Chapter 13. Memory, Learning, and Development
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Three-year outcomes from an ongoing clinical trial suggest that high-dose immunosuppressive therapy followed by transplantation of a person's own blood-forming stem cells may induce sustained remission in some people with relapsing-remitting multiple sclerosis (RRMS). RRMS is the most common form of MS, a progressive autoimmune disease in which the immune system attacks the brain and spinal cord. The trial is funded by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and conducted by the NIAID-funded Immune Tolerance Network (ITN) External Web Site Policy. Three years after the treatment, called high-dose immunosuppressive therapy and autologous hematopoietic cell transplant or HDIT/HCT, nearly 80 percent of trial participants had survived without experiencing an increase in disability, a relapse of MS symptoms or new brain lesions. Investigators observed few serious early complications or unexpected side effects, although many participants experienced expected side effects of high-dose immunosuppression, including infections and gastrointestinal problems. The three-year findings are published in the Dec. 29, 2014, online issue of JAMA Neurology. “These promising results support the need for future studies to further evaluate the benefits and risks of HDIT/HCT and directly compare this treatment strategy to current MS therapies,” said NIAID Director Anthony S. Fauci, M.D. “If the findings from this study are confirmed, HDIT/HCT may become a potential therapeutic option for people with this often-debilitating disease, particularly those who have not been helped by standard treatments.”
George Johnson Training a dog to salivate at the sound of a bell would have seemed pretty stupid to Ivan Pavlov. He was after much bigger things. Using instruments like metronomes and harmoniums, he demonstrated that a dog could make astonishingly fine discriminations — distinguishing between a rhythm of 96 and 104 beats a minute or an ascending and a descending musical scale. But what he really wanted to know was what his animals were thinking. His dream was a grand theory of the mind. He couldn’t put his subjects on a couch like his colleague Freud and ask them to free-associate, so he gauged their reactions to a variety of stimuli, meticulously counting their “psychic secretions,” those droplets of drool. He knew he was pricking at the skin of something deeper. “It would be stupid,” he said, “to reject the subjective world.” This is not the Pavlov most people think they know. In an excellent new biography, “Ivan Pavlov: A Russian Life in Science,” Daniel P. Todes, a medical historian, describes a man whose laboratory in pre-Soviet Russia was like an early-20th-century version of the White House Brain Initiative, with its aim “to revolutionize our understanding of the human mind.” That was also Pavlov’s goal: to build a science that would “brightly illuminate our mysterious nature” and “our consciousness and its torments.” He spoke those words 111 years ago and spent his life pursuing his goal. Yet when we hear his name, we reflexively think of a drooling dog and a clanging bell. Our brains have been conditioned with the myth. © 2014 The New York Times Company
Keyword: Learning & Memory
Link ID: 20439 - Posted: 12.23.2014
By James Gallagher Health editor, BBC News website A link between autism and air pollution exposure during pregnancy has been suggested by scientists. The Harvard School of Public Health team said high levels of pollution had been linked to a doubling of autism in their study of 1,767 children. They said tiny particulate matter, which can pass from the lungs to the bloodstream, may be to blame. Experts said pregnant women should minimise their exposure, although the link had still to be proven. Air pollution is definitely damaging. The World Health Organization estimates it causes 3.7 million deaths each year. The study, published in Environmental Health Perspectives, investigated any possible link with autism. It analysed 245 children with autism and 1,522 without. By looking at estimated pollution exposure during pregnancy, based on the mother's home address, the scientists concluded high levels of pollution were more common in children with autism. The strongest link was with fine particulate matter - invisible specks of mineral dust, carbon and other chemicals - that enter the bloodstream and cause damage throughout the body. Yet, the research is unable to conclusively say that pollution causes autism as there could be other factors that were not accounted for in the study. Consistent pattern There is a large inherited component to autism, but lead researcher Dr Marc Weisskopf said there was mounting evidence that air pollution may play a role too. BBC © 2014
by Helen Thomson HAVE you read this before? A 23-year-old man from the UK almost certainly feels like he has – he's the first person to report persistent déjà vu stemming from anxiety rather than any obvious neurological disorder. Nobody knows exactly how or why déjà vu happens, but for most of us it is rare. Some people experience it more often, as a side effect associated with epileptic seizures or dementia. Now, researchers have discovered the first person with what they call "psychogenic déjà vu" – where the cause appears to be psychological. The man's episodes began just after he started university, a period when he felt anxious and was also experiencing obsessive compulsions. As time went on, his déjà vu became more and more prolonged, and then fairly continuous after he tried LSD. Now, he avoids television and radio, and finds newspapers distressing as the content feels familiar. There are different theories as to what is going on, says Christine Wells at Sheffield Hallam University in the UK, who has written a paper on the man's experiences. "The general theory is that there's a misfiring of neurons in the temporal lobes – which deal with recollection and familiarity. That misfiring during the process of recollection means we interpret a moment in time as something that has already been experienced," she says. Surprisingly, when Wells gave the man a standard recall test, he scored more similarly to people of his own age without the condition than those with epilepsy-related déjà vu. An MRI and an EEG scan of his brain activity also showed no abnormalities. © Copyright Reed Business Information Ltd.
|By Marissa Fessenden Songbirds stutter, babble when young, become mute if parts of their brains are damaged, learn how to sing from their elders and can even be "bilingual"—in other words, songbirds' vocalizations share a lot of traits with human speech. However, that similarity goes beyond behavior, researchers have found. Even though humans and birds are separated by millions of years of evolution, the genes that give us our ability to learn speech have much in common with those that lend birds their warble. A four-year long effort involving more than 100 researchers around the world put the power of nine supercomputers into analyzing the genomes of 48 species of birds. The results, published this week in a package of eight articles in Science and 20 papers in other journals, provides the most complete picture of the bird family tree thus far. The project has also uncovered genetic signatures in song-learning bird brains that have surprising similarities to the genetics of speech in humans, a finding that could help scientists study human speech. The analysis suggests that most modern birds arose in an impressive speciation event, a "big bang" of avian diversification, in the 10 million years immediately following the extinction of dinosaurs. This period is more recent than posited in previous genetic analyses, but it lines up with the fossil record. By delving deeper into the rich data set, research groups identified when birds lost their teeth, investigated the relatively slow evolution of crocodiles and outlined the similarities between birds' and humans' vocal learning ability, among other findings. © 2014 Scientific American,
By Candy Schulman My mother’s greatest fear was Alzheimer’s. She got Lewy body dementia, or LBD, instead. This little known, oddly named, debilitating illness afflicts an estimated 1.3 million Americans, the actor and comedian Robin Williams possibly among them. It is often misdiagnosed because its signs, such as hallucinations and body rigidity, do not seem like those of dementia, but in the end it robs people of themselves even more painfully. I first noticed my mother’s cognitive difficulties when she was 88. Until then, she’d led an extraordinarily active life: She was a competitive golfer with a bureau full of trophies, a painter and a sculptor. Every Hanukkah she hosted a lively feast for her eight grandchildren and nine great-grandchildren. This time, though, she needed my help planning, shopping and cooking. She was having difficulty with the guest list, trying to write every family member’s name on a piece of paper, adding up the numbers to see how many potatoes to buy for latkes. Her concentration became frayed and she kept ripping it up and starting again, close to tears. Several months before that, she had sent me a Mother’s Day card that was illustrated with childlike prose, colorful illustrations and glitter hearts. The poem on the cover was printed in a playful purple font: “For you, Mom. For kissing my boo-boos, for wiping my face. . . . For calming my fears with your loving embrace.” On Mother’s Day and the rest of the year, Mom added in a shaky script, “thanks.”
Link ID: 20422 - Posted: 12.16.2014
|By Emilie Reas If you carried a gene that doubled your likelihood of getting Alzheimer's disease, would you want to know? What if there was a simple lifestyle change that virtually abolished that elevated risk? People with a gene known as APOE e4 have a higher risk of cognitive impairment and dementia in old age. Even before behavioral symptoms appear, their brains show reduced metabolism, altered activity and more deterioration than those without the high-risk gene. Yet accumulating research is showing that carrying this gene is not necessarily a sentence for memory loss and confusion—if you know how to work it to your advantage with exercise. Scientists have long known that exercise can help stave off cognitive decline. Over the past decade evidence has mounted suggesting that this benefit is even greater for those at higher genetic risk for Alzheimer's. For example, two studies by a team in Finland and Sweden found that exercising at least twice a week in midlife lowers one's chance of getting dementia more than 20 years later, and this protective effect is stronger in people with the APOE e4 gene. Several others reported that frequent exercise—at least three times a week in some studies; up to more than an hour a day in others—can slow cognitive decline only in those carrying the high-risk gene. Furthermore, for those who carry the gene, being sedentary is associated with increased brain accumulation of the toxic protein beta-amyloid, a hallmark of Alzheimer's. More recent studies, including a 2012 paper published in Alzheimer's & Dementia and a 2011 paper in NeuroImage, found that high-risk individuals who exercise have greater brain activity and glucose uptake during a memory task compared with their less active counterparts or with those at low genetic risk. © 2014 Scientific American
By Nicholas Bakalar Poor sleep in older adults may be linked to brain changes associated with dementia, a new study has found. Researchers studied 167 men who underwent sleep tests in 1999 and died by 2010. The study, in Neurology, recorded sleep duration, periods of waking up and episodes of apnea, and used pulse oximetry to measure oxygen saturation of their blood. On autopsy, they found that those in the highest one-quarter for duration of sleep at oxygen saturation of less than 95 percent were almost four times as likely to have higher levels microinfarcts, small areas of dead tissue caused by deprivation of blood supply, as those in the lowest one-quarter. Compared with those in the lowest 25 percent for duration of slow-wave (deep) sleep, those in the highest one-quarter were about a third as likely to have moderate or high levels of generalized brain atrophy. “Prior studies have shown an association between certain types of sleep disturbance and dementia,” said the lead author, Dr. Rebecca P. Gelber, an epidemiologist with the Veterans Administration in Hawaii. “These lesions may help explain the association.” © 2014 The New York Times Company
By David Noonan It was the day before Christmas, and the normally busy MIT laboratory on Vassar Street in Cambridge was quiet. But creatures were definitely stirring, including a mouse that would soon be world famous. Steve Ramirez, a 24-year-old doctoral student at the time, placed the mouse in a small metal box with a black plastic floor. Instead of curiously sniffing around, though, the animal instantly froze in terror, recalling the experience of receiving a foot shock in that same box. It was a textbook fear response, and if anything, the mouse’s posture was more rigid than Ramirez had expected. Its memory of the trauma must have been quite vivid. Which was amazing, because the memory was bogus: The mouse had never received an electric shock in that box. Rather, it was reacting to a false memory that Ramirez and his MIT colleague Xu Liu had planted in its brain. “Merry Freaking Christmas,” read the subject line of the email Ramirez shot off to Liu, who was spending the 2012 holiday in Yosemite National Park. The observation culminated more than two years of a long-shot research effort and supported an extraordinary hypothesis: Not only was it possible to identify brain cells involved in the encoding of a single memory, but those specific cells could be manipulated to create a whole new “memory” of an event that never happened. “It’s a fantastic feat,” says Howard Eichenbaum, a leading memory researcher and director of the Center for Neuroscience at Boston University, where Ramirez did his undergraduate work. “It’s a real breakthrough that shows the power of these techniques to address fundamental questions about how the brain works.” In a neuroscience breakthrough, the duo implanted a false memory in a mouse
By Gail Sullivan Chemicals found in food and common household products have been linked to lower IQ in kids exposed to high levels during pregnancy. Previous research linked higher exposure to chemicals called "phthalates" to poor mental and motor development in preschoolers. This study was said to be the first to report a link between prenatal exposure to the chemicals and childhood development. Researchers from Columbia University’s Mailman School of Public Health studied exposure to five types of phthalates, which are sometimes referred to as “hormone disruptors” or “endocrine disruptors.” Among these, di-n-butyl phthalate (DnBP) is used in shower curtains, raincoats, hairspray, food wraps, vinyl and pill coating, among other things — but according to the EPA, the largest source of exposure may be seafood. Di-isobutyl phthalate (DiBP) and Butylbenzyl phthalate (BBzP) are added to plastics to make them flexible. These chemicals may also used in makeup, nail polish, lacquer and explosives. The researchers linked prenatal exposure to phthalates to a more than six-point drop in IQ score compared with kids with less exposure. The study, “Persistent Associations between Maternal Prenatal Exposure to Phthalates on Child IQ at Age 7 Years," was published Wednesday in the journal PLOS One. "The magnitude of these IQ differences is troubling," one of the study’s authors, Robin Whyatt, said in a press release. "A six- or seven-point decline in IQ may have substantial consequences for academic achievement and occupational potential."
By Gary Stix Our site recently ran a great story about how brain training really doesn’t endow you instantly with genius IQ. The games you play just make you better at playing those same games. They aren’t a direct route to a Mensa membership. Just a few days before that story came out—Proceedings of the National Academy of Sciences—published a report that suggested that playing action video games, Call of Duty: Black Ops II and the like—actually lets gamers learn the essentials of a particular visual task (the orientation of a Gabor signal—don’t ask) more rapidly than non-gamers, a skill that has real-world relevance beyond the confines of the artificial reality of the game itself. As psychologists say, it has “transfer effects.” Gamers appear to have learned how to do stuff like home in quickly on a target or multitask better than those who inhabit the non-gaming world. Their skills might, in theory, make them great pilots or laparoscopic surgeons, not just high scorers among their peers. Action video games are not billed as brain training, but both Call of Duty and nominally accredited training programs like Lumosity are both structured as computer games. So that leads to the question of what’s going on here? Every new finding about brain training as B.S. appears to be contradicted by another that points to the promise of cognitive exercise, if that’s what you call a session with Call of Duty. It may boil down to a realization that the whole story about exercising your neurons to keep the brain supple may be a lot less simple than proponents make it out to be. © 2014 Scientific American
Keyword: Learning & Memory
Link ID: 20409 - Posted: 12.13.2014
by Helen Thomson Zapping your brain might make you better at maths tests – or worse. It depends how anxious you are about taking the test in the first place. A recent surge of studies has shown that brain stimulation can make people more creative and better at maths, and can even improve memory, but these studies tend to neglect individual differences. Now, Roi Cohen Kadosh at the University of Oxford and his colleagues have shown that brain stimulation can have completely opposite effects depending on your personality. Previous research has shown that a type of non-invasive brain stimulation called transcranial direct current stimulation (tDCS) – which enhances brain activity using an electric current – can improve mathematical ability when applied to the dorsolateral prefrontal cortex, an area involved in regulating emotion. To test whether personality traits might affect this result, Kadosh's team tried the technique on 25 people who find mental arithmetic highly stressful, and 20 people who do not. They found that participants with high maths anxiety made correct responses more quickly and, after the test, showed lower levels of cortisol, an indicator of stress. On the other hand, individuals with low maths anxiety performed worse after tDCS. "It is hard to believe that all people would benefit similarly [from] brain stimulation," says Cohen Kadosh. He says that further research could shed light on how to optimise the technology and help to discover who is most likely to benefit from stimulation. © Copyright Reed Business Information Ltd.
Ian Sample, science editor Electrical brain stimulation equipment – which can boost cognitive performance and is easy to buy online – can have bad effects, impairing brain functioning, research from scientists at Oxford University has shown. A steady stream of reports of stimulators being able to boost brain performance, coupled with the simplicity of the devices, has led to a rise in DIY enthusiasts who cobble the equipment together themselves, or buy it assembled on the web, then zap themselves at home. In science laboratories brain stimulators have long been used to explore cognition. The equipment uses electrodes to pass gentle electric pulses through the brain, to stimulate activity in specific regions of the organ. Roi Cohen Kadosh, who led the study, published in the Journal of Neuroscience, said: “It’s not something people should be doing at home at this stage. I do not recommend people buy this equipment. At the moment it’s not therapy, it’s an experimental tool.” The Oxford scientists used a technique called transcranial direct current stimulation (tDCS) to stimulate the dorsolateral prefrontal cortex in students as they did simple sums. The results of the test were surprising. Students who became anxious when confronted with sums became calmer and solved the problems faster than when they had sham stimulation (the stimulation itself lasted only 30 seconds of the half hour study). The shock was that the students who did not fear maths performed worse with the same stimulation.
Kelly Servick* Anesthesiologists and surgeons who operate on children have been dogged by a growing fear—that being under anesthesia can permanently damage the developing brain. Although the few studies of children knocked out for surgeries have been inconclusive, evidence of impaired development in nematodes, zebrafish, rats, guinea pigs, pigs, and monkeys given common anesthetics has piled up in recent years. Now, the alarm is reaching a tipping point. “Anything that goes from [the roundworm] C. elegans to nonhuman primates, I've got to worry about,” Maria Freire, co-chair of the U.S. Food and Drug Administration (FDA) science advisory board, told attendees at a meeting the agency convened here last month to discuss the issue. The gathering came as anesthesia researchers and regulators consider several moves to address the concerns: a clinical trial of anesthetics in children, a consensus statement about their possible risks, and an FDA warning label on certain drugs. But each step stirs debate. Many involved in the issue are reluctant to make recommendations to parents and physicians based on animal data alone. At the same time, more direct studies of anesthesia's risks in children are plagued by confounding factors, lack of funding, and ethical issues. “We have to generate—very quickly—an action item, because I don't think the status quo is acceptable,” Freire said at the 19 November meeting. “Generating an action item without having the data is where things become very, very tricky.” © 2014 American Association for the Advancement of Science
|By Bret Stetka When University of Bonn psychologist Monika Eckstein designed her latest published study, the goal was simple: administer a hormone into the noses of 62 men in hopes that their fear would go away. And for the most part, it did. The hormone was oxytocin, often called our “love hormone” due to its crucial role in mother-child relationships, social bonding, and intimacy (levels soar during sex). But it also seems to have a significant antianxiety effect. Give oxytocin to people with certain anxiety disorders, and activity in the amygdala—the primary fear center in human and other mammalian brains, two almond-shaped bits of brain tissue sitting deep beneath our temples—falls. The amygdala normally buzzes with activity in response to potentially threatening stimuli. When an organism repeatedly encounters a stimulus that at first seemed frightening but turns out to be benign—like, say, a balloon popping—a brain region called the prefrontal cortex inhibits amygdala activity. But in cases of repeated presentations of an actual threat, or in people with anxiety who continually perceive a stimulus as threatening, amygdala activity doesn’t subside and fear memories are more easily formed. To study the effects of oxytocin on the development of these fear memories, Eckstein and her colleagues first subjected study participants to Pavlovian fear conditioning, in which neutral stimuli (photographs of faces and houses) were sometimes paired with electric shocks. Subjects were then randomly assigned to receive either a single intranasal dose of oxytocin or a placebo. Thirty minutes later they received functional MRI scans while undergoing simultaneous fear extinction therapy, a standard approach to anxiety disorders in which patients are continually exposed to an anxiety-producing stimulus until they no longer find it stressful. In this case they were again exposed to images of faces and houses, but this time minus the electric shocks. © 2014 Scientific American
By recording from the brains of bats as they flew and landed, scientists have found that the animals have a "neural compass" - allowing them to keep track of exactly where and even which way up they are. These head-direction cells track bats in three dimensions as they manoeuvre. The researchers think a similar 3D internal navigation system is likely to be found throughout the animal kingdom. The findings are published in the journal Nature. Lead researcher Arseny Finkelstein, from the Weizmann Institute of Science in Rehovot, Israel, explained that this was the first time measurements had been taken from animals as they had flown around a space in any direction and even carried out their acrobatic upside-down landings. "We're the only lab currently able to conduct wireless recordings in flying animals," he told BBC News. "A tiny device attached to the bats allows us to monitor the activity of single neurons while the animal is freely moving." Decades of study of the brain's internal navigation system garnered three renowned neuroscientists this year's Nobel Prize for physiology and medicine. The research, primarily in rats, revealed how animals had "place" and "grid" cells - essentially building a map in the brain and coding for where on that map an animal was at any time. Mr Finkelstein and his colleagues' work in bats has revealed that their brains also have "pitch" and "roll" cells. These tell the animal whether it is pointing upwards or downwards and whether its head is tilted one way or the other. BBC © 2014
by Andy Coghlan How does this make you feel? Simply asking people to think about emotion-laden actions as their brains are scanned could become one of the first evidence-based tests for psychiatric illness. Assessing people in this way would be a step towards a more scientific approach to diagnosis, away from that based on how someone behaves or how they describe their symptoms. The US National Institute of Mental Health has had such a goal in mind since 2013. Marcel Just of Carnegie Mellon University in Pittsburgh, Pennsylvania, and his colleagues developed the brain scanning technique and used it to identify people with autism. "This gives us a whole new perspective to understanding psychiatric illnesses and disorders," says Just. "We've discovered a biological thought-marker for autism." The technique builds on work by the group showing that specific thoughts and emotions are represented in the brain by certain patterns of neural activation. The idea is that deviations from these patterns, what Just refers to as thought-markers, can be used to diagnose different psychiatric conditions. The team asked a group of adults to imagine 16 actions, some of which required emotional involvement, such as "hugging", "persuading" or "adoring", while they lay in an fMRI scanner. © Copyright Reed Business Information Ltd.
By CHRISTOPHER F. CHABRIS and DANIEL J. SIMONS NEIL DEGRASSE TYSON, the astrophysicist and host of the TV series “Cosmos,” regularly speaks to audiences on topics ranging from cosmology to climate change to the appalling state of science literacy in America. One of his staple stories hinges on a line from President George W. Bush’s speech to Congress after the 9/11 terrorist attacks. In a 2008 talk, for example, Dr. Tyson said that in order “to distinguish we from they” — meaning to divide Judeo-Christian Americans from fundamentalist Muslims — Mr. Bush uttered the words “Our God is the God who named the stars.” Dr. Tyson implied that President Bush was prejudiced against Islam in order to make a broader point about scientific awareness: Two-thirds of the named stars actually have Arabic names, given to them at a time when Muslims led the world in astronomy — and Mr. Bush might not have said what he did if he had known this fact. This is a powerful example of how our biases can blind us. But not in the way Dr. Tyson thought. Mr. Bush wasn’t blinded by religious bigotry. Instead, Dr. Tyson was fooled by his faith in the accuracy of his own memory. In his post-9/11 speech, Mr. Bush actually said, “The enemy of America is not our many Muslim friends,” and he said nothing about the stars. Mr. Bush had indeed once said something like what Dr. Tyson remembered; in 2003 Mr. Bush said, in tribute to the astronauts lost in the Columbia space shuttle explosion, that “the same creator who names the stars also knows the names of the seven souls we mourn today.” Critics pointed these facts out; some accused Dr. Tyson of lying and argued that the episode should call into question his reliability as a scientist and a public advocate. © 2014 The New York Times Company
Keyword: Learning & Memory
Link ID: 20387 - Posted: 12.03.2014
|By David Z. Hambrick If you’ve spent more than about 5 minutes surfing the web, listening to the radio, or watching TV in the past few years, you will know that cognitive training—better known as “brain training”—is one of the hottest new trends in self improvement. Lumosity, which offers web-based tasks designed to improve cognitive abilities such as memory and attention, boasts 50 million subscribers and advertises on National Public Radio. Cogmed claims to be “a computer-based solution for attention problems caused by poor working memory,” and BrainHQ will help you “make the most of your unique brain.” The promise of all of these products, implied or explicit, is that brain training can make you smarter—and make your life better. Yet, according to a statement released by the Stanford University Center on Longevity and the Berlin Max Planck Institute for Human Development, there is no solid scientific evidence to back up this promise. Signed by 70 of the world’s leading cognitive psychologists and neuroscientists, the statement minces no words: "The strong consensus of this group is that the scientific literature does not support claims that the use of software-based “brain games” alters neural functioning in ways that improve general cognitive performance in everyday life, or prevent cognitive slowing and brain disease." The statement also cautions that although some brain training companies “present lists of credentialed scientific consultants and keep registries of scientific studies pertinent to cognitive training…the cited research is [often] only tangentially related to the scientific claims of the company, and to the games they sell.” © 2014 Scientific American,
Keyword: Learning & Memory
Link ID: 20380 - Posted: 12.02.2014
By Nicholas Bakalar Researchers have found that people diagnosed with diabetes in their 50’s are significantly more likely than others to suffer mental decline by their 70’s. The study, published Monday in the Annals of Internal Medicine, started in 1990. Scientists examined 13,351 black and white adults, aged 48 to 67, for diabetes and prediabetes using self-reported physician diagnoses and glucose control tests. They also administered widely used tests of memory, reasoning, problem solving and planning. About 13 percent had diabetes at the start. The researchers followed them with five periodic examinations over the following 20 years. By that time, 5,987 participants were still enrolled. After adjusting for numerous health and behavioral factors, and for the large attrition in the study, the researchers found people with diabetes suffered a 30 percent larger decline in mental acuity than those without the disease. Diabetes can impair blood circulation, and the authors suggest that the association of diabetes with thinking and memory problems may be the result of damage to small blood vessels in the brain. “People may think cognitive decline with age is inevitable, but it’s not,” said the senior author, Elizabeth Selvin, an associate professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health. “Factors like diabetes are potentially modifiable. If we can better control diabetes we can stave off cognitive decline and future dementia.” © 2014 The New York Times Company