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

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Laura Sanders In stark contrast to earlier findings, adults do not produce new nerve cells in a brain area important to memory and navigation, scientists conclude after scrutinizing 54 human brains spanning the age spectrum. The finding is preliminary. But if confirmed, it would overturn the widely accepted and potentially powerful idea that in people, the memory-related hippocampus constantly churns out new neurons in adulthood. Adult brains showed no signs of such turnover in that region, researchers reported November 13 at a meeting of the Society for Neuroscience in Washington, D.C. Previous studies in animals have hinted that boosting the birthrate of new neurons, a process called neurogenesis, in the hippocampus might enhance memory or learning abilities, combat depression and even stave off the mental decline that comes with dementia and old age (SN: 9/27/08, p. 5). In rodents, exercise, enriched environments and other tweaks can boost hippocampal neurogenesis — and more excitingly, memory performance. But the new study may temper those ambitions, at least for people. Researchers studied 54 human brain samples that ranged from fetal stages to age 77, acquired either postmortem or during brain surgery. These samples were cut into thin slices and probed with molecular tools that can signal dividing or young cells, both of which are signs that nerve cells are being born. As expected, fetal and infant samples showed evidence of both dividing cells that give rise to new neurons and young neurons themselves in the hippocampus. But with age, these numbers declined. In brain tissue from a 13-year-old, the researchers spotted only a handful of young neurons. And in adults, there were none. |© Society for Science & the Public 2000 - 2017.

Keyword: Neurogenesis
Link ID: 24334 - Posted: 11.16.2017

By NICHOLAS BAKALAR Heart attack survivors have an increased risk for developing dementia, a new study has found. Danish researchers studied 314,911 heart attack patients and compared them with 1,573,193 controls who had not had a heart attack. They excluded anyone who had already been diagnosed with dementia or other memory disorders. The study, in Circulation, adjusted for heart failure, pulmonary disease, head trauma, kidney disease and many other variables. During 35 years of follow-up, there were 3,615 cases of Alzheimer’s disease, 2,034 cases of vascular dementia and 5,627 cases of other dementias among the heart attack patients. There was no association of heart attack with Alzheimer’s disease. But heart attack increased the risk for vascular dementia, the type caused by impaired blood flow to the brain, by 35 percent. There are several possible reasons for the link, including similar underlying causes for dementia and heart attack — among them, hypertension, stroke and having undergone coronary artery bypass surgery. The researchers had no data on smoking, and they acknowledge that there may be other variables they were unable to account for. “Dementia can’t be cured,” said the lead author, Dr. Jens Sundboll, a resident in cardiology at Aarhus University in Denmark. “What’s the solution? Prevention. And for prevention we have to identify risk factors. Here we’ve identified an important one.” © 2017 The New York Times Company

Keyword: Alzheimers
Link ID: 24330 - Posted: 11.16.2017

By Sarah DeWeerdt, Young adults with autism have an unusual gait and problems with fine motor skills. Researchers presented the unpublished findings today at the 2017 Society for Neuroscience annual meeting in Washington, D.C. Motor problems such as clumsiness, toe-walking and altered gait are well documented in autism. But most studies have been limited to children or have included adults only as part of a broad age range. “Studies haven’t focused on just adults,” says Cortney Armitano, a graduate student in Steven Morrison’s lab at Old Dominion University in Norfolk, Virginia, who presented the work. The researchers looked at 20 young adults with autism between the ages of about 17 and 25, and 20 controls of about the same age range. They put these participants through a battery of standard tests of fine motor skills, balance and walking. When it comes to simple tasks—such as tapping a finger rapidly against a hard surface or standing still without swaying—those with autism perform just as well as controls do. But with activities that require more back-and-forth between the brain and the rest of the body, differences emerge. Adults with autism have slower reaction times compared with controls, measured by how fast they can click a computer mouse in response to seeing a button light up. They also have a weaker grip. © 2017 Scientific American,

Keyword: Autism; Movement Disorders
Link ID: 24329 - Posted: 11.15.2017

The ready availability of technology may make the children of today faster at configuring a new smartphone, but does all of that screen time affect the development of their eyes? While conventional wisdom dictates that children should do less up-close viewing, sit farther from the television and perhaps even wear their eyeglasses less, we have found in recent studies that another factor may be at play: Kids need to go outside and, if not play, at least get some general exposure to outdoor light. To our surprise, more time outdoors had a protective effect and reduced the chances that a child would go on to need myopic refractive correction. The size of the effect was impressive. What causes nearsightedness? Myopia, or nearsightedness, is a condition in which you can’t see far away but can see up close without glasses or contact lenses. It typically starts during the early elementary-school years. Because kids don’t know how other kids see, they often think their blurry vision is normal, so regular eye examinations are important. With myopia, the eye is growing, but growing too long for distant rays of light to focus accurately on the back of the eye. A blurry image results. For children, eyeglasses or contact lenses move the focus back to the retina, and a clear image is formed. The too-long eye cannot be shrunk, so refractive correction is then a lifelong necessity. In adulthood, surgery is an option. © 1996-2017 The Washington Post

Keyword: Vision; Development of the Brain
Link ID: 24320 - Posted: 11.13.2017

By Ann Gibbons Ever since Alex Pollen was a boy talking with his neuroscientist father, he wanted to know how evolution made the human brain so special. Our brains are bigger, relative to body size, than other animals', but it's not just size that matters. "Elephants and whales have bigger brains," notes Pollen, now a neuroscientist himself at the University of California, San Francisco. Comparing anatomy or even genomes of humans and other animals reveals little about the genetic and developmental changes that sent our brains down such a different path. Geneticists have identified a few key differences in the genes of humans and apes, such as a version of the gene FOXP2 that allows humans to form words. But specifically how human variants of such genes shape our brain in development—and how they drove its evolution—have remained largely mysterious. "We've been a bit frustrated working so many years with the traditional tools," says neurogeneticist Simon Fisher, director of the Max Planck Institute for Psycholinguistics in Nijmegen, the Netherlands, who studies FOXP2. Now, researchers are deploying new tools to understand the molecular mechanisms behind the unique features of our brain. At a symposium at The American Society of Human Genetics here last month, they reported zooming in on the genes expressed in a single brain cell, as well as panning out to understand how genes foster connections among far-flung brain regions. Pollen and others also are experimenting with brain "organoids," tiny structured blobs of lab-grown tissue, to detail the molecular mechanisms that govern the folding and growth of the embryonic human brain. "We used to be just limited to looking at sequence data and cataloging differences from other primates," says Fisher, who helped organize the session. "Now, we have these exciting new tools that are helping us to understand which genes are important." © 2017 American Association for the Advancement of Science.

Keyword: Development of the Brain
Link ID: 24315 - Posted: 11.10.2017

By Sara B. Linker, Tracy A. Bedrosian, and Fred H. Gage For years, neurons in the brain were assumed to all carry the same genome, with differences in cell type stemming from epigenetic, transcriptional, and posttranscriptional differences in how that genome was expressed. But in the past decade, researchers have recognized an incredible amount of genomic diversity, in addition to other types of cellular variation that can affect function. Indeed, the human brain contains approximately 100 billion neurons, and we now know that there may be almost as many unique cell types. Our interest in this incredible diversity emerged from experiments that we initially labeled as failures. In 1995, we (F.H.G. and colleagues) found that a protein called fibroblast growth factor 2 (FGF2) is important for maintaining adult neural progenitor cells (NPCs) in a proliferative state in vitro. We could only expand NPCs by culturing them at high density, however, so we could not generate homogeneous populations of cells.1 Five years later, we identified a glycosylated form of the protein cystatin C (CCg) that, combined with FGF2, allowed us to isolate and propagate a very homogeneous population of NPCs—cells that would uniformly and exclusively differentiate into neurons.2 We compared gene expression of this homogeneous population of cells to that of rat stem cells and the oligodendrocytes, astroglia, and neurons derived from the NPCs. To our surprise and disappointment, the top nine transcripts that were unique to the NPC-derived population were all expressed components of long interspersed nuclear element-1, also known as LINE-1 or L1— an abundant retrotransposon that makes up about 20 percent of mammalian genomes. © 1986-2017 The Scientist

Keyword: Development of the Brain; Epigenetics
Link ID: 24305 - Posted: 11.08.2017

By Anna Cranston, Around 50m people worldwide are thought to have Alzheimer’s disease. And with rapidly ageing populations in many countries, the number of sufferers is steadily rising. We know that Alzheimer’s is caused by problems in the brain. Cells begin to lose their functions and eventually die, leading to memory loss, a decline in thinking abilities and even major personality changes. Specific regions of the brain also shrink, a process known as atrophy, causing a significant loss of brain volume. But what’s actually happening in the brain to cause this? Advertisement The main way the disease works is to disrupt communication between neurons, the specialised cells that process and transmit electrical and chemical signals between regions of the brain. This is what is responsible for the cell death in the brain – and we think its due to a build up of two types of protein, called amyloid and tau. The exact interaction between these two proteins is largely unknown, but amyloid accumulates into sticky clusters known as beta-amyloid “plaques”, while tau builds up inside dying cells as “neurofibrillary tangles”. One of the difficulties of diagnosing Alzheimer’s is that we’ve no reliable and accurate way of measuring this protein build-up during the early stages of the disease. In fact, we can’t definitively diagnose Alzheimer’s until after the patient has died, by examining their actual brain tissue. Another problem we have is that beta-amyloid plaques can also be found in the brains of healthy patients. This suggests the presence of the amyloid and tau proteins may not tell the whole story of the disease. © 2017 Scientific American,

Keyword: Alzheimers
Link ID: 24300 - Posted: 11.07.2017

For the first time, scientists have found a connection between abnormalities in how the brain breaks down glucose and the severity of the signature amyloid plaques and tangles in the brain, as well as the onset of eventual outward symptoms, of Alzheimer’s disease. The study was supported by the National Institute on Aging (NIA), part of the National Institutes of Health, and appears in the Nov. 6, 2017, issue of Alzheimer's & Dementia: the Journal of the Alzheimer's Association. Led by Madhav Thambisetty, M.D., Ph.D., investigator and chief of the Unit of Clinical and Translational Neuroscience in the NIA’s Laboratory of Behavioral Neuroscience, researchers looked at brain tissue samples at autopsy from participants in the Baltimore Longitudinal Study of Aging (BLSA), one of the world’s longest-running scientific studies of human aging. The BLSA tracks neurological, physical and psychological data on participants over several decades. Researchers measured glucose levels in different brain regions, some vulnerable to Alzheimer’s disease pathology, such as the frontal and temporal cortex, and some that are resistant, like the cerebellum. They analyzed three groups of BLSA participants: those with Alzheimer’s symptoms during life and with confirmed Alzheimer’s disease pathology (beta-amyloid protein plaques and neurofibrillary tangles) in the brain at death; healthy controls; and individuals without symptoms during life but with significant levels of Alzheimer’s pathology found in the brain post-mortem. They found distinct abnormalities in glycolysis, the main process by which the brain breaks down glucose, with evidence linking the severity of the abnormalities to the severity of Alzheimer’s pathology. Lower rates of glycolysis and higher brain glucose levels correlated to more severe plaques and tangles found in the brains of people with the disease. More severe reductions in brain glycolysis were also related to the expression of symptoms of Alzheimer’s disease during life, such as problems with memory.

Keyword: Alzheimers
Link ID: 24299 - Posted: 11.07.2017

By Roni Dengler The bills of even newly hatched ducks might be as sensitive as our hands, as touch sensors in their beaks are as abundant as those in our fingertips and palms. That’s the take-away of new research published today in the Proceedings of the National Academy of Sciences that describes the origins of touchiness in the common duck’s quacker. Researchers knew that duck bills can sense light touch but have muted responsiveness to temperature. This comes in handy (or bill-y) since the birds forage for food in cold, murky bottom waters. Now, researchers find the sensors duck bills use to perceive touch work even before hatching. That likely helps young ducklings scavenge for food alongside adults soon after birth. In keeping with the need to feel for food, the ducks have more nerve cells to relay touch signals than chickens, which rely on eyesight to find sustenance, they report. That means different developmental programs are at work in ducks and chickens, which could help scientists uncover how touch evolved. Because the duck’s touch sensors are similar to mammals’ and their bills aren’t covered in fur, the authors suggest embryonic duck bills might be a better model than standard laboratory rodents to study touch sensation as it applies to us relatively hairless humans. © 2017 American Association for the Advancement of Science

Keyword: Pain & Touch; Development of the Brain
Link ID: 24298 - Posted: 11.07.2017

Laura Sanders An Alzheimer’s-related protein can move from the blood to the brain and accumulate there, experiments on mice show for the first time. The results, published online October 31 in Molecular Psychiatry, suggest that the protein amyloid-beta outside the brain may contribute to the Alzheimer’s disease inside it, says Mathias Jucker, a neurobiologist at the University of Tübingen in Germany. This more expansive view of the disease may lead scientists to develop treatments that target parts of the body that are easier than the brain to access. The experiments don’t suggest that people could contract Alzheimer’s from another person’s blood. “The bottom line is that this study is thought-provoking but shouldn’t cause alarm,” says neurologist John Collinge of University College London. “There really isn’t any evidence that you can transmit Alzheimer’s disease by blood transfusion.” But researchers wondered whether, over time, A-beta might build up in the brain by moving there from the blood, where it’s normally found in small quantities. Earlier animal studies have shown that A-beta can move into the brain if it’s injected into the bloodstream, but scientists didn’t know whether A-beta from the blood can be plentiful enough to form plaques in the brain. To test this, researchers used a form of extreme blood-sharing in the experiment. Six pairs of mice — with one mouse engineered to produce gobs of human A-beta and one normal — were surgically joined for a year, causing blood mingling that’s far more extensive than that of a blood transfusion. After a year, the brains of the mice carrying the mutations were full of A-beta plaques, as expected. But these plaques were also inside the brains of the normal mice in the joined pairs. |© Society for Science & the Public 2000 - 2017.

Keyword: Alzheimers
Link ID: 24295 - Posted: 11.06.2017

BC's Hogan twins, featured in the documentary Inseparable, are unique in the world. Joined at the head, their brains are connected by a thalamic bridge which gives them neurological capabilities that researchers are only now beginning to understand. Still, they are like other Canadian ten-year-olds; they attend school, have a favourite pet and are part of a large, loving family determined to live each day to the fullest. Here are a few highlights: Craniopagus twins, joined at the head, are a rarity — one in 2.5 million. The vast majority do not survive 24 hours. Krista and Tatiana Hogan were born October 25, 2006, in Vancouver, B.C. A CT scan of the twins showed they could never be separated due to the risk of serious injury or death. The structure of the twins’ brains makes them unique in the world. Their brains are connected by a thalamic bridge, connecting the thalamus of one with that of the other. The thalamus acts like a switchboard relaying sensory and motor signals and regulating consciousness. Krista and Tatiana Hogan share the senses of touch and taste and even control one another’s limbs. Tatiana can see out of both of Krista’s eyes, while Krista can only see out of one of Tatiana’s. Tatiana controls three arms and a leg, while Krista controls three legs and an arm. They can also switch to self-control of their limbs. The twins say they know one another’s thoughts without having to speak. “Talking in our heads” is how they describe it. The girls are diabetic and have epilepsy. They take a regimen of pills, blood tests and need daily insulin injections. The twins go to a regular school and as of September 2017 have started Grade 6. Though academically delayed, they are learning to read, write and do arithmetic. ©2017 CBC/Radio-Canada.

Keyword: Development of the Brain; Consciousness
Link ID: 24288 - Posted: 11.04.2017

By Emily Willingham In their October 23 opinion piece “Why Does Autism Impact Boys More Often Than Girls?” Renee Joy Dufault and Steven G. Gilbert attempt to argue that autism diagnoses are on the increase because of inorganic mercury content in processed foods. Going a step further, they try to construct a rationale for blaming mercury for the perceived bias in autism rates among boys compared to girls. Using the example of one observational study reporting that mercury affects chemical tagging of a single gene in one cell type differently in boys and girls, the pair constructs a fragile chain of putative links between this single study and their claim that “inorganic mercury has been rising for many years in American blood.” The claims are problematic on many levels, but let’s just take a trip to the ground floor: evidence. First, mercury levels in “American blood” and urine are decreasing, not increasing. The latest analysis of values of inorganic mercury in urine and total blood mercury, published online September 6 in Environmental Toxicology and Pharmacology, finds that from 2005 to 2012 among all age groups, urinary inorganic mercury decreased. Total blood mercury, which includes organic (carbon-bound) and inorganic forms, also decreased in all age groups during that time. These conclusions are based on data from the U.S. Centers for Disease Control and Prevention (CDC) National Health and Nutrition Examination Survey (NHANES). Meanwhile, other CDC data indicate that autism prevalence has increased. The trends for autism prevalence and mercury levels in people living in the United States are in opposite directions. © 2017 Scientific American

Keyword: Autism; Neurotoxins
Link ID: 24287 - Posted: 11.04.2017

JoNel Aleccia People who abhor the thought of being kept alive with feeding tubes or other types of artificial nutrition and hydration have, for years, had a way out: They could officially document their wishes to halt such interventions using advance directives. Even patients diagnosed with progressive dementia who are able to record crucial end-of-life decisions before the disease robs them of their mental capacity could write advance directives. But caregivers and courts have rarely honored patients' wishes to refuse food and fluids offered by hand. Margot Bentley, 85, of British Columbia, died last year. She was a retired nurse who had cared for dementia patients before being diagnosed with Alzheimer's in 1999. In 1991, she wrote a statement stipulating that she wanted no nourishment or liquids if she developed an incurable illness. However, the nursing home where she was a patient continued to spoon-feed her, despite her family's protests. A court ruling upheld the nursing home's action, saying that food is basic care that cannot be withdrawn. Nora Harris, 64, of Medford, Ore., died on Oct. 11 after an eight-year struggle with early-onset Alzheimer's disease. More than a year earlier, her husband had gone to court to stop caregivers from spoon-feeding Harris, who had an advance directive that called for no artificial nourishment or hydration. A judge declined, siding with officials who said the state was required to feed vulnerable adults. © 2017 npr

Keyword: Alzheimers
Link ID: 24284 - Posted: 11.03.2017

Alison Abbott The first controlled, but controversial and small, clinical trial of giving young blood to people with dementia has reported that the procedure appears safe. It has also hinted that it may even produce modest improvements in the daily lives of people who have Alzheimer's disease. Researchers who conducted the trial and others caution that the results are based on just 18 people and therefore are only a first step in exploring this type of treatment. “This is a really very small trial and the results should not be over-interpreted,” says Tony Wyss-Coray, a neurologist at Stanford University in California who led the study. The trial was conducted by his start-up company Alkahest, which is based in San Carlos, California. The results suggest the procedure is safe and hint that it could even boost the ability of people with dementia to undertake everyday skills, such as shopping or preparing a meal. The team plans to present the results on 4 November at the 10th Clinical Trials on Alzheimer’s Disease conference in Boston, Massachusetts. Wyss-Coray and his colleagues tested people aged between 54 and 86 with mild to moderate Alzheimer's disease. The team gave the 18 subjects weekly infusions for four weeks. They received either a saline placebo or plasma — blood from which the red cells have been removed — from blood donors aged 18–30. During the study, the team monitored the patients to assess their cognitive skills, mood and general abilities to manage their lives independently. The study detected no serious adverse reactions. It saw no significant effect on cognition, but two different batteries of tests assessing daily living skills both showed significant improvement. © 2017 Macmillan Publishers Limited,

Keyword: Alzheimers; Hormones & Behavior
Link ID: 24279 - Posted: 11.02.2017

By NICHOLAS BAKALAR Chronic inflammation in middle age may be associated with an increased risk for brain shrinkage and Alzheimer’s disease later in life. A new study, published in Neurology, looked at 1,633 people whose average age was 53 in 1987-89, measuring white blood cell count and various blood proteins that indicate inflammation. They followed the participants for 24 years. In 2011-13, when the subjects’ average age was 77, the scientists measured their brain volume using M.R.I. and tested their mental agility with a word-memorization task. They found that the greater the number of elevated inflammatory markers earlier in life, the smaller the volume of several parts of the brain, including those associated with Alzheimer’s disease. Higher levels of inflammation were also associated with poorer performance on the memory test. The authors acknowledge that they had blood tests for only one point in time, and that they are assuming that brain loss occurred in the years after the inflammatory markers were assessed. “It’s important early in life that we prevent diseases like diabetes, heart disease or hypertension that cause systemic inflammation,” said the lead author, Keenan A. Walker, a postdoctoral fellow at Johns Hopkins. “This study shows a temporal relationship between early inflammation and later brain volume loss.” © 2017 The New York Times Company

Keyword: Alzheimers; Neuroimmunology
Link ID: 24277 - Posted: 11.02.2017

Teens are getting less sleep than they did before smartphones became commonplace, prompting concerns about potentially serious health consequences, researchers say. A study published in the current issue of the journal Sleep Medicine examined data from two surveys of U.S. adolescents conducted over many years and including questions about how many hours of sleep they got. Almost 370,000 adolescents participated. The researchers focused on how much sleep teens reported getting in the years from 2009 to 2015, "when the mobile technology really saturated the market among adolescents," said Zlatan Krizan, a psychologist specializing in sleep and social behaviour at Iowa State University and co-author of the study. Zlatan Krizan, a psychology researcher specializing in sleep, personality and social behaviour at Iowa State University, was one of the authors of a recent study that showed a trend of teens getting less sleep over the years they started using smartphones. (Iowa State University) Krizan and his colleagues found that teens were 16 to 17 per cent more likely to report getting less than seven hours of sleep a night in 2015 than they were in 2009. The recommended amount of sleep for 13 to 18-year-olds is eight to 10 hours per night, according to the U.S. Centers for Disease Control and Prevention. ©2017 CBC/Radio-Canada.

Keyword: Sleep; Development of the Brain
Link ID: 24273 - Posted: 11.01.2017

Sara Reardon Human genome databases are enabling researchers to take a deeper dive into the evolution of psychiatric disorders. Psychiatric disorders can be debilitating and often involve a genetic component, yet, evolution hasn’t weeded them out. Now, recent work is beginning to reveal the role of natural selection — offering a peek at how the genetic underpinnings of mental illness has changed over time. Many psychiatric disorders are polygenic: they can involve hundreds or thousands of genes and DNA mutations. It can be difficult to track how so many genetic regions evolved, and such studies require large genome data sets. But the advent of massive human genome databases is enabling researchers to look for possible connections between mental illnesses and the environmental and societal conditions that might have driven their emergence and development. Others are looking to Neanderthal genetic sequences to help inform the picture of these disorders, as well as cognitive abilities, in humans. Several of these teams presented their findings at the American Society of Human Genetics (ASHG) meeting in Orlando, Florida, in late October. One project found that evolution selected for DNA variants thought to protect against schizophrenia. The study, led by population geneticist Barbara Stranger of the University of Chicago in Illinois, looked at hundreds of thousands of human genomes using a statistical method that identified signals of selection over the past 2,000 years1. There were no signs of selection in genetic regions associated with any other mental illness. Many of schizophrenia's symptoms, such as auditory hallucinations and jumbling sentences, involve brain regions tied to speech, says Bernard Crespi, an evolutionary biologist at Simon Fraser University in Burnaby, Canada. Over the course of hominid evolution, he says, the ability to speak could have outweighed the small, but unavoidable risk that the genes involved in language could malfunction and result in schizophrenia in a small percentage of the population. © 2017 Macmillan Publishers Limited

Keyword: Schizophrenia; Depression
Link ID: 24270 - Posted: 10.31.2017

By Jessica Hamzelou Can you catch Alzheimer’s disease? Fear has been growing that the illness might be capable of spreading via blood transfusions and surgical equipment, but it has been hard to find any evidence of this happening. Now a study has found that an Alzheimer’s protein can spread between mice that share a blood supply, causing brain degeneration, and suggesting that the disease may transmissible in a similar way to Creutzfeldt-Jacob Disease (CJD). We already know from CJD that misfolded proteins can spread brain diseases. Variant CJD can spread through meat products or blood transfusions infected with so-called prion proteins, for example. Like CJD, Alzheimer’s also involves a misfolded protein called beta-amyloid. Plaques of this protein accumulate in the brains of people with the illness, although we still don’t know if the plaques cause the condition, or are merely a symptom. There has been evidence that beta-amyloid may spread like prions. Around 50 years ago, many people with a growth disorder were treated with growth hormone taken from cadavers. Many of the recipients went on to develop CJD, as these cadavers turned out to be carrying prions. But decades later, it emerged in postmortems that some of these people had also developed Alzheimer’s plaques, despite being 51 or younger at the time. The team behind this work suggested investigating whether beta-amyloid was spreading via blood products or surgical instruments, just as they can spread prions. © Copyright New Scientist Ltd

Keyword: Alzheimers; Prions
Link ID: 24266 - Posted: 10.31.2017

There is no good evidence that a nutrient drink being sold online in the UK to "help" people with early Alzheimer's actually slows the disease, say experts. Latest trial results in patients who took Souvenaid did not find it preserves memory and thinking. The authors say in Lancet Neurology that bigger studies are needed to show if the product can work as hoped. And consumers should be aware that the £3.49 per bottle drink "is not a cure". Manufacturer Nutricia says its drink should only be taken under the direction of a doctor, specialist nurse or pharmacist. Souvenaid comes in strawberry or vanilla flavour and contains a combination of fatty acids, vitamins and other nutrients. Taken once daily, the idea is that the boost of nutrients it provides will help keep Alzheimer's at bay in people with the earliest signs of this type of dementia. But the latest phase two clinical trial results do not prove this. What the trial found The study involved 311 patients with very early Alzheimer's or mild cognitive impairment. All of them were asked to take a daily drink, but only half were given Souvenaid - the other half received one with no added nutrients. After two years of participating, the patients were reassessed to see if there was any difference between the two groups in terms of dementia progression, measured by various memory and cognitive tests. The treatment did not appear to offer an advantage, although patients in the Souvenaid group did have slightly less brain shrinkage on scans, which the researchers say is promising because shrinkage in brain regions controlling memory is seen with worsening dementia. But experts remain cautious. Prof Tara Spires-Jones, a dementia expert at the University of Edinburgh, said: "Some of the other tests of brain structure and function were promising, but overall this study indicates that a specific change in nutrition is unlikely to make a large difference to people with Alzheimer's, even in the early stages. © 2017 BBC.

Keyword: Alzheimers
Link ID: 24265 - Posted: 10.31.2017

By Nicholas Kristof The colored parts of the image above, prepared by Columbia University scientists, indicate where a child’s brain is physically altered after exposure to this pesticide. This chemical, chlorpyrifos, is hard to pronounce, so let’s just call it Dow Chemical Company’s Nerve Gas Pesticide. Even if you haven’t heard of it, it may be inside you: One 2012 study found that it was in the umbilical cord blood of 87 percent of newborn babies tested. And now the Trump administration is embracing it, overturning a planned ban that had been in the works for many years. The Environmental Protection Agency actually banned Dow’s Nerve Gas Pesticide for most indoor residential use 17 years ago — so it’s no longer found in the Raid you spray at cockroaches (it’s very effective, which is why it’s so widely used; then again, don’t suggest this to Dow, but sarin nerve gas might be even more effective!). The E.P.A. was preparing to ban it for agricultural and outdoor use this spring, but then the Trump administration rejected the ban. That was a triumph for Dow, but the decision stirred outrage among public health experts. They noted that Dow had donated $1 million for President Trump’s inauguration. So Dow’s Nerve Gas Pesticide will still be used on golf courses, road medians and crops that end up on our plate. Kids are told to eat fruits and vegetables, but E.P.A. scientists found levels of this pesticide on such foods at up to 140 times the limits deemed safe. © 2017 The New York Times Company

Keyword: Neurotoxins; Development of the Brain
Link ID: 24264 - Posted: 10.30.2017