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By Karen Weintraub Research on Alzheimer’s has mainly focused on Caucasians. New findings, however, suggest the disease process that leads to dementia may differ in African–Americans. According to a study published Monday in JAMA Neurology, the brains of African–Americans diagnosed with Alzheimer’s have less buildup of a protein called tau—one of the two hallmark proteins that characterize the disease. It is not clear why African–Americans would have less tau while still suffering from Alzheimer’s, says neurologist John Morris, who led the research. But the finding is significant because it means the medical community needs to exercise caution when defining Alzheimer’s by measures of tau buildup alone. The study also suggests race might affect other aspects of the disease’s pathology, says Morris, who directs the Knight Alzheimer Disease Research Center at Washington University in Saint Louis. “The study of Alzheimer’s disease, which really began formally in the United States in the mid-1980s, has largely been of white people,” he notes. “The U.S. in general and the older adult portion of the U.S. population is increasingly diverse, so we really do need to study all populations to try to understand the disease and its forms.” For the moment, the differences detected in the disease’s pathology will not change existing treatment protocols, which do not yet look at certain aberrant proteins to make a diagnosis. Physicians today diagnose Alzheimer’s largely based on a patient’s neuropsychological characteristics. But once researchers have developed a more practical way to measure levels of key proteins involved in the disease, such differences could be crucial for accurate diagnoses, Morris says. Brain scans can detect tau as well as amyloid beta—another protein that builds up in the brains of Alzheimer’s sufferers—but the scans are expensive and not widely available. © 2019 Scientific American,

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25849 - Posted: 01.09.2019

Jon Hamilton Scientists have found a biological clue that could help explain why African-Americans appear to be more vulnerable than white Americans to Alzheimer's disease. A study of 1,255 people, both black and white, found that cerebrospinal fluid from African-Americans tended to contain lower levels of a substance associated with Alzheimer's, researchers report Monday in the journal JAMA Neurology. Yet these low levels did not seem to protect black participants from the disease. The finding "implies that the biological mechanisms underlying Alzheimer's disease may be very different in [different] racial groups," says Dr. John Morris, an author of the paper and director of the Knight Alzheimer's Disease Research Center at Washington University in St. Louis. And if Alzheimer's works differently in African-Americans, that difference could make them more vulnerable to the disease, Morris says. The study has limitations, though, says Lisa Barnes, a cognitive neuropsychologist at the Rush Alzheimer's Disease Center in Chicago, who wrote an accompanying editorial. For example, it could not fully account for the effects of some other known Alzheimer's risk factors — including hypertension, diabetes and obesity — or some suspected risk factors, including stress and poverty. Also, the study included just 173 African-Americans and was able to obtain spinal fluid samples from only half of them. Even so, Barnes says she was excited to see the study "because we have so little data" on African-Americans and other racial and ethnic minorities. © 2019 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25846 - Posted: 01.08.2019

By Paula Span He was a retired factory worker, living with his wife outside a small town in Wales, in the United Kingdom. Once outgoing and sociable, engaged in local activities including a community choir, he’d been jolted by a diagnosis of early dementia. A few months later, at 70, he wouldn’t leave the house alone, fearful that if he needed help, he couldn’t manage to use a cellphone to call his wife. He avoided household chores he’d previously undertaken, such as doing laundry. When his frustrated wife tried to show him how to use the washer, he couldn’t remember her instructions. “He’d lost a lot of confidence,” said Linda Clare, a clinical psychologist at the University of Exeter. “He was actually capable, but he was frightened of making a mistake, getting it wrong.” Dr. Clare directed a recent trial of cognitive rehabilitation in England and Wales in which the patient was enrolled. Cognitive rehabilitation, which Dr. Clare has been researching for 20 years, evolved from methods used to help people with brain injuries. The practice brings occupational and other therapists into the homes of dementia patients to learn which everyday activities they’re struggling with and which abilities they want to preserve or improve upon. Organizing a visit with a friend, perhaps. Keeping track of the day’s appointments and plans. Heating a prepared lunch without burning it. In weekly sessions over several months, the therapists devise individual strategies that can help, at least in the early and moderate stages of the disease. The therapists show patients how to compensate for memory problems and to practice new techniques. Cognitive rehab has its limitations. “We never suggest this can reverse the effects of dementia,” Dr. Clare said. It will not raise participants’ scores on tests of mental ability. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 25840 - Posted: 01.05.2019

In a study of fruit flies, NIH scientists suggested that the body’s immune system may play a critical role in the damage caused by aging brain disorders. The results are based on experiments in which the researchers altered the activity of Cdk5, a gene that preclinical studies have suggested is important for early brain development and may be involved in neurodegenerative diseases, such as ALS, Alzheimer’s and Parkinson’s disease. Previously, they found that altering Cdk5 sped up the genetic aging process, causing the flies to die earlier than normal and have problems with walking or flying late in life and greater signs of neurodegenerative brain damage. In this study, published in Cell Reports, they suggested that altering Cdk5 resulted in the death of dopamine releasing neurons, especially in the brains of older flies. Typically, Parkinson’s disease damages the same types of cells in humans. Further experiments in flies suggested the neuron loss happened because altering Cdk5 slowed autophagy, or a cell’s waste disposal system that rids the body of damaged cells in a contained, controlled fashion, which in turn triggered the immune system to attack the animal’s own neurons. This immune system attack is a much “messier” and more diffuse process than autophagy. Genetically restoring the waste system or blocking the immune system’s responses prevented the reduction in dopamine neurons caused by altering Cdk5. The authors concluded that this chain reaction in which a breakdown in autophagy triggers a widely destructive immune reaction may occur in human brain during several neurodegenerative disorders and that researchers may want to look to these systems for new treatment targets and strategies.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 25836 - Posted: 01.03.2019

Incorporating genetic diversity into a mouse model of Alzheimer’s disease resulted in greater overlap with the genetic, molecular and clinical features of this pervasive human disease, according to a study funded by the National Institute on Aging (NIA), part of the National Institutes of Health. The study also suggests that adding genetic diversity may be key to improving the predictive power of studies using mouse models and increasing their usability for precision medicine research for Alzheimer’s. This research comes out of the newly established Resilience-Alzheimer’s Disease Consortium (Resilience-AD) and was published online Dec. 27, 2018 in the journal Neuron. “This is the first study to show that you can replicate many of the molecular features of Alzheimer’s disease in a genetically diverse mouse model,” said NIA Director Richard J. Hodes, M.D. “It points to a strategy for better use of mouse models for precision medicine research—both basic and translational—for Alzheimer’s disease.” Alzheimer's disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out simple tasks. As many as 5.5 million Americans age 65 and older are estimated to be living with Alzheimer’s disease, the most common form of dementia. A key tool among the multiple efforts to find a treatment or cure for Alzheimer’s, mouse models allow researchers to explore genetic, molecular and even behavioral aspects of disease that can’t be done in humans. The researchers, led by Catherine C. Kaczorowski, Ph.D. (link is external), an associate professor and Evnin Family Chair in Alzheimer’s Research at the Jackson Laboratory, Bar Harbor, Maine, and her graduate student, first author Sarah Neuner, noted that mouse models with Alzheimer’s mutations are important for defining high-risk as well as protective genes and disease mechanisms, and to efficiently test new potential interventions and therapeutics.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25826 - Posted: 12.28.2018

By Laura Spinney A disease mystery with no shortage of leads now has an intriguing new one. Since the 1960s, thousands of children in poor, war-torn regions of East Africa have developed epilepsy-like seizures in which their heads bob to their chest; over time, the seizures worsen, cognitive problems develop, and the victims ultimately die. Researchers have proposed causes for nodding syndrome that include malnutrition, parasites, and viruses, but have not proved a clear link to any of them. Now, the first published examination of the brains of children who died after developing the condition suggests it has a key similarity to certain brain diseases of old age, such as Alzheimer's and Parkinson's: It leaves victims' brains riddled with fibrous tangles containing a protein called tau. "Nodding syndrome is a tauopathy," concludes Michael Pollanen, a pathologist at the University of Toronto in Canada who is lead author of a report published last month in Acta Neuropathologica. Pollanen believes the finding "suggests a totally new line of investigation" into the syndrome. As significant as the discovery of the tangles may be what his group of Canadian and Ugandan researchers didn't find: any sign of the brain inflammation that might be triggered by a parasite or virus. "Our hypothesis is that nodding syndrome is a neurodegenerative disease, like Alzheimer's," Pollanen says. Some who study the condition are skeptical, but the possibility excites researchers working on other tauopathies including Alzheimer's. Childhood forms of those diseases are exceedingly rare, but the nodding syndrome finding "means [tau deposition] is not an age-dependent problem," says John Hardy, of the UK Dementia Research Institute at University College London. Something else must have triggered the tauopathy in these children. And because nodding syndrome struck a small region of East Africa, over a specific time period—in Uganda, the condition appears to be vanishing—its trigger might be relatively easy to identify, and could shed light on the causes of diseases like Alzheimer's, Hardy and others say. © 2018 American Association for the Advancement of Science.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 25805 - Posted: 12.20.2018

Robin McKie Scientists have found an unexpected use for virtual reality headsets: to help pinpoint people who may later develop Alzheimer’s disease. The devices, widely used by computer gamers, display images that can be used to test the navigational skills of people thought to be at risk of dementia. Those who do worse in the tests will be the ones most likely to succumb to Alzheimer’s later in life, scientists now believe. By identifying potential patients far earlier than is possible at present, researchers hope it should then become easier in the long term to develop treatments aimed at halting or slowing their condition. “It is usually thought memory is the first attribute affected in Alzheimer’s,” said project leader Dennis Chan, a neuroscientist based at Cambridge University. “But difficulty with navigation is increasingly recognised as one of the very earliest symptoms. This may predate the onset of other symptoms. “By pinpointing those who are beginning to lose their navigational skills, we hope to show that we can target people at a much earlier stage of the condition and one day become far more effective in treating them.” The discovery that loss of navigational skills was associated with Alzheimer’s disease was made several years ago by Chan and colleagues based at several centres in the UK. These studies used tablet computers to test navigational tasks. © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25790 - Posted: 12.17.2018

Laura Sanders An Alzheimer’s protein found in contaminated vials of human growth hormone can spread in the brains of mice. That finding, published online December 13 in Nature, adds heft to the idea that, in very rare cases, amyloid-beta can travel from one person’s brain to another’s. Decades ago, over a thousand young people in the United Kingdom received injections of growth hormone derived from cadavers’ brains as treatment for growth deficiencies. Four of these people died with unusually high levels of A-beta in their brains, a sign of Alzheimer’s disease (SN: 10/17/15, p. 12). The results hinted that A-beta may have been delivered along with the growth hormone. Now researchers have confirmed not only that A-beta was in some of those old vials, but also that it can spark A-beta accumulation in mice’s brains. Neurologist John Collinge of University College London and colleagues found that brain injections of the contaminated growth hormone led to clumps of A-beta in the brains of mice genetically engineered to produce the protein, while brain injections with synthetic growth hormone did not. The results suggest that A-beta can “seed” the protein in people’s brains, under the right circumstances. Still, that doesn’t mean that Alzheimer’s disease is transmissible in day-to-day life. |© Society for Science & the Public 2000 - 2018

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 25788 - Posted: 12.15.2018

Doing crossword puzzles and Sudoku does not appear to protect against mental decline, according to a new study. The idea of "use it or lose it" when it comes to our brains in later life has previously been widely accepted. The new Scottish study showed that people who regularly do intellectual activities throughout life have higher mental abilities. This provides a "higher cognitive point" from which to decline, say the researchers. But the study did not show that they decline any slower. The work, published in the BMJ, was undertaken by Dr Roger Staff at Aberdeen Royal Infirmary and the University of Aberdeen. It looked at 498 people born in 1936 who had taken part in a group intelligence test at the age of 11. This current study started when they were about 64 years old and they were recalled for memory and mental-processing-speed testing up to five times over a 15-year period. It found engagement in problem solving did not protect an individual from decline. However, engaging in intellectually stimulating activities on a regular basis was linked to level of mental ability in old age. The study uses modelling to look at associations and cannot prove any causal link. Also, many of the participants were unable to complete the whole study - some dropped out, others died. Image copyright Getty Images Previously, some studies have found that cognitive training can improve some aspects of memory and thinking, particularly for people who are middle-aged or older. They found so-called brain training may help older people to manage their daily tasks better. No studies have shown that brain training prevents dementia. And last year a report from the Global Council on Brain Health recommended that people should take part in stimulating activities such as learning a musical instrument, designing a quilt or gardening rather than brain training to help their brain function in later life. © 2018 BBC

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 25771 - Posted: 12.11.2018

By Philip S. Gutis With a slow moving disease like Alzheimer’s, there’s still time for doubt. Perhaps the diagnosis is wrong and the memory holes and struggle for words are just normal aging. Deep in your psyche, there’s still a little spark of hope. But there comes a moment when denial is no longer an option. Like Alzheimer’s itself, the moment creeps up slowly, taking care to not give away too much too soon. My moment came recently, as I was walking past the Bucks County Playhouse in downtown New Hope, Pa. I correctly remembered that my husband, Tim, and I recently saw a show there. I even remembered who went with us. But I had no recollection of what show I had seen. Tim reminded me that it was “Guys and Dolls,” but the memory wasn’t there. No songs, no story, no scenes. Nothing at all. The next morning, I sat quietly on my bed. “Tim,” I said, “It’s coming, isn’t it?” Without asking what I meant, Tim gently said, “Yes, it’s coming.” I cried, of course, but just a little. I’ve known, obviously, that change is coming. I’ve been tested, prodded, injected and studied for well over two years as part of a clinical trial. But looking back, I realize that I’ve still harbored a shadow of doubt. The shadow is gone. The spark of hope has been extinguished. Now we have to seriously plan for the future. Alzheimer’s will continue to steal from me, and, unless there’s an unlikely medical miracle, nothing is going to stop the creeping loss. Loss of memory. Loss of mobility. Loss of freedom. Despite this, I haven’t thrown in the towel. Deep down, I know there’s much more life to live, much more time to fight and to love. The years since my diagnosis haven’t been all bad. A few months after we learned the news, my partner of 12 years and I went to the county courthouse to get married. My sister and my nieces and nephew joined us and took pictures as we kissed for the first time as a married couple and fulfilled the Jewish tradition of breaking a glass for good luck. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25748 - Posted: 12.04.2018

By Mitch Leslie Unlike most cells in our bodies, the neurons in our brain can scramble their genes, scientists have discovered. This genome tampering may expand the brain’s protein repertoire, but it may also promote Alzheimer’s disease, their study suggests. “It’s potentially one of the biggest discoveries in molecular biology in years,” says Geoffrey Faulkner, a molecular biologist at the University of Queensland in Brisbane, Australia, who wasn’t connected to the research. “It is a landmark study,” agrees clinical neurologist Christos Proukakis of University College London. Scientists first discovered that certain cells could shuffle and edit DNA in the 1970s. Some immune cells snip out sections of genes that code for proteins that detect or fight pathogens and splice the remaining pieces together to create new varieties. Our B cells, for example, can potentially spawn about 1 quadrillion types of antibodies, enough to fend off an enormous range of bacteria, viruses, and other attackers. Scientists have seen hints that such genomic reshuffling—known as somatic recombination—happens in our brain. Neurons there often differ dramatically from one another. They often have more DNA or different genetic sequences than the cells around them. To look for definitive evidence of somatic recombination in the brain, neuroscientist Jerold Chun of the Sanford Burnham Prebys Medical Discovery Institute in San Diego, California, and colleagues analyzed neurons from the donated brains of six healthy elderly people and seven patients who had the noninherited form of Alzheimer’s disease, which accounts for most cases. The researchers tested whether the cells harbored different versions of the gene for the amyloid precursor protein (APP), the source of the plaques in the brains of people with Alzheimer’s disease. APP’s gene was a good candidate to examine, the researchers thought, because one of their previous studies suggested neurons from patients with Alzheimer’s disease can harbor extra copies of the gene, an increase that could arise from somatic recombination. © 2018 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25716 - Posted: 11.24.2018

Sara Reardon Drug companies have spent billions of dollars searching for therapies to reverse or significantly slow Alzheimer’s disease, to no avail. Some researchers argue that the best way to make progress is to create better animal models for research, and several teams are now developing mice that more closely simulate how the disease devastates people’s brains. The US National Institutes of Health (NIH), the UK Dementia Research Institute and Jackson Laboratory (JAX) — one of the world’s biggest suppliers of lab mice — are among the groups trying to genetically engineer more sophisticated rodents. Scientists are also probing the complex web of mutations that influences neurological decline in mice and people. “We appreciate that the models we had were insufficient,” says Bruce Lamb, a neuroscientist at Indiana University in Indianapolis who directs the NIH-funded programme. “I think it’s sort of at a critical juncture right now.” Alzheimer’s is marked by cognitive impairment and the build-up of amyloid-protein plaques in the brains of people, but the disease does not occur naturally in mice. Scientists get around this by studying mice that have been genetically modified to produce high levels of human amyloid protein. These mice develop plaques in their brains, but they still do not display the memory problems seen in people. Many experimental drugs that have successfully removed plaques from mouse brains have not lessened the symptoms of Alzheimer’s disease in people. One high-profile stumble came last month, when three companies reported that their Alzheimer’s drugs — from a class called BACE inhibitors — had failed in large, late-stage clinical trials. Although the drugs successfully blocked the accumulation of amyloid protein in mice, they seemed to worsen cognitive decline and brain shrinkage in people. © 2018 Springer Nature Limited.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25715 - Posted: 11.24.2018

By Pam Belluck It’s a rare person in America who doesn’t know of someone with Alzheimer’s disease. The most common type of dementia, it afflicts about 44 million people worldwide, including 5.5 million in the United States. Experts predict those numbers could triple by 2050 as the older population increases. So why is there still no effective treatment for it, and no proven way to prevent or delay its effects? Why is there still no comprehensive understanding of what causes the disease or who is destined to develop it? The answer, you could say, is: “It’s complicated.” And that is certainly part of it. For nearly two decades, researchers, funding agencies and clinical trials have largely focused on one strategy: trying to clear the brain of the clumps of beta amyloid protein that form the plaques integrally linked to the disease. But while some drugs have reduced the accumulation of amyloid, none have yet succeeded in stopping or reversing dementia. And amyloid doesn’t explain everything about Alzheimer’s — not everyone with amyloid plaques has the disease. “It’s not that amyloid is not an important factor,” said Dr. John Morris, director of the Knight Alzheimer’s Disease Research Center at the Washington University School of Medicine in St. Louis. “On the other hand, we’ve had some 200-plus trials since 2001 that have been negative.” Not all trials have targeted amyloid. Some have focused on tau, a protein that, in Alzheimer’s, forms threads that stick together in tangles inside neurons, sandbagging their communications with one another. Tau tangles seem to spread after amyloid accumulates into plaques between neurons. But so far, anti-tau drugs haven’t successfully attacked Alzheimer’s itself. Only five drugs have been approved to treat this dementia, but they address early symptoms and none have been shown to work very well for very long. It’s been 15 years since the last one was approved. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25704 - Posted: 11.20.2018

by Bianca Nogrady It’s a rainy Wednesday morning and Dr Andrew Affleck is driving more carefully than usual on his way to the Neuroscience Research Australia building in Randwick. It’s not just the slick, crowded roads putting the edge on his caution; in the boot of his car, cocooned in several layers of protective container and nestled in ice, is the brain of a human being who was alive only a few hours earlier. It’s no ordinary brain – if any brain could be said to be ordinary – but one that has a deadly secret buried inside. The individual who was until recently embodied within this mass of pink, grey and white tissue died of one of the neurodegenerative diseases that are increasingly a cause of death for our ageing population. Perhaps it was Alzheimer’s disease that gradually robbed them of their connection to reality, or frontotemporal dementia that transformed their personality, or Parkinson’s disease that shook their body and mind. “I really hope that this is the brain that will get us across the line,” says Affleck. At the Sydney Brain Bank, housed within NeuRA, the hope is that scientists will be able to glean some new and vital insight from their tissue. And maybe, one day, that insight will lead to a better understanding, a better treatment, or even a cure. “Every donation, bringing the tissue back into the laboratory, I say to myself, I really hope that this is the tipping point,” says Affleck, a research associate at the Sydney Brain Bank. © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25678 - Posted: 11.14.2018

By Alex Therrien Health reporter, BBC News A five-minute scan could be used to spot people at risk of dementia before symptoms appear, researchers claim. Scientists used ultrasound scanners to look at blood vessels in the necks of more than 3,000 people and monitored them over the next 15 years. They found those with the most intense pulses went on to experience greater cognitive decline over the next decade than the other study participants. Researchers hope it may offer a new way to predict cognitive decline. An international team of experts, led by University College London (UCL), measured the intensity of the pulse travelling towards the brain in 3,191 people in 2002. A more intense pulse can cause damage to the small vessels of the brain, structural changes in the brain's blood vessel network and minor bleeds known as mini-strokes. Over the next 15 years, researchers monitored participants' memory and problem-solving ability. Those with the highest intensity pulse (the top quarter of participants) at the beginning of the study were about 50% more likely to show accelerated cognitive decline over the next decade compared with the rest of the participants, the study found. Researchers said this was the equivalent of about an extra one to one-and-half years of decline. Cognitive decline is often one of the first signs of dementia, but not everyone who experiences it will go on to develop the condition. Researchers said the test could provide a new way to identify people who are at risk of developing dementia, leading to earlier treatments and lifestyle interventions. Controlling blood pressure and cholesterol, having a healthy diet, doing regular exercise and not smoking can all help to stave off dementia, evidence suggests. © 2018 BBC

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25670 - Posted: 11.12.2018

By Paula Span The spouses arriving for the Wednesday afternoon caregivers’ class at the Penn Memory Center in Philadelphia had something on their minds even before Alison Lynn, the social worker leading the session, could start the conversation. A few days before, retired Supreme Court Justice Sandra Day O’Connor had released a letter announcing that she’d been diagnosed with dementia, probably Alzheimer’s disease. “As this condition has progressed, I am no longer able to participate in public life,” she wrote. “I want to be open about these changes, and while I am still able, share some personal thoughts.” It meant something to Ms. Lynn’s participants that the first woman to serve on the Supreme Court would acknowledge, at 88, that she had the same relentless disease that was claiming their husbands and wives (and that killed Justice O’Connor’s husband, too, in 2009). “There’s so much stigma,” Ms. Lynn said. “Caregivers feel so isolated and lonely. They were happy that she would bring light and public attention to this disease.” Justice O’Connor had joined a growing but still tiny group: public figures who choose to share a dementia diagnosis. The breakthrough came in 1994, when Ronald and Nancy Reagan released a handwritten letter disclosing his Alzheimer’s disease. “In opening our hearts, we hope this might promote greater awareness of this condition,” the former president wrote. “Perhaps it will encourage a clearer understanding of the individuals and families who are affected by it.” Musician Glen Campbell and his family reached a similar decision in 2011, announcing his Alzheimer’s diagnosis, and several farewell concerts, in a magazine interview. The concerts became a 15-month tour and an intimate, unflinching documentary. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25662 - Posted: 11.10.2018

Jon Hamilton A substance that gives pot its kick appears to reduce the brain changes associated with Alzheimer's disease – at least in mice. In mice that had been genetically tweaked to develop symptoms like those of Alzheimer's, animals that received a synthetic form of tetrahydrocannabinol for six weeks performed as well as healthy mice on a memory test, scientists reported Tuesday at the Society for Neuroscience meeting in San Diego. Meanwhile, mice given a placebo instead of THC lost the ability to remember where to find the shallow spot in a pool of water. The treated mice also lost fewer brain cells and their brains contained 20 percent less of the sticky plaques associated with Alzheimer's, said researcher Yvonne Bouter of the University Medical Center Goettingen in Goettingen, Germany. Bouter presented the results, which haven't been published in a peer-reviewed journal, at a press conference. The findings suggest that "cannabis could be beneficial for Alzheimer's disease," Bouter said. But even if that's true, she said, it doesn't mean the growing number of healthy older people who smoke pot should celebrate by lighting up. "We did this same experiment in healthy mice," she said, "and they had problems learning." "Should you give Grandpa THC? You should probably be cautious," said Michael Taffe of the Scripps Research Institute, who moderated the press conference. "You could have something that is detrimental, if this does not translate to humans, or the person did not have the disorder." © 2018 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25657 - Posted: 11.09.2018

Richard Harris Powerful drugs that have been used for decades to treat delirium are ineffective for that purpose, according to a study published online Monday in the New England Journal of Medicine. Antipsychotic medications, such as haloperidol (brand name, Haldol), are widely used in intensive care units, emergency rooms, hospital wards and nursing homes. "In some surveys up to 70 percent of patients [in the ICU] get these antipsychotics," says Dr. E. Wesley "Wes" Ely, an intensive care specialist at Vanderbilt University Medical Center. They're prescribed by "very good doctors at extremely good medical centers," he says. "Millions of people worldwide are getting these drugs to treat their delirium." But the drugs can have serious side effects. And Ely says there is no solid research showing that they are effective at treating delirium. Patients with delirium are often confused and incoherent and sometimes can suffer hallucinations. This condition can lead to long-term cognitive problems, including a form of dementia. Ely and colleagues at 16 U.S. medical centers decided to put antipsychotic drugs to a rigorous test. They divided nearly 600 patients who were suffering from delirium into three groups. One group got the powerful antipsychotic haloperidol. A second group got ziprasidone, which is a related medication from a class of drugs called "atypical antipsychotics." A third group got a placebo. © 2018 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25602 - Posted: 10.23.2018

Allison Aubrey By age 40, about one in 10 adults will experience some hearing loss. It happens so slowly and gradually, says audiologist Dina Rollins, "you don't realize what you're missing." And even as it worsens, many people are in denial. By the time someone is convinced they have a hearing problem, age-related memory loss may have already set in. But, here's the good news: Restoring hearing with hearing aids can help slow down cognitive decline. Consider these findings: Researchers tracked about 2,000 older adults in the U.S. both before and after they started using hearing aids. The adults were participants in a big, national study, the Health and Retirement Study. "We found the rate of cognitive decline was slowed by 75 percent following the adoption of hearing aids," says Asri Maharani, a researcher at the University of Manchester in the division of neuroscience and experimental psychology and an author of the paper. "It is a surprising result," Maharani says. The study was published this spring in the Journal of the American Geriatrics Society. To assess cognition over time, researchers performed a battery of tests face-to-face with participants. This was done every two years from 1996 to 2014. One test to assess memory required participants to recall a list of 10 words, both immediately after the words were read aloud, and then again after the participants had been distracted by other tasks. © 2018 npr

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 25599 - Posted: 10.22.2018

By Nicholas Bakalar Having pre-eclampsia — dangerously high blood pressure during pregnancy — is linked to an increased risk for dementia later in life, according to a new study. Up to 5 percent of pregnant women develop pre-eclampsia, usually after the 20th week. In addition to hypertension, the condition can include signs of diminished kidney or liver function. Researchers followed the 1,178,005 Danish women who had given birth between 1978 and 2015. More than 58,000 of them had pre-eclampsia during pregnancy. The study is in BMJ. Having pre-eclampsia doubled the risk for vascular dementia, and quadrupled the risk for women over 65. There was a modest association of pre-eclampsia with Alzheimer’s disease, and none with any other type of dementia. “My advice to a woman who has had pre-eclampsia is the same for dementia as it would be for cardiovascular risk,” said the senior author, Heather A. Boyd, a researcher at the Statens Serum Institut in Copenhagen. “Get the hypertension down, get the weight within normal range, work on lowering the risk for Type 2 diabetes. We still need to confirm this finding in other populations, and then we need to figure out what to do about it. We don’t know at this point what the intervention should be.” © 2018 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 25587 - Posted: 10.18.2018