Chapter 13. Memory, Learning, and Development

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By Michael Price First piloted as an experiment to reduce dental cavities in Grand Rapids, Michigan, in 1945, fluoridated drinking water has since been hailed by the U.S. Centers for Disease Control and Prevention in Atlanta as “one of public health’s greatest success stories.” Today, about two-thirds of people in the United States receive fluoridated tap water, as do many people in Australia, Brazil, Canada, New Zealand, Spain, and the United Kingdom. Now, a controversial new study links fluoridation to lower IQ in young children, especially boys whose mothers drank fluoridated water while pregnant. Longtime fluoridation critics are lauding the study, but other researchers say it suffers from numerous flaws that undercut its credibility. Either way, “It’s a potential bombshell,” says Philippe Grandjean, an environmental health researcher at Harvard University who wasn’t involved in the work. Fluoride is well-known for protecting teeth against cavities by strengthening tooth enamel. It’s found naturally in low concentrations in both freshwater and seawater, as well as in plant material, especially tea leaves. Throughout the 1940s and ’50s, public health researchers and government officials in cities around the world experimentally added fluoride to public drinking water; they found it reduced the prevalence of cavities by about 60%. Today, fluoridated water flows through the taps of about 5% of the world’s population, including 66% of Americans and 38% of Canadians. Yet skepticism has dogged the practice for as long as it has existed. Some have blamed fluoridated water for a wide range of illnesses including cancer, but most criticism has been dismissed as pseudoscience. Over the years, though, a small number of scientists have published meta-analyses casting doubt on the efficacy of water fluoridation in preventing cavities. More recently, scientists have published small-scale studies that appear to link prenatal fluoride exposure to lower IQ, although dental research groups were quick to challenge them. © 2019 American Association for the Advancement of Science.

Keyword: Development of the Brain; Intelligence
Link ID: 26516 - Posted: 08.19.2019

Ashley Yeager Drops of blood, filter paper, bacteria, a bacterial inhibitor, and a baking dish—that’s all it took for microbiologist Robert Guthrie to develop a basic test for phenylketonuria, a genetic metabolic disease that, if left untreated in infants, soon leads to neurological dysfunction and intellectual disability. The test would lay the foundation for screening newborns for diseases. In 1957, Guthrie met Robert Warner, a specialist who diagnosed individuals with mental disabilities. Warner told Guthrie about phenylketonuria (PKU), now known to affect roughly 1 in 10,000 children. The disease makes it impossible to break down the amino acid phenylalanine, so that it builds up to toxic levels in the body and disrupts neuronal communication. Once a child was diagnosed, a strict low-phenylalanine diet could prevent further damage, but Warner had no easy way to measure phenylalanine levels in his PKU patients’ blood to monitor the diet’s effects. He asked Guthrie for help. Guthrie reported back to Warner three days later with a solution. Guthrie knew from past work that the bacterial inhibitor β-2-thienylalanine blocked Bacillus subtilis from flourishing by substituting for phenylalanine in growing peptide chains, resulting in inactive proteins. He also knew that adding phenylalanine to the cell cultures restored normal protein function and spurred the bacterium’s growth. So his solution was simple: prick the skin, collect a few drops of blood on filter paper, and place the filter paper in a baking pan covered in β-2-thienylalanine. Add Bacillus subtilis to the filter paper and heat the pan overnight. If the bacterium grows exponentially, the level of phenylalanine is high. The assay worked well, so Guthrie used it as a model to develop tests for other metabolic diseases. © 1986–2019 The Scientist

Keyword: Development of the Brain; Genes & Behavior
Link ID: 26515 - Posted: 08.19.2019

Researchers believe that stuttering — a potentially lifelong and debilitating speech disorder — stems from problems with the circuits in the brain that control speech, but precisely how and where these problems occur is unknown. Using a mouse model of stuttering, scientists report that a loss of cells in the brain called astrocytes are associated with stuttering. The mice had been engineered with a human gene mutation previously linked to stuttering. The study (link is external), which appeared online in the Proceedings of the National Academy of Sciences, offers insights into the neurological deficits associated with stuttering. The loss of astrocytes, a supporting cell in the brain, was most prominent in the corpus callosum, a part of the brain that bridges the two hemispheres. Previous imaging studies have identified differences in the brains of people who stutter compared to those who do not. Furthermore, some of these studies in people have revealed structural and functional problems in the same brain region as the new mouse study. The study was led by Dennis Drayna, Ph.D., of the Section on Genetics of Communication Disorders, at the National Institute on Deafness and Other Communication Disorders (NIDCD), part of the National Institutes of Health. Researchers at the Washington University School of Medicine in St. Louis and from NIH’s National Institute of Biomedical Imaging and Bioengineering, and National Institute of Mental Health collaborated on the research. “The identification of genetic, molecular, and cellular changes that underlie stuttering has led us to understand persistent stuttering as a brain disorder,” said Andrew Griffith, M.D., Ph.D., NIDCD scientific director. “Perhaps even more importantly, pinpointing the brain region and cells that are involved opens opportunities for novel interventions for stuttering — and possibly other speech disorders.”

Keyword: Language; Glia
Link ID: 26513 - Posted: 08.19.2019

Laura Sanders Seconds before a memory pops up, certain nerve cells jolt into collective action. The discovery of this signal, described in the Aug. 16 Science, sheds light on the mysterious brain processes that store and recall information. Electrodes implanted in the brains of epilepsy patients picked up neural signals in the hippocampus, a key memory center, while the patients were shown images of familiar people and places, including former President Barack Obama and the Eiffel Tower in Paris. As the participants took in this new information, electrodes detected a kind of brain activity called sharp-wave ripples, created by the coordinated activity of many nerve cells in the hippocampus. Later blindfolded, the patients were asked to remember the pictures. One to two seconds before the participants began describing each picture, researchers noticed an uptick in sharp-wave ripples, echoing the ripples detected when the subjects had first seen the images. That echo suggests that these ripples are important for learning new information and for recalling it later, Yitzhak Norman of the Weizmann Institute of Science in Rehovot, Israel, and colleagues write in the study. Earlier studies suggested that these ripples in the hippocampus were important for forming memories. But it wasn’t clear if the ripples also had a role in bringing memories to mind. In another recent study, scientists also linked synchronized ripples in two parts of the brain to better memories of word pairs (SN Online: 3/5/19). |© Society for Science & the Public 2000 - 2019

Keyword: Learning & Memory
Link ID: 26512 - Posted: 08.19.2019

By John Horgan At the beginning of my book Mind-Body Problems, I describe one of my earliest childhood memories: I am walking near a river on a hot summer day. My left hand grips a fishing rod, my right a can of worms. One friend walks in front of me, another behind. We’re headed to a spot on the river where we can catch perch, bullheads and large-mouth bass. Weeds bordering the path block my view of the river, but I can smell its dank breath and feel its chill on my skin. The seething of cicadas builds to a crescendo. I stop short. I’m me, I say. My friends don’t react, so I say, louder, I’m me. The friend before me glances over his shoulder and keeps walking, the friend behind pushes me. I resume walking, still thinking, I’m me, I’m me. I feel lonely, scared, exhilarated, bewildered. Advertisement That moment was when I first became self-conscious, aware of myself as something weird, distinct from the rest of the world, demanding explanation. Or so I came to believe when I recalled the incident in subsequent decades. I never really talked about it, because it was hard to describe. It meant a lot to me, but I doubted it would mean much to anyone else. Then I learned that others have had similar experiences. One is Rebecca Goldstein, the philosopher and novelist, whom I profiled in Mind-Body Problems. Before interviewing Goldstein, I read her novel 36 Arguments for the Existence of God, and I came upon a passage in which the hero, Cass, a psychologist, recalls a recurrent “metaphysical seizure” or “vertigo” that struck him in childhood. Lying in bed, he was overcome by the improbability that he was just himself and no one else. “The more he tried to get a fix on the fact of being Cass here,” Goldstein writes, “the more the whole idea of it just got away from him.” Even as an adult, Cass kept asking himself, “How can it be that, of all things, one is this thing, so that one can say, astonishingly, ‘Here I am’”? © 2019 Scientific American

Keyword: Consciousness; Development of the Brain
Link ID: 26510 - Posted: 08.17.2019

Laura Sanders Alzheimer’s disease destroys command centers in the brain that keep people awake. That finding could explain why the disease often brings daytime drowsiness. Sleep problems can precede dementias, including Alzheimer’s, sometimes by decades. But the new result, described online August 12 in Alzheimer’s & Dementia, suggests that disordered sleeping isn’t just an early harbinger of Alzheimer’s. Instead, sleep trouble is “part of the disease,” says Lea Grinberg, a neuropathologist at the University of California, San Francisco. Grinberg and colleagues focused on the brain stem and a structure perched above it called the hypothalamus. Together, these parts of the nervous system oversee crucial jobs such as keeping people awake and paying attention. Though important, the brain stem and its neighbors have been largely overlooked in studies of dementia, Grinberg says. In particular, the researchers searched for evidence of tau, a protein that can form tangles inside nerve cells, in postmortem brains of people who died with Alzheimer’s disease. Three small regions of the hypothalamus and brain stem, all of which usually contain nerve cells that keep people awake during the day, were packed with tau, the team found. And two of the three areas had lost over 70 percent of their nerve cells, or neurons. These areas “are hit hard, and they are hit by tau,” Grinberg says. That destruction could be part of the reason people with Alzheimer’s disease often feel tired during the day, even if they slept the night before. |© Society for Science & the Public 2000 - 2019.

Keyword: Alzheimers
Link ID: 26509 - Posted: 08.17.2019

By John Williams The first, startling epigraph in Nicci Gerrard’s new book, “The Last Ocean,” comes from Emily Dickinson: “Abyss has no Biographer.” Gerrard sets out to tell the story of dementia, a disease that can appear to consume those it afflicts. After her father, John, died in 2014, the author — who writes best-selling thrillers with her husband under the name Nicci French — embarked on learning more about the disease as both a journalist and an activist. The result is a tender, inquisitive tour of a subject that can be raw and painful. Below, Gerrard talks about loss, art that punches you in the solar plexus and the experience of writing a book that doesn’t answer questions. When did you first get the idea to write this book? I first had the idea when my father, who’d been living with dementia for over 10 years, went into hospital in February 2014. After four weeks without anyone to see him — we were allowed in for very limited times and then not at all, because of a norovirus outbreak — I barely recognized him. I will, for the rest of my life, feel terribly that I didn’t get him out earlier. Then he lived at home for nine months. He had become skeletal, immobile, inarticulate, and in a way he felt utterly lost, like a ghost in our lives and in his own life. He would lay downstairs in a hospital bed, looking outside at the garden he used to love. There was this clear sense that he’d already lost everything he had, everything he was, all his capacity, there was nothing left — and yet somehow that he didn’t lose himself. In the book I say that if I were religious, I would call that self he retained his soul. Something very indelible remained. © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26508 - Posted: 08.17.2019

By Dylan Loeb McClain Kary B. Mullis, a biochemist who won the 1993 Nobel Prize in Chemistry for discovering a way to analyze DNA easily and cheaply and thus pave the way for major advances in medical diagnostics, molecular biology and forensic science, died on Aug. 7 at his home in Newport Beach, Calif. He was 74. The cause was heart and respiratory failure brought on by pneumonia, his wife, Nancy Cosgrove Mullis, said. The process for analyzing DNA that Dr. Mullis invented is called polymerase chain reaction, or PCR. It replicates a single strand of DNA millions of times, enabling scientists to pinpoint a segment of the strand and amplify it for identification. Polymerase, an enzyme that synthesizes polymers and nucleic acids, is essential in creating DNA and RNA, the molecules that are responsible for coding DNA. Before PCR, amplifying DNA took weeks, because it had to be generated in bacteria. Once Dr. Mullis’s process was perfected, it took only hours, opening up a world of possibilities. We’ll bring you stories that capture the wonders of the human body, nature and the cosmos. Today, his method is used to detect genetic mutations that can lead to diagnoses of diseases, like sickle cell anemia; analyze ancient sources of DNA, like bones; assist in obtaining crime scene evidence; and determine paternity. It was used as well to decode and map the entire human DNA as part of the Human Genome Project, the landmark international research effort that ran from 1990 to 2003. As he told the story in his Nobel lecture, Dr. Mullis found his inspiration one night in 1983 while driving to his cabin in Mendocino, Calif. © 2019 The New York Times Company

Keyword: Genes & Behavior
Link ID: 26505 - Posted: 08.16.2019

By Bret Stetka Among the human body’s many maladies, few have stumped medical researchers like those that decimate the brain. After decades of effort, effectively treating—let alone curing—neurodegenerative disorders such as Huntington’s and Alzheimer's disease has been a source of frustration for many, as old theories are questioned and clinical trials fail. Basic scientists have achieved some progress. Over the past few decades, they have made serious headway in identifying single inherited genes responsible for genetic forms of various neurodegenerative diseases such as Alzheimer’s—and also the molecular and neural mechanisms behind nongenetic, or sporadic, forms of brain maladies. Yet translating these findings into working therapies has proved challenging. With genetic engineering technologies, such as CRISPR, that literally rewrite our DNA still a ways away from routine use, a number of clinical researchers have turned to a more immediate genome-based approach to treat disorders of the brain: manipulating RNA to modify levels of proteins associated with disease. DNA provides our genetic code, with its sister molecule RNA translating that code into the proteins that run our brains and myriad bodily functions. Scientists can now use molecules called antisense oligonucleotides (ASOs) to modify this process by binding to RNA and altering translation. ASOs are DNA-like molecules that greatly resemble the DNA that produced the RNA they correspond to in the first place. Depending on where they are designed to bind, these antisense molecules can prevent an RNA from being translated into a protein, which reduces levels of that protein in the body or brain. Alternatively, these same DNA-like molecules can be crafted to interfere with RNA machinery that normally inhibits or slows translation. In this case, more protein is made. © 2019 Scientific American

Keyword: Alzheimers; ALS-Lou Gehrig's Disease
Link ID: 26504 - Posted: 08.15.2019

Patti Neighmond Most children enrolled in Medicaid who get a diagnosis of attention deficit hyperactivity disorder don't get timely or appropriate treatment afterward. That's the conclusion of a report published Thursday by a federal watchdog agency, the Department of Health and Human Services' Office of Inspector General. "Nationwide, there were 500,000 Medicaid-enrolled children newly prescribed an ADHD medication who did not receive any timely follow-up care," says Brian Whitley, a regional inspector general with OIG. The report analyzed Medicaid claims data from 2014 and 2015. Those kids didn't see a health care provider regarding their ADHD within a month of being prescribed the medication, though pediatric guidelines recommend that, he says. And one in five of those children didn't get the two additional check-ins with a doctor they should get within a year. "That's a long time to be on powerful medications without a practitioner checking for side effects or to see how well the medication is working," Whitley says. Additionally, according to the OIG report, "Nearly half of Medicaid-enrolled children who were newly prescribed an ADHD medication did not receive behavioral therapy," though that, too, is recommended by pediatricians. Elizabeth Cavey, who lives with her family in Arlington, Va., knows just how important it is to get a child with ADHD accurately diagnosed and treated. Kindergarten, Cavey says, was a disaster for her daughter. "She was constantly being reprimanded and forced to sit still," Cavey recalls. "And she's a bright child, but she kept falling further and further behind in learning letters and language, because she could not concentrate." © 2019 npr

Keyword: ADHD; Development of the Brain
Link ID: 26500 - Posted: 08.15.2019

­­­In a nationwide study, researchers used magnetic resonance imaging (MRI) to scan the brains of hundreds of participants in the National Institutes of Health’s Systolic Blood Pressure Intervention Trial (SPRINT) and found that intensively controlling a person’s blood pressure was more effective at slowing the accumulation of white matter lesions than standard treatment of high blood pressure. The results complement a previous study published by the same research group which showed that intensive treatment significantly lowered the chances that participants developed mild cognitive impairment. “These initial results support a growing body of evidence suggesting that controlling blood pressure may not only reduce the risk of stroke and heart disease but also of age-related cognitive loss,” said Walter J. Koroshetz, M.D., director of the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). “I strongly urge people to know your blood pressure and discuss with your doctors how to optimize control. It may be a key to your future brain health.” Brain white matter is made up of billions of thin nerve fibers, called axons, that connect the neurons with each other. The fibers are covered by myelin, a white fatty coating that protects axons from injury and speeds the flow of electrical signals. White matter lesions, which appear bright white on MRI scans, represent an increase in water content and reflect a variety of changes deep inside the brain, including the thinning of myelin, increased glial cell reactions to injury, leaky brain blood vessels, or multiple strokes. These changes are associated with high blood pressure, or “hypertension”.

Keyword: Alzheimers
Link ID: 26496 - Posted: 08.14.2019

Todd Golde and Steven DeKosky Dr. Todd Golde is a co-founder of Lacerta Therapeutics, Inc. and serves on their scientific advisory board (SAB). He is on the SAB for Promis Neuroscience, Inc. In the past he has served, ad hoc, on SABs related to neurodegenerative disease programs for Eli Lilly, Novartis, Bristol Myers Squib, Abbvie, Lundbeck, Biogen and Pfizer. He is co-editor in chief of Alzheimer’s Research and Therapy for which he receives an honorarium. He has served on the medical and scientific advisory board for the Alzheimer’s Association. He serves as a scientific advisor and participates in grant reviews for BrightFocus Foundation and the American Federation for Aging Research. He is a co-inventor on multiple patents and patent applications relating to AD therapeutics. He currently receives funding from the NIH. Steven DeKosky receives grant funding from the National Institute of Aging, serves as a consultant for Amgen, Biogen, and Cognition Therapeutics, and serves as editor for dementia for Up-To-Date, a point-of-care electronic textbook. He has chaired study sections for the NIH, served on two NIH councils, for the National Center for Complementary and Alternative Medicine (now the National Center for Complementary and Integrative Health; NCCIH) and the Director's Council (Council of Councils). He has served on the board of the Alzheimer's Association and chaired their Medical and Scientific Advisory Council, as well as chairing the Medical and Scientific Advisory Panel of Alzheimer's Disease International. © 2010–2019, The Conversation US, Inc.

Keyword: Alzheimers
Link ID: 26495 - Posted: 08.14.2019

By Jane E. Brody Early to bed, early to rise — a fine plan for a dairy farmer who has to get up long before dawn to milk the cows. But if you’re someone who works all day with stocks and clients and may want to enjoy an evening out now and then, it would be better not to be getting up at 2 a.m. and have to struggle to stay awake through dinner or a show. Such is the challenge faced by a friend who has what sleep specialists call an advanced sleep phase. Her biological sleep-wake cycle, or circadian rhythm, is out of sync with the demands of the modern world. My friend, who asked to remain anonymous, has always been an early riser, even as a teenager. Getting up at 5 was an advantage in high school — she never had to worry about being late. But as she aged, her nights kept getting shorter. Now at age 63 she’s ready to go to sleep before 9 p.m., but that rarely fits with the demands of her life. No matter how delayed her bedtime, she gets up by 4 in the morning — and sometimes as early as 1:30 — and can’t get back to sleep. She said that given her stimulating job as an investment products specialist, she’s not sleepy during the day, nor does she nap. Still, she’s concerned about her short nights, partly because she’s read that insufficient sleep — especially not enough REM sleep, when dreams occur — has been linked to a possible increased risk of Alzheimer’s disease. She knows that late dinners, especially with wine, contribute to her sleep problem. But it’s also likely that her lifelong dairy-farmer sleep pattern is programmed by her genes, not the result of unavoidable disruptions or unwise living habits. And, it seems, her early-to-sleep, early-to-wake rhythm may not be as extremely rare as has long been believed. In a new study in the journal Sleep by researchers in San Francisco, Salt Lake City and Madison, Wis., of more than 2,400 patients who visited a sleep clinic for complaints like sleep apnea or insomnia, a small number of them were found to have a previously unrecognized familial form of advanced sleep phase, a kind of permanent jet lag that the study showed often runs in families. © 2019 The New York Times Company

Keyword: Biological Rhythms; Genes & Behavior
Link ID: 26488 - Posted: 08.12.2019

By Paula Span Juli Engel was delighted when a neurologist recommended a PET scan to determine whether amyloid — the protein clumps associated with an increased risk of Alzheimer’s disease — was accumulating in her mother’s brain. “My internal response was, ‘Yay!’” said Ms. Engel, 65, a geriatric care manager in Austin, Tex., who has been making almost monthly trips to help her mother in Florida. “He’s using every tool to try to determine what’s going on.” Sue Engel, who’s 83 and lives in a retirement community in Leesburg, Fla., has been experiencing memory problems and other signs of cognitive decline for several years. Her daughter checked off the warning signs: her mother has been financially exploited, suffered an insurance scam, caused an auto accident. Medicare officials decided in 2013, shortly after PET (positron emission tomography) amyloid imaging became available, that they lacked evidence of its health benefits. So outside of research trials, Medicare doesn’t cover the scans’ substantial costs ($5,000 to $7,000, the Alzheimer’s Association says); private insurers don’t, either. Juli Engel thinks Medicare should reimburse for the scan, but “if necessary, we’ll pay for it out of pocket,” she said. Her mother already has an Alzheimer’s diagnosis and is taking a commonly prescribed dementia drug. So she probably doesn’t meet the criteria developed by the Alzheimer’s Association and nuclear medicine experts, which call for PET scans only in cases of unexplained or unusual symptoms and unclear diagnoses. But as evidence mounts that brain damage from Alzheimer’s begins years before people develop symptoms, worried patients and their families may start turning to PET scans to learn if they have this biomarker. © 2019 The New York Times Company

Keyword: Alzheimers; Brain imaging
Link ID: 26484 - Posted: 08.03.2019

By Michael Buchanan Social affairs correspondent, BBC News Alcohol-related brain damage, a condition similar to dementia, is poorly understood and often missed by health professionals, a study by charity Alcohol Change UK says. And patients struggling with the "double stigma" of brain impairment and alcohol addiction often end up in accident and emergency units because of a lack of community services. The condition affects balance and makes it difficult for patients to process new information. They can also become confused and experience memory loss. At its most basic, the injury is caused by damage to brain cells from alcohol, which causes them to shrink and die or deprives them of vital vitamins. Heavy drinking A man who drinks more than 50 units of alcohol a week, or a woman drinking more than 35 units, for five years or more is at risk of the disease, Alcohol Change says. "You're talking about a condition that's the result of long-term heavy drinking, which a lot of people are going to say, 'Well someone's done that themselves, it's his own fault,'" Andrew Misell, from Alcohol Change UK, said. "And then you're talking about a condition which makes someone's behaviour difficult to manage - people can be aggressive, inappropriate, confused and confusing to others" Last year, the alcohol care team at the Royal Liverpool Hospital treated 79 patients with alcohol-related brain disease. Patients are asked to sit a test used to diagnose dementia, which has been adapted for this condition. A low score can lead to scans to see if the patient's alcohol intake has shrunk their brain. If it has, an occupational therapist is then brought in to find out how the brain damage has affected that person's daily life. © 2019 BBC

Keyword: Drug Abuse; Alzheimers
Link ID: 26483 - Posted: 08.03.2019

By Emily S. Rueb Excessive alcohol consumption is not safe for a person at any age, but it is particularly dangerous for older adults. And according to a study published this week, about one in 10 older adults is considered a binge drinker. “Binge drinking, even episodically or infrequently, may negatively affect other health conditions by exacerbating disease, interacting with prescribed medications and complicating disease management,” said Dr. Benjamin Han, the lead author of the study that was published on Wednesday in the Journal of the American Geriatrics Society. Alcohol is also a risk factor for injury, Dr. Han said, but the consequences and recovery from a fall are much more serious for an 81-year-old than a 21-year-old. The study defined binge drinking as consuming five or more drinks in a sitting for men, and four or more drinks in a sitting for women. And a drink equaled a can or bottle of beer, a glass of wine or a wine cooler, a shot of liquor, or a mixed drink with liquor in it. Dr. Han’s group analyzed data from the annual U.S. National Survey on Drug Use and Health between 2015 and 2017. In all, the findings included 10,927 adults aged 65 or older who reported their drinking habits in the previous 30 days. The group did not include adults living in long-term-care facilities or nursing homes, Dr. Han added. The prevalence of binge drinking among adults 65 and older is still relatively low compared with other age groups, Dr. Han said. Over 38 percent of college-aged adults, 18 to 25, had recently drunk excessively, the highest prevalence of any age group. Adults ages 26 to 34 had only slightly fewer binge drinkers, and the second highest percentage, the study found. © 2019 The New York Times Company

Keyword: Drug Abuse; Development of the Brain
Link ID: 26482 - Posted: 08.03.2019

By Gina Kolata For decades, researchers have sought a blood test for beta amyloid, the protein that is a hallmark of Alzheimer’s disease. Several groups and companies have made progress, and on Thursday, scientists at Washington University in St. Louis reported that they had devised the most sensitive blood test yet. The test will not be available for clinical use for years, and in any event, amyloid is not a perfect predictor of Alzheimer’s disease: Most symptomless older people with amyloid deposits in their brains will not develop dementia. But the protein is a significant risk factor, and the new blood test identified patients with amyloid deposits before brain scans did. That will be important to scientists conducting trials of drugs to prevent Alzheimer’s. They need find participants in the earliest stages of the disease. At present, a diagnosis of Alzheimer’s disease is not easy to make. Doctors rely mostly on tests of mental acuity and interviews with the patient and family members. Studies have shown that community doctors are only 50 to 60 percent accurate in diagnosing the condition — about the same as tossing a coin. Methods that can improve accuracy, like PET scans of the brain, are expensive and often not available. The new test relies on mass spectrometry, a tool used in analytical chemistry that, with recent technical advances, can find elusive beta amyloid molecules in blood with high precision. The lead investigator, Dr. Randall Bateman, a neurologist at Washington University, has been working on a mass spectrometry test for 20 years. He and a colleague, Dr. David Holtzman, founded a company ten years ago and licensed patents from their university to commercialize a mass spectrometry test if they ever developed one. © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26481 - Posted: 08.02.2019

By Judith Graham By all accounts, the woman, in her late 60s, appeared to have severe dementia. She was largely incoherent. Her short-term memory was terrible. She couldn’t focus on questions that medical professionals asked her. But Malaz Boustani, a doctor and professor of aging research at Indiana University School of Medicine, suspected something else might be going on. The patient was taking Benadryl for seasonal allergies, another antihistamine for itching, Seroquel (an antipsychotic medication) for mood fluctuations, as well as medications for urinary incontinence and gastrointestinal upset. To various degrees, each of these drugs blocks an important chemical messenger in the brain, acetylcholine. Boustani thought the cumulative impact might be causing the woman’s cognitive difficulties. He was right. Over six months, Boustani and a pharmacist took the patient off those medications and substituted alternative treatments. Miraculously, she appeared to recover completely. Her initial score on the Mini-Mental State Examination had been 11 of 30 — signifying severe dementia — and it shot up to 28, in the normal range. An estimated 1 in 4 older adults take anticholinergic drugs — a wide-ranging class of medications used to treat allergies, insomnia, leaky bladders, diarrhea, dizziness, motion sickness, asthma, Parkinson’s disease, chronic obstructive pulmonary disease and various psychiatric disorders. Older adults are highly susceptible to negative responses to these medications. Since 2012, anticholinergics have been featured prominently on the American Geriatrics Society Beers Criteria list of medications that are potentially inappropriate for seniors. © 1996-2019 The Washington Post

Keyword: Alzheimers
Link ID: 26479 - Posted: 08.02.2019

By Lydia Denworth An elderly woman suffering from late-stage Alzheimer’s disease had neither talked to nor reacted to any of her family members for years. Then, one day, she suddenly started chatting with her granddaughter, asking for news of other family members and even giving her granddaughter advice. “It was like talking to Rip van Winkle,” the granddaughter told University of Virginia researchers of her astonishment. Unfortunately, the reawakening did not last—the grandmother died the next week. That event got written up as what the case study authors called terminal lucidity—a surprising, coherent episode of meaningful communication just before death in someone presumed incapable of social interaction. Yet it was by no means unique. Physician Basil Eldadah, who heads the geriatric branch at the National Institute on Aging (NIA), had heard such stories and filed them away as intriguing accounts. But in 2018, spurred by the need to make progress combatting Alzheimer’s, Eldadah began to think it was time to do more and organized a workshop for interested scientists. After all, if the grandmother was able to tap into mysterious neural reserves, cases such as hers might help scientists explore how cognition could possibly be restored—even briefly—in patients with the most advanced neurodegenerative disease. This summer Eldadah and the scientists he assembled have taken the first steps toward systematic and rigorous study of what they are now calling paradoxical lucidity, a broader label intended to capture the dramatic, unexpected and puzzling nature of the phenomenon. The workshop participants published two papers on it in the August issue of Alzheimer’s and Dementia, and the NIA announced plans to fund relevant research next year. The early goals are modest—the formulation of an operational definition and a gauging of the phenomenon’s prevalence. The possible long-term implications, however, are tantalizing. “If the brain were able to access that normal state, even if it’s transient, it would suggest that there’s some requisite level of machinery that can work under some kind of unique circumstance,” anesthesiologist and neuroscientist George Mashour, director of the Center for Consciousness Science at the University of Michigan and lead author of one of the papers, says. © 2019 Scientific American

Keyword: Alzheimers
Link ID: 26474 - Posted: 08.01.2019

By Nicholas Bakalar A new study confirms earlier reports that anemia — a condition caused by having too little hemoglobin, the oxygen-carrying component of red blood cells — increases the risk for dementia. It found that having high hemoglobin levels does so as well. Dutch researchers looked at 12,305 people without dementia at the start of the study, measuring their hemoglobin levels and following them for an average of 12 years. Over the period, 1,520 developed dementia, including 1,194 with Alzheimer’s disease. The study is in Neurology. The scientists divided the hemoglobin levels into five groups, low to high. Compared with those in the middle one-fifth, those in the highest fifth had a 20 percent increased risk for any dementia type, and a 22 percent increased risk for Alzheimer’s. Those in the lowest were at a 29 percent increased risk for dementia and a 36 percent increased risk for Alzheimer’s. The researchers controlled for education level, blood pressure, diabetes, lipid-lowering medication, alcohol intake and other health and behavioral characteristics. “We don’t have the intervention studies that would show that modifying hemoglobin could prevent dementia,” said the lead author, Frank J. Wolters, a researcher at Erasmus University Medical Center in Rotterdam, “and we can’t recommend interventions based on this study. In the meantime, given the other beneficial effects of treating anemia, this study provides an extra incentive.” © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26473 - Posted: 08.01.2019