Chapter 7. Life-Span Development of the Brain and Behavior
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By Andy Coghlan A woman in her 80s has become the first person to be successfully treated with induced pluripotent stem (iPS) cells. A slither of laboratory-made retinal cells has protected her eyesight, fighting her age-related macular degeneration – a common form of progressive blindness. Such stem cells can be coaxed to form many other types of cell. Unlike other types of stem cell, such as those found in an embryo, induced pluripotent ones can be made from adult non-stem cells – a discovery that earned a Nobel prize in 2012. Now, more than a decade after they were created, these stem cells have helped someone. Masayo Takahashi at the RIKEN Laboratory for Retinal Regeneration in Kobe, Japan, and her team took skin cells from the woman and turned them into iPS cells. They then encouraged these to form retinal pigment epithelial cells, which are important for supporting and nourishing the retina cells that capture light for vision. The researchers made a slither of cells measuring just 1 by 3 millimetres. Before transplanting this into the woman’s eye in 2014, they first removed diseased tissue on her retina that was gradually destroying her sight. They then inserted the small patch of cells they had created, hoping they would become a part of her eye and stop her eyesight from degenerating. © Copyright Reed Business Information Ltd.
Heidi Ledford Like a zombie that keeps on kicking, legal battles over mutant mice used for Alzheimer’s research are haunting the field once again — four years after the last round of lawsuits. In the latest case, the University of South Florida (USF) in Tampa has sued the US National Institutes of Health (NIH) for authorizing the distribution of a particular type of mouse used in the field. The first pre-trial hearing in the case is set to begin in a federal court on 21 March. The university holds a patent on the mouse, but the NIH has contracted the Jackson Laboratory, a non-profit organization in Bar Harbor, Maine, to supply the animals to researchers. The USF is now claiming that it deserves some of the money that went to the contractor. If the suit, filed in December 2015, is successful, it could set a precedent for other universities, cautions Robert Cook-Deegan, an intellectual-property scholar at the Washington DC centre of Arizona State University in Tempe. And that would threaten the affordability of and access to lab animals used to investigate. “It feels greedy to me,” Cook-Deegan says. “If other universities start doing this, all it does is push up the cost of research tools.” The mice, on which the USF filed a patent in 1997, express mutated forms of two genes1. These modifications help researchers to study how amyloid plaques develop in the brain, and enable them to investigate behavioural changes that manifest before those plaques appear. © 2017 Macmillan Publishers Limited,
Link ID: 23356 - Posted: 03.15.2017
By Knvul Sheikh As we get older, we start to think a little bit more slowly, we are less able to multitask and our ability to remember things gets a little wobblier. This cognitive transformation is linked to a steady, widespread thinning of the cortex, the brain's outermost layer. Yet the change is not inevitable. So-called super agers retain their good memory and thicker cortex as they age, a recent study suggests. Researchers believe that studying what makes super agers different could help unlock the secrets to healthy brain aging and improve our understanding of what happens when that process goes awry. “Looking at successful aging could provide us with biomarkers for predicting resilience and for things that might go wrong in people with age-related diseases like Alzheimer's and dementia,” says study co-author Alexandra Touroutoglou, a neuroscientist at Harvard Medical School. Touroutoglou and her team gave standard recall tests to a group of 40 participants between the ages of 60 and 80 and 41 participants aged 18 to 35. Among the older participants, 17 performed as well as or better than adults four to five decades younger. When the researchers looked at MRI scans of the super agers' brains, they found that their brains not only functioned more like young brains, they also looked very similar. Two brain networks in particular seemed to be protected from shrinking: the default mode network, which helps to store and recall new information, and the salience network, which is associated with directing attention and identifying important details. In fact, the thicker these regions were, the better the super agers' memory was. © 2017 Scientific American,
By Michael Price The objects and people children play with as early as toddlerhood may provide clues to their eventual sexual orientation, reveals the largest study of its kind. The investigation, which tracked more than 4500 kids over the first 15 years of their lives, seeks to answer one of the most controversial questions in the social sciences, but experts are mixed on the findings. “Within its paradigm, it’s one of the better studies I’ve seen,” says Anne Fausto-Sterling, professor emerita of biology and gender studies at Brown University. The fact that it looks at development over time and relies on parents’ observations is a big improvement over previous studies that attempted to answer similar questions based on respondents’ own, often unreliable, memories, she says. “That being said … they’re still not answering questions of how these preferences for toys or different kinds of behaviors develop in the first place.” The new study builds largely on research done in the 1970s by American sex and gender researcher Richard Green, who spent decades investigating sexuality. He was influential in the development of the term “gender identity disorder” to describe stress and confusion over one’s sex and gender, though the term—and Green’s work more broadly—has come under fire from many psychologists and social scientists today who say it’s wrong to label someone’s gender and sexuality “disordered.” In the decades since, other studies have reported that whether a child plays along traditional gender lines can predict their later sexual orientation. But these have largely been criticized for their small sample sizes, for drawing from children who exhibit what the authors call “extreme” gender nonconformity, and for various other methodological shortcomings. © 2017 American Association for the Advancement of Science
Researchers at Vanderbilt University in Nashville, Tennessee, have discovered that in zebrafish, decreased levels of the neurotransmitter gamma-aminobutyric acid (GABA) cue the retina, the light-sensing tissue in the back of the eye, to produce stem cells. The finding sheds light on how the zebrafish regenerates its retina after injury and informs efforts to restore vision in people who are blind. The research was funded by the National Eye Institute (NEI) and appears online today in Stem Cell Reports. NEI is part of the National Institutes of Health. “This work opens up new ideas for therapies for blinding diseases and has implications for the broader field of regenerative medicine,” said Tom Greenwell, Ph.D., NEI program officer for retinal neuroscience. For years, vision scientists have studied zebrafish to understand their retinal regenerative capacity. Zebrafish easily recover from retinal injuries that would permanently blind a person. Early studies in zebrafish led to the idea that dying retinal cells release signals that trigger support cells in the retinal called Muller glia to dedifferentiate — return to a stem-like state — and proliferate. However, recent studies in the mouse brain and pancreas suggest GABA, a well-characterized neurotransmitter, might also play an important role in regeneration distinct from its role in communicating local signals from one neuron to the next. Scientists studying a part of the brain called the hippocampus found that GABA levels regulate the activity of neural stem cells. When GABA levels are high, the stem cells stay quiet, and if GABA levels decrease, then the stem cells start to divide, explained James Patton, Ph.D., Stevenson Professor of Biological Sciences at Vanderbilt and senior author of the new study in zebrafish retina. A similar phenomenon was reported in mouse pancreas.
By Bahar Gholipour, Spectrum An analysis of whole-genome sequences from more than 5,000 people has unearthed 18 new candidate genes for autism. The study, the largest yet of its kind, was published this week in Nature Neuroscience. The new work identified 61 genes associated with autism, 43 of which turned up in previous studies. An independent study published last month looked at several autism genes and made a strong case for three of the new genes2. Most of the new candidates play roles in cellular processes already implicated in autism and intellectual disability. They also point to possible new treatments. “Eighty percent of them involve common biological pathways that have potential targets for future medicines,” says study investigator Ryan Yuen, research associate at the Hospital for Sick Children in Toronto, Canada. The study is the largest analysis of whole genomes from people with autism and their family members to date. Participants are enrolled in MSSNG, an effort funded by Google and the nonprofit group Autism Speaks to analyze sequences from 10,000 people. Other studies typically focus on the coding regions of the genome, called theexomes. Most of the mutations identified in the new work land in genes, but some affect noncoding regions of the genome. Understanding the role of these noncoding mutations is a “challenging task,” says Ivan Iossifov, associate professor at Cold Spring Harbor Laboratory in New York, who was not involved in the study. “The more data that’s available, the better,” he says. “This paper provides a very useful resource for the community to further study.” © 2017 Scientific American,
by Laura Sanders If your young child is facing ear tubes, an MRI or even extensive dental work, you’ve probably got a lot of concerns. One of them may be about whether the drugs used to render your child briefly unconscious can permanently harm his brain. Here’s the frustrating answer: No one knows. “It’s a tough conundrum for parents of kids who need procedures,” says pediatric anesthesiologist Mary Ellen McCann, a pediatric anesthesiologist at Boston Children’s Hospital. “Everything has risks and benefits,” but in this case, the decision to go ahead with surgery is made more difficult by an incomplete understanding of anesthesia’s risks for babies and young children. Some studies suggest that single, short exposures to anesthesia aren’t dangerous. Still, scientists and doctors say that we desperately need more data before we really understand what anesthesia does to developing brains. It helps to know this nonanswer comes with a lot of baggage, a sign that a lot of very smart and committed people are trying to answer the question. In December, the FDA issued a drug safety communication about anesthetics that sounded alarming, beginning with a warning that “repeated or lengthy use of general anesthetic and sedation drugs during surgeries or procedures in children younger than 3 years or in pregnant women during their third trimester may affect the development of children’s brains.” FDA recommended more conversations between parents and doctors, in the hopes of delaying surgeries that can safely wait, and the amount of anesthesia exposure in this potentially vulnerable population. |© Society for Science & the Public 2000 - 2017.
By Jia Naqvi He loves dancing to songs, such as Michael Jackson’s "Beat It" and the "Macarena," but he can't listen to music in the usual way. He laughs whenever someone takes his picture with a camera flash, which is the only intensity of light he can perceive. He loves trying to balance himself, but his legs don't allow him to walk without support. He is one in a million, literally. Born deaf-blind and with a condition, osteopetrosis, that makes bones both dense and fragile, 6-year-old Orion Theodore Withrow is among an unknown number of children with a newly identified genetic disorder that researchers are just beginning to decipher. It goes by an acronym, COMMAD, that gives little away until each letter is explained, revealing an array of problems that also affect eye formation and pigmentation in eyes, skin and hair. The rare disorder severely impairs the person's ability to communicate. Children such as Orion, who are born to genetically deaf parents, are at a higher risk, according to a recent study published in the American Journal of Human Genetics. The finding has important implications for the deaf community, said its senior author, Brian Brooks, clinical director and chief of the Pediatric, Developmental and Genetic Ophthalmology Section at the National Eye Institute. “It is relatively common for folks in deaf community to marry each other,” he said, and what's key is whether each of the couple has a specific genetic "misspelling" that causes a syndrome called Waardenburg 2A. If yes, there's the likelihood of a child inheriting the mutation from both parents. The result, researchers found, is COMMAD. © 1996-2017 The Washington Post
Amanda Montañez A couple of weeks ago I listened to an excellent podcast series on poverty in America. One message that stuck with me is just how many factors the poor have working against them—factors that, if you’re not poor, are all too easy to deny, disregard, or simply fail to notice. In the March issue of Scientific American, neuroscientist Kimberly Noble highlights one such invisible, yet very real, element of poverty: its effect on brain development in children. When considering such a complex topic, any sort of data-driven approach can feel mired in confounding factors and variables. After all, it’s not as if money itself has any impact on the structure or function of one’s brain; rather, it is likely to be an amalgamation of environmental and/or genetic influences accompanying poverty, which results in an overall trend of relatively low achievement among poor children. By definition, this is a multifaceted problem in which correlation and causation seem virtually impossible to untangle. Nonetheless, Noble’s lab is tackling this challenge using the best scientific tools and methods available. First, it is essential to define the problem: in what specific ways does poverty impact brain function? To address this question, Noble recruited some 150 children from various socioeconomic backgrounds and used standard psychological testing methods to evaluate their abilities in several cognitive areas associated with particular parts of the brain. As outlined in the graphs below, the relationships are clear, especially in terms of language skills. © 2017 Scientific American,
By Jessica Wright, Spectrum The prevalence of autism in the United States has risen steadily since researchers first began tracking it in 2000. The rise in the rate has sparked fears of an autism ‘epidemic.’ But experts say the bulk of the increase stems from a growing awareness of autism and changes to the condition’s diagnostic criteria. Here’s how researchers track autism’s prevalence and explain its apparent rise. How do clinicians diagnose autism? There is no blood test, brain scan or any other objective test that can diagnose autism—although researchers are actively trying to develop such tests. Clinicians rely on observations of a person’s behavior to diagnose the condition. In the U.S., the criteria for diagnosing autism are laid out in the “Diagnostic and Statistical Manual of Mental Disorders” (DSM). The criteria are problems with social communication and interactions, and restricted interests or repetitive behaviors. Both of these ‘core’ features must be present in early development. What is the prevalence of autism in the U.S.? The Centers for Disease Control and Prevention (CDC) estimates that 1 in 68children in the U.S. have autism. The prevalence is 1 in 42 for boys and 1 in 189 for girls. These rates yield a gender ratio of about five boys for every girl. © 2017 Scientific American,
Link ID: 23305 - Posted: 03.03.2017
By Andy Coghlan People who have autoimmune disorders may be 20 per cent more likely to develop dementia. That’s according to an analysis of 1.8 million hospital cases in England. Based on data collected between 1999 and 2012, the study’s findings add to mounting evidence that chronic inflammation – a common feature of many autoimmune disorders – may be a trigger of dementia and Alzheimer’s disease. Previous studies have found that if infections or chronic inflammatory diseases – including diabetes – have pushed a person’s immune system into overdrive, this can lead to immune cells attacking healthy brain tissue. Varying effect According to the analysis, people with multiple sclerosis are among those with autoimmune disorders who are most likely to develop dementia. This finding isn’t very surprising, as the disorder is caused by the immune system attacking the central nervous system. The study, led by Michael Goldacre at the University of Oxford, found that people with the condition have double the risk of developing dementia. But other autoimmune disorders were also associated with rises in dementia risk. The skin condition psoriasis was linked to a 29 per cent increase, while the risk of developing dementia was 46 per cent higher in people who have lupus erythematosus, a disorder that involves rashes and fatigue. © Copyright Reed Business Information Ltd.
By Edward G. Barrett It’s no secret that fewer than 10 percent of investigational drugs achieve regulatory approval and reach the marketplace. But the chances of success for drugs developed to treat Alzheimer’s disease are even more grim. Despite researchers’ valiant efforts to stall, slow, or even beat this devastating neurodegenerative condition, there are still no effective drugs available to the estimated 5.4 million Americans with the disease. The scientific community has watched in dismay, time and again, as potential Alzheimer’s drugs that produced promising data in rodent models failed to work as expected in humans. For the most part, these drugs have pursued the promising “amyloid hypothesis,” which states that the disease may be caused by accumulation of beta-amyloid peptide in brain tissue resulting in neuron-killing plaques. But so far, no drug candidates targeting the beta-amyloid pathway have prevailed through late-stage clinical trials. Earlier this year, for example, Merck halted a Phase 2/3 trial of verubecestat, a small molecule inhibitor of a protein implicated in the buildup of beta-amyloid, called beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), due to a lack of efficacy. Another high-profile example occurred late last year, when Eli Lilly’s solanezumab, a monoclonal antibody active against the beta-amyloid peptide, failed to prevent cognitive decline in a Phase 3 trial. These accumulating failures call into question the promise of targeting the formation and occurrence of amyloid plaques as a viable approach for treating Alzheimer’s. So how do we break the chain? Are there other approaches we could be taking that could give us valuable insight before investing in human studies? © 1986-2017 The Scientist
Link ID: 23295 - Posted: 03.01.2017
By GRETCHEN REYNOLDS For some people with early-stage Alzheimer’s disease, frequent, brisk walks may help to bolster physical abilities and slow memory loss, according to one of the first studies of physical activity as an experimental treatment for dementia. But the study’s results, while encouraging, showed that improvements were modest and not universal, raising questions about just how and why exercise helps some people with dementia and not others. Alzheimer’s disease affects more than five million people in the United States and more than 35 million worldwide, a number that is expected to double within 20 years. There are currently no reliable treatments for the disease. But past studies of healthy elderly people have found relationships between regular exercise and improved memories. Physically active older people are, for instance, significantly less likely than those who are sedentary to develop mild cognitive impairment, a frequent precursor to Alzheimer’s disease. Physically fit older people also tend to have more volume in their brain’s hippocampus than do sedentary people of the same age, brain scans show. The hippocampus is the portion of the brain most intimately linked with memory function. But most of this research has examined whether exercise might prevent Alzheimer’s disease. Little has been known about whether it might change the trajectory of the disease in people who already have the condition. So for the new study, published in February in PLoS One, researchers at the University of Kansas decided to work directly with people who had previously been given a diagnosis of Alzheimer’s disease. Because the disease can affect coordination as it progresses, the researchers focused on men and women in its early stages, who were still living at home and could safely walk by themselves or perform other types of light exercise. © 2017 The New York Times Company
Link ID: 23294 - Posted: 03.01.2017
By Melissa Pandika Groundbreaking research suggests that a treatment for autism may come in the form of a probiotic. Stress can send your stomach into a painful tailspin, causing cramps, spasms and grumbling. But trouble in the gut can also affect the brain. This two-way relationship may be an unlikely key to solving one of medicine’s most pressing — and perplexing — mysteries: autism. Nearly 60 years after the disorder was first identified, the number of cases has surged, and the United Nations estimates that up to 70 million people worldwide fall on the autism spectrum. Yet there is no known cause or cure. But scientists have found promising clues in the gut. Research has revealed striking differences in the trillions of bacteria — a.k.a., the microbiome — in the intestines of children with and without autism. But the gut bacteria in individuals with autism aren’t just different. Researchers at the California Institute of Technology have shown for the first time that they may actually contribute to the disorder. They reported in the journal Cell in December 2013 that an experimental probiotic therapy alleviated autism-like behaviors in mice and are already planning a clinical trial. Today autism is treated primarily through behavioral therapy. But the new study suggests that treatment may one day come in the form of a probiotic — live, beneficial bacteria like those found in yogurt. “If you block the gastrointestinal problem, you can treat the behavioral symptoms,” Paul Patterson, a professor of biology at Caltech who co-authored the study told SFARI.org. University of Colorado Boulder professor Rob Knight hailed the finding as “groundbreaking” in a commentary in Cell. © OZY 2017 Terms & Conditions
By Joshua A. Krisch When Kathleen Gardiner first encountered female mice with Down syndrome, she was surprised to find that the rodents’ brains showed unexpected abnormalities. Gardiner, a neuroscientist at the University of Colorado School of Medicine in Aurora, knew that trisomic male mice typically had perturbed protein levels in their hippocampuses. But these trisomic female mice showed the most serious changes in their cerebellums. “Right away, there’s a brain region sex difference,” Gardiner said. “It’s very interesting to ponder the fact that this could lead to sex differences in the learning, memory, or behavioral abnormalities associated with [Down syndrome].” Although Gardiner recognized that differences between mouse sexes would not necessarily translate into sex differences in humans, she considered the potential implications for clinical studies on Down syndrome therapies. “If we find that males or females are differing not only in their baseline impairment, but in their response to drugs, we need to know that,” she said. “We could be missing a big piece of information that could lead to better or different clinical trials.” Indeed, sex differences in model organisms are becoming increasingly apparent. Studies have shown sex differences in mice can affect cardiovascular health, liver disease, and cancer risk. Many of these studies are now published in Biology of Sex Differences, where Gardiner’s own work on the trisomic female mice appeared. © 1986-2017 The Scientist
By Claudia Wallis Dinosaurs, Star Wars, train schedules, Disney princesses, maps, LEGO—subjects such as these can become all-consuming passions for children on the autism spectrum. What therapists and educators often call “circumscribed” or “restricted” interests (or, more generously, “special” interests) make up a characteristic symptom of autism spectrum disorder (ASD). The current edition of psychiatry’s Diagnostic and Statistical Manual of Mental Disorders describes them as “highly restricted, fixated interests that are abnormal in intensity or focus.” Roughly 90 percent of high-functioning kids with ASD display at least one such interest during their elementary school years, according to a 2007 survey conducted at the Yale University Child Study Center, one of the few studies to have examined the topic. For a family with an affected child, this kind of narrow preoccupation can be tedious and exhausting. Imagine a kid who will talk about nothing but the exits on the New Jersey Turnpike or the Captain Underpants book series. (Both actual examples.) Therapists and educators have traditionally tried to suppress or modulate a child’s special interest, or use it as a tool for behavior modification: Keep your hands still and stop flapping, and you will get to watch a Star Wars clip; complete your homework or no Harry Potter. But what if these obsessions themselves can be turned into pathways to growth? What if these intellectual cul-de-sacs can open up worlds? That is the idea explored in the film Life, Animated, a contender for the Academy Award for Best Documentary this Sunday night. © 2017 Scientific American
Link ID: 23277 - Posted: 02.24.2017
Jon Brock What if I told you that we can now identify babies who are going to develop autism based on a simple brain scan? This, in essence, is the seductive pitch for a study published last week in the journal Nature, and making headlines around the world. Early identification and diagnosis is one of the major goals of autism research. By definition, people with autism have difficulties with social interaction and communication. But these skills take many years to develop, even in typically developing (i.e., non-autistic) children. Potential early signs of autism are extremely difficult to pick out amidst the natural variation in behaviour and temperament that exists between all babies. A brain scan for autism would be a major step forward. But is the hype justified? Are we really on the brink of a new era in autism diagnostics? Without wishing to detract from the efforts of everyone involved in the study, it’s important to look at the results critically, both in terms of the scientific findings and their potential implications for clinical practice. The study, led by Heather Cody Hazlett at the University of North Carolina, was part of a larger research program investigating the development of babies who have an older sibling with autism. Because autism runs in families, these babies are much more likely to develop autism than babies from the general population.
Laurel Hamers Clusters of a toxic bacterial protein have a surprising structure, differing from similar clumps associated with Alzheimer’s and Parkinson’s in humans, scientists report in the Feb. 24 Science. These clusters, called amyloids, are defined in part by their structure: straight regions of protein chains called beta strands, folded accordion-style into flat beta sheets, which then stack up to form a fiber. That definition might now need to be broadened. “All the amyloids that have been structurally looked at so far have certain characteristics,” says Matthew Chapman, a biologist at the University of Michigan in Ann Arbor who wasn’t part of the work. “This is the odd amyloid out right now.” In the human brain, misfolded proteins can form amyloids that trigger neurodegenerative diseases. But amyloids aren’t always a sign of something gone wrong — some bacteria make amyloids to help defend their turf. In Staphylococcus aureus, for example, the PSMα3 protein assembles into amyloids that help the bacteria kill other cells. Previous research suggested that PSMα3 clusters were like any other amyloid. But researchers using X-ray crystallography found that instead of straight beta strands, the PSMα3 fiber was made up of curly structures called alpha helices that resemble an old-fashioned phone cord. The helices still formed a familiar fiber shape just like the beta strands did, but the sheets making up that fiber were rippled instead of flat. |© Society for Science & the Public 2000 - 2017.
Link ID: 23274 - Posted: 02.24.2017
By RONI CARYN RABIN Older adults who started sleeping more than nine hours a night — but had not previously slept so much — were at more than double the risk of developing dementia a decade later than those who slept nine hours or less, researchers report. The increased risk was not seen in people who had always slept more than nine hours. “We’re not suggesting you go wake up Grandpa. We think this might be a marker for the risk of dementia, not a cause” of the illness, said Dr. Sudha Seshadri, a professor of neurology at Boston University School of Medicine and the senior author of the study, in Neurology. Using data from 2,457 people, average age 72, who were part of a study in Framingham, Mass., the researchers found that those with a new habit of excessive slumber were at a greater risk of all forms of dementia, including Alzheimer’s, which is characterized by a buildup of beta amyloid, a toxic protein fragment that forms plaques in the brain. “My suspicion is that this is a compensatory mechanism: that at a time when amyloid is building up in the brain, people may be sleeping longer as the body is reacting and trying to remove it from the brain,” Dr. Seshadri added. © 2017 The New York Times Company
Link ID: 23270 - Posted: 02.24.2017
Hannah Devlin Rambling and long-winded anecdotes could be an early sign of Alzheimer’s disease, according to research that suggests subtle changes in speech style occur years before the more serious mental decline takes hold. The scientists behind the work said it may be possible to detect these changes and predict if someone is at risk more than a decade before meeting the threshold for an Alzheimer’s diagnosis. Janet Cohen Sherman, clinical director of the Psychology Assessment Center at Massachusetts General Hospital, said: “One of the greatest challenges right now in terms of Alzheimer’s disease is to detect changes very early on when they are still very subtle and to distinguish them from changes we know occur with normal ageing.” Speaking at the American Association for the Advancement of Science in Boston, Sherman outlined new findings that revealed distinctive language deficits in people with mild cognitive impairment (MCI), a precursor to dementia. “Many of the studies to date have looked at changes in memory, but we also know changes occur in language,” she said. “I’d hope in the next five years we’d have a new linguistic test.” Sherman cites studies of the vocabulary in Iris Murdoch’s later works, which showed signs of Alzheimer’s years before her diagnosis, and the increasingly repetitive and vague phrasing in Agatha Christie’s final novels – although the crime writer was never diagnosed with dementia. Another study, based on White House press conference transcripts, found striking changes in Ronald Reagan’s speech over the course of his presidency, while George HW Bush, who was a similar age when president, showed no such decline.