misses nature’s inspiring vistas and inhabitants that fueled his writing, though he can still hear birds chatter in the trees, leaves rustle in the wind and waves crash on the shore. Mr. Hoagland is hardly alone in his distress. According to Action for Blind People, a British support organization, those who have lost some or all sight “struggle with a range of emotions — from shock, anger, sadness and frustration to depression and grief.” When eyesight fails, some people become socially disengaged, leading to isolation and loneliness. Anxiety about a host of issues — falls, medication errors, loss of employment, social blunders — is common. A recent study from researchers at the Wilmer Eye Institute at Johns Hopkins University School of Medicine found that most Americans regard loss of eyesight as the worst ailment that could happen to them, surpassing such conditions as loss of limb, memory, hearing or speech, or having H.I.V./AIDS. Indeed, low vision ranks behind arthritis and heart disease as the third most common chronic cause of impaired functioning in people over 70, Dr. Eric A. Rosenberg of Weill Cornell Medical College and Laura C. Sperazza, a New York optometrist, wrote in American Family Physician. © 2017 The New York Times Company
Bret Stetka In a series of recent interviews, President Donald Trump's longtime personal physician Dr. Harold N. Bornstein told The New York Times that our new commander in chief has what amounts to a pretty unremarkable medical chart. Like about a quarter of American adults, Trump is on a statin for high cholesterol. He also takes a daily baby aspirin for heart health, an occasional antibiotic for rosacea, a skin condition, and Propecia, a pill to promote hair growth. Bornstein also told the Times that should he be appointed White House doctor, he probably wouldn't test the president for baseline dementia risk, something many doctors have argued should be mandatory. At 70, Trump is the oldest American president to ever take office. Couple his age with a family history of dementia — his father Fred developed Alzheimer's disease in his 80s — and one could argue that the question of baseline cognitive testing for the U.S. head of state has taken on new relevance. An assortment of fairly simple tests exist that can establish a reference point for cognitive capacity and detect early symptoms of mental decline. One of the most common such screens is the Mini-Mental Status Examination, a series of questions that gauges attention, orientation and short-term memory. It takes about five to 10 minutes to complete. Yet admitting vulnerability of any kind isn't something politicians have been keen to do. The true health of politicians has likely been cloaked in secrecy since the days of Mesopotamian kings, but definitely since the Wilson administration. © 2017 npr
Link ID: 23243 - Posted: 02.17.2017
Ewen Callaway Researchers have no way to tell whether young babies may later be diagnosed with autism. But brain scans could help, a small study suggests. By scanning the brains of babies whose siblings have autism, researchers say they have been able to make reasonably accurate forecasts about which of these high-risk infants will later develop autism themselves. The findings raise the prospect of diagnosing autism spectrum disorder (ASD) months before children develop symptoms, a goal that has proved elusive. Nature looks at the new study and its implications. Why has it been so tough to diagnose autism in infants? Children typically show symptoms of ASD, such as difficulty making eye contact, after the age of 2. Researchers believe that the brain changes underlying ASD begin much earlier — possibly even in the womb. But behavioural assessments haven't been helpful in predicting who will get autism, says Joseph Piven, a psychiatrist at the University of North Carolina (UNC) in Chapel Hill, who co-led the study, published online in Nature1. “Children who end up with autism at 2 or 3, they don’t look like they have autism in the first year," he says. Certain rare mutations are linked to ASD, but the vast majority of cases cannot be pinned to a single or even a handful of genetic risk factors. Beginning in the 1990s, Piven and other researchers noticed that children with autism tended to have larger brains than developmentally normal children, suggesting that brain growth could be a biomarker for ASD. But Piven and colleague Heather Cody Hazlett, a psychologist at UNC-Chapel Hill, say it had not been clear when overgrowth occurred. What did their latest study look at? © 2017 Macmillan Publishers Limited,
By Amy Ellis Nutt For the first time, scientists can point to substantial empirical evidence that people with attention-deficit/hyperactivity disorder have brain structures that differ from those of people without ADHD. The common disorder, they conclude, should be considered a problem of delayed brain maturation and not, as it is often portrayed, a problem of motivation or parenting. In conducting the largest brain imaging study of its kind, an international team of researchers found that ADHD involves decreased volume in key brain regions, in particular the amygdala, which is responsible for regulating the emotions. Although the study, published Wednesday in the Lancet Psychiatry, included children, adolescents and adults, the scientists said the greatest differences in brain volume appeared in the brains of children. Of seven subcortical brain regions targeted in the study, five, including the amygdala, were found to be smaller in those with ADHD, compared with those in a control group. The other regions that showed reductions in volume were: the caudate nucleus (which has been linked to goal-directed action), the putamen (involved in learning and responding to stimuli), the nucleus accumbens (which processes rewards and motivation) and the hippocampus (where memories are formed). © 1996-2017 The Washington Post
By John Carroll, Scratch yet another Phase III Alzheimer’s drug hopeful. Merck announced late Tuesday that it is shuttering its EPOCH trial for the BACE inhibitor verubecestat in mild-to-moderate Alzheimer’s after the external data monitoring committee concluded that the drug was a bust, with “virtually” no chance of success. A separate Phase III study in prodromal patients, set to read out in two years, will continue as investigators found no signs of safety issues. This is one of Merck’s top late-stage drugs, and news of the failure drove down the pharma giant’s shares in after-market trading by 2.45%. BACE drugs essentially seek to interfere in the process that creates amyloid beta, a toxic protein often found in the brains of Alzheimer’s patients. As the top amyloid beta drugs like bapineuzumab and solanezumab — which sought to extract existing amyloid beta loads — ground their way to repeated failures, developers in the field turned increasingly to BACE therapies as an alternative mechanism that could provide the key to slowing this disease down. Merck’s effort was the most advanced in the pipeline, but Eli Lilly and others are still in hot pursuit with their own persistent BACE efforts. Teams from Biogen/Eisai and Novartis/Amgen are also beavering away on BACE. “Alzheimer’s disease is one of the most pressing and daunting medical issues of our time, with inherent, substantial challenges to developing an effective disease-modifying therapy for people with mild-to-moderate disease. Studies such as EPOCH are critical, and we are indebted to the patients in this study and their caregivers,” said Dr. Roger M. Perlmutter, president, Merck Research Laboratories. © 2017 American Association for the Advancement of Science.
Link ID: 23238 - Posted: 02.16.2017
By Jesse Singal Those who advocate for sound, evidence-based research about autism are extremely alarmed about Donald Trump, and for good reason: In addition to Trump’s ties to Andrew Wakefield, the disgraced British doctor whose debunked research helped fuel the false idea of links between childhood vaccines and autism, Robert F. Kennedy Jr., a notorious anti-vaxxer himself, told reporters back in January that Trump planned to tap him as chair of a commission on “vaccine safety.” There is no question at this point that Trump has significant connections to a pseudoscientific medical movement that spreads dangerous, disproven ideas. Today, Trump gave nervous observers yet more reason to worry. It occurred at a White House event in which Trump and Secretary of Education Betsy DeVos met with a bunch of educators. Trump seemed to fixate, for a moment, on one educator named Jane (her last name is hard to make out) after she explained that she is the principal of a special education center in Virginia. The sequence starts at about 5:38 in this video: After Jane noted that many of her students have autism, Trump asked, “Have you seen a big increase in the autism, with the children?” Jane replied in the affirmative, but seemed to couch her response as being more about an increase in demand for services — she didn’t explicitly agree there’s been a big increase in the overall rate. Trump continued: “So what’s going on with autism? When you look at the tremendous increase, it’s really — it’s such an incredible — it’s really a horrible thing to watch, the tremendous amount of increase. Do you have any idea? And you’re seeing it in the school?” Jane replied — again, in a way that seems a bit noncommittal vis-à-vis Trump’s claim — that the rate of autism is something like 1-in-66 or 1-in-68 children. To which Trump responds: “Well now, it’s gotta be even lower [presumably meaning higher, rate-wise] than that, which is just amazing — well, maybe we can do something.” (Jane had the rate right, and Trump is incorrect that it has crept higher.) © 2017, New York Media LLC.
Link ID: 23233 - Posted: 02.15.2017
Ian Sample Science editor Children who are born very prematurely are at greater risk of developing mental health and social problems that can persist well into adulthood, according to one of the largest reviews of evidence. Those with an extremely low birth weight, at less than a kilogram, are more likely to have attention disorders and social difficulties as children, and feel more shyness, anxiety and depression as adults, than those born a healthy weight. The review draws on findings from 41 published studies over the past 26 years and highlights the need for doctors to follow closely how children born very prematurely fare as they become teenagers and adults. “It is important that families and doctors be aware of the potential for these early-emerging mental health problems in children born at extremely low birth weight, since at least some of them endure into adulthood,” said Karen Mathewson, a psychologist at McMaster University in Ontario. Improvements in neonatal care in the past two decades mean that more children who are born very prematurely now survive. In a healthy pregnancy, a baby can reach 1kg (a little more than 2lbs) within 27 weeks, or the end of the second trimester. The study, which involves data from 13,000 children in 12 different countries, follows previous research that found a greater tendency for very low birth weight children to have lower IQs and autism and more trouble with relationships and careers as they reach adulthood and venture into the world. © 2017 Guardian News and Media Limited
Katherine Bourzac Kristopher Boesen, who broke his neck in a car accident, regained the ability to move his arms and hands after his spinal cord was injected with stem cells. Two years after having a stroke at 31, Sonia Olea Coontz remained partially paralysed on her right side. She could barely move her arm, had slurred speech and needed a wheelchair to get around. In 2013, Coontz enrolled in a small clinical trial. The day after a doctor injected stem cells around the site of her stroke, she was able to lift her arm up over her head and speak clearly. Now she no longer uses a wheelchair and, at 36, is pregnant with her first child. Coontz is one of stem-cell therapy's “miracle patients”, says Gary Steinberg, chair of neurosurgery at Stanford School of Medicine in California, and Coontz's doctor. Conventional wisdom said that her response was impossible: the neural circuits damaged by the stroke were dead. Most neuroscientists believed that the window for functional recovery extends to only six months after the injury. Stem-cell therapies have shown great promise in the repair of brain and spinal injuries in animals. But animal models often behave differently from humans — nervous-system injuries in rats, for example, heal more readily than they do in people. Clinical trial results have been mixed. Interesting signals from small trials have faded away in larger ones. There are plenty of unknowns: which stem cells are the right ones to use, what the cells are doing when they work and how soon after an injury they can be used. © 2016 Macmillan Publishers Limited,
“Bench-to-bedside” describes research that has progressed from basic science in animal models that has led to therapies used in patients. Now, a study in the journal Brain describes what could be considered a direct “aquarium-to-bedside” approach, taking a drug discovered in a genetic zebrafish model of epilepsy and testing it, with promising results, in a small number of children with the disease. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This is the first time that scientists have taken a potential therapy discovered in a fish model directly into people in a clinical trial,” said Vicky Whittemore, Ph.D., program director at the NINDS. “These findings suggest that it may be possible to treat neurological disorders caused by genetic mutations through an efficient and precision medicine-style approach.” Scott C. Baraban, Ph.D., the William K. Bowes Jr. Endowed Chair in Neuroscience Research and professor of neurological surgery at the University of California, San Francisco (UCSF), postdoctoral fellow Aliesha Griffin, Ph.D., and colleagues used a zebrafish model of Dravet syndrome to test the drug lorcaserin and found that it suppressed seizure activity in the fish. Dravet syndrome is a severe form of pediatric epilepsy characterized by frequent daily drug-resistant seizures and developmental delays. It is caused by a genetic mutation, which Dr. Baraban’s group was able to introduce into the zebrafish to cause epilepsy. Dr. Baraban and his colleague Kelly Knupp, M.D. at the University of Colorado, Denver, then tested lorcaserin in five children with Dravet syndrome. The children were resistant to other anti-epileptic drugs and participated in this study through a compassionate use, off-label program.
In a study of mice and monkeys, National Institutes of Health funded researchers showed that they could prevent and reverse some of the brain injury caused by the toxic form of a protein called tau. The results, published in Science Translational Medicine, suggest that the study of compounds, called tau antisense oligonucleotides, that are genetically engineered to block a cell’s assembly line production of tau, might be pursued as an effective treatment for a variety of disorders. Cells throughout the body normally manufacture tau proteins. In several disorders, toxic forms of tau clump together inside dying brain cells and form neurofibrillary tangles, including Alzheimer’s disease, tau-associated frontotemporal dementia, chronic traumatic encephalopathy and progressive supranuclear palsy. Currently there are no effective treatments for combating toxic tau. "This compound may literally help untangle the brain damage caused by tau,” said Timothy Miller, M.D., Ph.D., the David Clayson Professor of Neurology at Washington University, St. Louis, and the study's senior author. Antisense oligonucleotides are short sequences of DNA or RNA programmed to turn genes on or off. Led by Sarah L. DeVos, a graduate student in Dr. Miller’s lab, the researchers tested sequences designed to turn tau genes off in mice that are genetically engineered to produce abnormally high levels of a mutant form of the human protein. Tau clusters begin to appear in the brains of 6-month-old mice and accumulate with age. The mice develop neurologic problems and die earlier than control mice.
Link ID: 23205 - Posted: 02.09.2017
By SHARON LERNER IN the fall, I began to research an article that I gave the working title “The Last Days of Chlorpyrifos.” A widely used pesticide, chlorpyrifos affects humans as well as the bugs it kills. Back in the halcyon days before the election, the optimism of the title seemed warranted. After years of study, the Environmental Protection Agency had announced in October 2015 that it could no longer vouch for the safety of chlorpyrifos on food. The agency had acknowledged for decades that chlorpyrifos can cause acute poisoning and in the early 2000s it had prohibited its use in most home products and reduced the amounts that could be used on some crops. But the 2015 announcement stemmed from the agency’s recognition of mounting evidence that prenatal exposure to chlorpyrifos could have lasting effects on children’s brains. Though the process of re-evaluating the safety of the pesticide had stretched on for years, at long last, chlorpyrifos seemed to be going down. Another report was expected to provide all the ammunition necessary to stop its use on fruits and vegetables, and I was eager to document its demise. For a reporter who covers the environment, this was going to be the rare happy story. The election of President Trump has thrown that outcome — indeed, the fate of many of the E.P.A.’s public health protections — into question. On Monday, Mr. Trump signed an executive order requiring federal agencies to scrap two regulations for every one they institute on small businesses. In its first week, his administration suspended 30 environmental regulations issued under President Barack Obama. And Myron Ebell, who oversaw the agency’s transition team, suggested recently that the E.P.A.’s staff may soon be reduced by as much as two-thirds. How will the agency’s mission “to protect human health and the environment” fare under this assault? What happens with chlorpyrifos may be our best indication. “I think it’ll be a very early test of their commitment to environmental protection,” Jim Jones, who oversaw the evaluation of chlorpyrifos as the E.P.A.’s assistant administrator for chemical safety and pollution prevention, told me, not long after he stepped down on Inauguration Day. © 2017 The New York Times Company
By CATHERINE SAINT LOUIS During her pregnancy, she never drank alcohol or had a cigarette. But nearly every day, Stacey, then 24, smoked marijuana. With her fiancé’s blessing, she began taking a few puffs in her first trimester to quell morning sickness before going to work at a sandwich shop. When sciatica made it unbearable to stand during her 12-hour shifts, she discreetly vaped marijuana oil on her lunch break. “I wouldn’t necessarily say, ‘Go smoke a pound of pot when you’re pregnant,’” said Stacey, now a stay-at-home mother in Deltona, Fla., who asked that her full name be withheld because street-bought marijuana is illegal in Florida. “In moderation, it’s O.K.” Many pregnant women, particularly younger ones, seem to agree, a recent federal survey shows. As states legalize marijuana or its medical use, expectant mothers are taking it up in increasing numbers — another example of the many ways in which acceptance of marijuana has outstripped scientific understanding of its effects on human health. Often pregnant women presume that cannabis has no consequences for developing infants. But preliminary research suggests otherwise: Marijuana’s main psychoactive ingredient — tetrahydrocannabinol, or THC — can cross the placenta to reach the fetus, experts say, potentially harming brain development, cognition and birth weight. THC can also be present in breast milk. “There is an increased perception of the safety of cannabis use, even in pregnancy, without data to say it’s actually safe,” said Dr. Torri Metz, an obstetrician at Denver Health Medical Center who specializes in high-risk pregnancies. Ten percent of her patients acknowledge recent marijuana use. © 2017 The New York Times Company
By Emma Hiolski Imagine cells that can move through your brain, hunting down cancer and destroying it before they themselves disappear without a trace. Scientists have just achieved that in mice, creating personalized tumor-homing cells from adult skin cells that can shrink brain tumors to 2% to 5% of their original size. Although the strategy has yet to be fully tested in people, the new method could one day give doctors a quick way to develop a custom treatment for aggressive cancers like glioblastoma, which kills most human patients in 12–15 months. It only took 4 days to create the tumor-homing cells for the mice. Glioblastomas are nasty: They spread roots and tendrils of cancerous cells through the brain, making them impossible to remove surgically. They, and other cancers, also exude a chemical signal that attracts stem cells—specialized cells that can produce multiple cell types in the body. Scientists think stem cells might detect tumors as a wound that needs healing and migrate to help fix the damage. But that gives scientists a secret weapon—if they can harness stem cells’ natural ability to “home” toward tumor cells, the stem cells could be manipulated to deliver cancer-killing drugs precisely where they are needed. Other research has already exploited this method using neural stem cells—which give rise to neurons and other brain cells—to hunt down brain cancer in mice and deliver tumor-eradicating drugs. But few have tried this in people, in part because getting those neural stem cells is hard, says Shawn Hingtgen, a stem cell biologist at the University of North Carolina in Chapel Hill. © 2017 American Association for the Advancement of Science.
New clinical trial results provide evidence that high-dose immunosuppressive therapy followed by transplantation of a person's own blood-forming stem cells can induce sustained remission of relapsing-remitting multiple sclerosis (MS), an autoimmune disease in which the immune system attacks the central nervous system. Five years after receiving the treatment, called high-dose immunosuppressive therapy and autologous hematopoietic cell transplant (HDIT/HCT), 69 percent of trial participants had survived without experiencing progression of disability, relapse of MS symptoms or new brain lesions. Notably, participants did not take any MS medications after receiving HDIT/HCT. Other studies have indicated that currently available MS drugs have lower success rates. The trial, called HALT-MS, was sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and conducted by the NIAID-funded Immune Tolerance Network (link is external) (ITN). The researchers published three-year results from the study in December 2014, and the final five-year results appear online Feb. 1 in Neurology, the medical journal of the American Academy of Neurology. “These extended findings suggest that one-time treatment with HDIT/HCT may be substantially more effective than long-term treatment with the best available medications for people with a certain type of MS,” said NIAID Director Anthony S. Fauci, M.D. “These encouraging results support the development of a large, randomized trial to directly compare HDIT/HCT to standard of care for this often-debilitating disease.”
James Gorman What fly is famous on TV? Think corpses and detectives wanting to know how long that body has been in a storage locker or suitcase. It’s the blowfly, of course. Its larvae, a.k.a. maggots, feed on rotting flesh, which could be that spouse or business partner who got in the way. Or, in a good police procedural, both the spouse and the business partner, sent to the great beyond together for their transgressions. By seeing whether the eggs have hatched and how big the larvae are, forensic scientists can get an idea of how much time has passed since the victims met their end and began the final chapter in the way of all flesh. By the way, if you have a problem with a spouse or business partner, it’s worth keeping in mind that the flies can indeed get into a suitcase. They stick their ovipositor through the gaps in the zipper. Or the newly hatched larvae themselves can sneak through. But there are aspects of the maggot’s life that have remained somewhat obscure. Martin Hall, a forensic entomologist at the Natural History Museum in London, thought that one part of the fly’s development in particular needed further study. The maggots are a bit like caterpillars in that at a certain point in their development they wrap themselves up in a case and go through one of the most astonishing events in the natural world: metamorphosis. In 10 days, the maggot, which has no legs or eyes and is something like “an animated sock,” Dr. Hall said, turns into the extraordinarily complex blowfly. No doubt blowflies are not as appealing as butterflies to most people, but chalk that up to a human bias for pretty fluttery things that land on flowers. It’s certainly not the fly’s fault. Any close-up image of its multifaceted, jewel-like eye shows that it is marvelous in its own way, even if it does feed on the dead. Science Times © 2017 The New York Times Company
Keyword: Development of the Brain
Link ID: 23169 - Posted: 01.31.2017
By Emily Underwood LOS ANGELES, CALIFORNIA—In a barbed wire–enclosed parking lot 100 meters downwind of the Route 110 freeway, an aluminum hose sticks out of a white trailer, its nozzle aimed at an overpass. Every minute, the hose sucks up hundreds of liters of air mixed with exhaust from the roughly 300,000 cars and diesel-burning freight trucks that rumble by each day. Crouched inside the trailer, a young chemical engineer named Arian Saffari lifts the lid off a sooty cylinder attached to the hose, part of a sophisticated filtration system that captures and sorts pollutants by size. Inside is a scientific payload: particles of sulfate, nitrate, ammonium, black carbon, and heavy metal at least 200 times smaller than the width of a human hair. The particles are too fine for many air pollution sensors to accurately measure, says Saffari, who works in a lab led by Constantinos Sioutas at the University of Southern California (USC) here. Typically smaller than 0.2 µm in diameter, these “ultrafine” particles fall within a broader class of air pollutants commonly referred to as PM2.5 because of their size, 2.5 µm or less. When it comes to toxicity, size matters: The smaller the particles that cells are exposed to, Saffari says, the higher their levels of oxidative stress, marked by the production of chemically reactive molecules such as peroxides, which can damage DNA and other cellular structures. © 2017 American Association for the Advancement of Science.
By Meredith Wadman Many children with congenital heart disease (CHD)—the most common major birth defect in the United States—sustain brain damage that often leads to problems with behavior, thinking, and learning. Now, for the first time, researchers have described how the lack of brain oxygen that results from heart malformations might stunt the brains of newborns, opening avenues to potential therapies that could be used even before babies are born. The results are “incredibly exciting,” says Caitlin Rollins, a child neurologist at Boston Children’s Hospital. “This kind of study allows us to start understanding the cellular mechanisms” behind the brain damage, she says. In the future, she adds, “we might be able to alter the course of brain development” with drugs targeted at the cellular anomalies and delivered during pregnancy. CHD reduces oxygen delivery to the brain at a time when the fetus most needs it. This lack of oxygen is thought to be a primary cause of the brain aberrations, which first become visible on MRI scans in the third trimester of pregnancy. (The heart anomalies themselves are commonly identified in the second trimester, on routine ultrasound scans.) Yet until now, scientists have been unclear about the underlying cellular process causing the brain problems. So a research team led by scientists at Children’s National Health System in Washington, D.C., delivered subpar levels of oxygen to newborn piglets, whose course of brain development and whose highly evolved brain structure mirrors in many respects those of humans. © 2017 American Association for the Advancement of Science.
Keyword: Development of the Brain
Link ID: 23150 - Posted: 01.26.2017
By Andy Coghlan NEW drug will finally cure Alzheimer’s! Sound familiar? Seemingly every other week, the results of one preliminary trial or another promise that a game-changing drug for Alzheimer’s disease is just around the corner. Check back a few months later, though, and all mention of the drug has vanished, save perhaps for a terse story about a failed trial. Almost all clinical trials of new drugs to combat Alzheimer’s fail. No drug has bucked the trend in 20 years, but you wouldn’t know it from the constant promises of a breakthrough. Last November, after the failure of a particularly high-profile trial, for some the jig was up. “There are no treatments that can slow or reverse this devastating condition,” says Bryce Vissel at the University of Technology in Sydney, Australia. “There is no question that we have to look at Alzheimer’s in a different way.” So are we heading in the right direction, or do we need to rip up all the textbooks and start over? Alzheimer’s is the most common cause of dementia, and by some metrics its prevalence is rising. Alzheimer’s Disease International estimates that in 2015, 46.8 million people worldwide had dementia, a number that is set to double every 20 years, mostly because of an increasing number of older people in developing countries like India and China, leading to a global healthcare crisis. © Copyright Reed Business Information Ltd.
Link ID: 23149 - Posted: 01.26.2017