Chapter 7. Life-Span Development of the Brain and Behavior
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By Andrea Anderson Mom's ovaries could hold clues to some autism cases, new research suggests—and this time it's not because of genetic vulnerabilities carried in her eggs. A new, large-scale study out of Sweden suggests that women with polycystic ovarian syndrome (PCOS)—an endocrine disorder that affects 5 to 10 percent of women of childbearing age—have an increased risk of giving birth to children with autism spectrum disorder (ASD). The Karolinska Institute's Renee Gardner, along with colleagues from Sweden and the U.S., tapped into a Swedish national population health database to look at potential ties between PCOS and ASD. As they reported online December 8 in Molecular Psychiatry, the team looked at 23,748 individuals with ASD and nearly 209,000 unaffected individuals, all born in Sweden between 1984 and 2007. Although identifying information about the individuals was removed, the researchers had access to information about their relationships to others in the database as well as documented diagnoses and use of health care services. The group found that ASD was 59 percent more prevalent in children born to women with PCOS—a relationship that was independent of PCOS complications such as increased neonatal distress or C-section delivery. This risk level is roughly comparable with that of having a father over age 50 (estimated to be 66 percent) but lower than it is in those with certain rare genetic syndromes or mutations. The authors of the analysis believe PCOS increases ASD risk in offspring to a greater extent than maternal infection, one of many factors previously implicated in autism. © 2015 Scientific American
Laura Sanders You can thank your parents for your funny-looking hippocampus. Genes influence the three-dimensional shape of certain brain structures, scientists report in a paper posted online December 1 at bioRxiv.org. Showing a new way that genes help sculpt the brain opens up more ways to explore how the brain develops and operates. Earlier work linked genes to simple measurements of brain structures, such as overall volume or length. The new work goes beyond that by mathematically analyzing complex 3-D shapes and tying those shapes to a particular genetic makeup. A team led by researchers at Massachusetts General Hospital and Harvard Medical School analyzed MRI brain scans and genome data from 1,317 healthy young adults. Particular genetic profiles influenced the 3-D shape of structures including the hippocampus, caudate and cerebellum, the scientists found. In some brains, for instance, genes played a role in making the seahorse-shaped right hippocampus skinnier on the top and wider on the bottom. Genes also influenced whether the tail of the caudate was short or long. Quirks of brain structure shapes might play a role in disorders such as schizophrenia, autism spectrum disorder and bipolar disorder, which are known to be influenced by genes, the authors write. Citations T. Ge et al. Heritability of neuroanatomical shape. bioRxiv.org. Posted December 1, 2015. doi: 10.1101/033407. © Society for Science & the Public 2000 - 2015
By Darold A. Treffert The headlines read “New study suggests autism can be outgrown”, or “outgrowing autism: a doctor’s surprise and wonder.” The stories are based on studies reporting that 7-9% of children with a documented early autistic syndrome disorder (ASD) have no symptoms of the disorder on follow-up later in childhood or adolescence. That is good news. The question is how to account for it. Is it possible to simply “outgrow” autism? Was the initial diagnosis wrong? Did some interventions work? Or might there be other explanations for this welcome news? "In an earlier column titled “Oops. When “autism” isn’t autistic disorder,” I outlined three types of hyperlexia, or precocious reading ability, which is sometimes an element of a diagnosis of ASD. Type 1 are neurotypical children who simply read way ahead of their chronological age. Listening to a 4 year old reading books to his or her nursery school classmates is a startling experience. Type 2 are children in which intense fascination with letters and numbers, along with early reading and remarkable memory represent ‘splinter skills’ as a part of autistic syndrome disorder (ASD) Type 3 are children who likewise show intense fascination and preoccupation with numbers and letters very early, along with precocious reading skills and remarkable memory. They do have “autistic-like” symptoms or behaviors but those disappear over time as the child gets older. The outcome in these children is much more positive than those with ASD to their benefit and the great relief of their parents. Following the “Oops” article I received numerous reports from parents who identified with hyperlexia 3. “You just described my child,” the puzzled, and relieved parents would write as they read the case examples in my Wisconsin Medical Journal article in December, 2011. © 2015 Scientific American
Link ID: 21689 - Posted: 12.10.2015
By Gretchen Reynolds Physical fitness may be critical for maintaining a relatively youthful and nimble brain as we age, according to a new study of brain activation patterns in older people. For most of us, our bodies begin to lose flexibility and efficiency as we enter our 40s. Running and other movements slow down and become more awkward, and something similar seems to occur within our heads. As middle age encroaches, our thinking becomes less efficient. We don’t toggle between mental tasks as nimbly as we once did or process new information with the same aplomb and clarity. Recently, neuroscientists have begun to quantify how those cognitive changes play out in our brains, to disquieting effect. In studies comparing brain activation in young people with that of people past 40, they have found notable differences, especially during mental tasks that require attention, problem solving, decision-making and other types of high-level thinking. Such thinking primarily involves activation of the brain’s prefrontal cortex. In young people, activation in the cortex during these cognitive tasks tends to be highly localized. Depending on the type of thinking, young people’s brains light up almost exclusively in either the right or left portion of the prefrontal cortex. But in older people, studies show, brain activity during the same mental tasks requires far more brainpower. They typically display activity in both hemispheres of their prefrontal cortex. In effect, they require more of their brains’ resources to complete the same tasks that young people do with less cognitive effort. Neuroscientists coined an acronym for this phenomenon: Harold, for hemispheric asymmetry reduction in older adults. Most agree that it represents a general reorganization and weakening of the brain’s function with age. © 2015 The New York Times Company
By Lindzi Wessel Nighttime restlessness is common among people with Alzheimer’s, and many stay awake agitated and pacing long after their family members have gone to sleep. Now, scientists may have figured out why: The disease appears to degrade a special type of eye cell that tells the brain when it’s day or night. If the discovery holds up, it might offer clinicians a new way to monitor the progression of Alzheimer’s and could lead to treatments that restore a good night’s sleep. The cells in question are known as melanopsin retinal ganglion cells. They send signals to the brain center responsible for circadian rhythms, our body’s daily clock. The cells make up 1% to 2% of the eye’s light-responsive sensors, but they play no role in vision, says lead author Chiara La Morgia, a neuroscientist at the University of Bologna in Italy. Rather, they sense light levels around us, telling us when to get sleepy and when to be alert. La Morgia and her colleagues, aware of the profound sleep problems often seen in Alzheimer’s, wondered whether the cells may stop doing their job as the disease progresses. “If you lose them, you should see dysfunction of the circadian rhythms and see disrupted sleep,” says Alfredo Sadun, neuro-opthamologist at the University of California, Los Angeles, and co-author of the study. “That is the exact symptomology we see in Alzheimer’s disease.” To learn more, the researchers used dyes to mark melanopsin cells in the eyes of 30 recently deceased organ donors. They found approximately 24% fewer melanopsin cells in the eyes of people with Alzheimer’s than in the eyes of donors without the disease. © 2015 American Association for the Advancement of Science.
Ian Sample Science editor Scientists have discovered a chemical that destroys toxic plaques which build up in the brain in the early stages of Alzheimer’s disease. Preliminary tests found that when added to drinking water, the compound cleared amyloid beta plaques from the brains of mice with Alzheimer’s-like symptoms, and restored their cognitive function to normal. The work is at a very early stage, but raises hopes for drugs that can prevent the accumulation of amyloid plaques and potentially halt the progression of the disease. Amyloid plaques are one of the first hallmarks of Alzheimer’s disease and are thought to contribute to neurodegeneration by killing off brain cells. Researchers in Korea discovered the chemical, EPPS, while screening a variety of molecules for their effects on amyloid plaques. In the latest study, they added the substance to the drinking water of mice that had symptoms of Alzheimer’s disease. They found that administering EPPS for a week improved how well mice performed on maze tests, and cleared amyloid plaques from the animals’ brains. “Our findings clearly support the view that aggregated amyloid-beta is the pathological culprit of Alzheimer’s disease,” said YoungSoo Kim, who led the team at the Korea Institute of Science and Technology in Seoul. The study used mice that had amyloid plaques injected into their brains. The animals suffered cognitive impairments as a result, but they did not develop the kind of widespread brain damage seen in Alzheimer’s patients which would not be reversed by removing amyloid plaques. © 2015 Guardian News and Media Limited
Link ID: 21685 - Posted: 12.09.2015
A new, open-source software that can help track the embryonic development and movement of neuronal cells throughout the body of the worm, is now available to scientists. The software is described in a paper published in the open access journal, eLife on December 3rd by researchers at the National Institute of Biomedical Imaging and Bioengineering (NIBIB) and the Center for Information Technology (CIT); along with Memorial Sloan-Kettering Institute, New York City; Yale University, New Haven, Connecticut; Zhejiang University, China; and the University of Connecticut Health Center, Farmington. NIBIB is part of the National Institutes of Health. As far as biologists have come in understanding the brain, much remains to be revealed. One significant challenge is determining the formation of complex neuronal structures made up of billions of cells in the human brain. As with many biological challenges, researchers are first examining this question in simpler organisms, such as worms. Although scientists have identified a number of important proteins that determine how neurons navigate during brain formation, it’s largely unknown how all of these proteins interact in a living organism. Model animals, despite their differences from humans, have already revealed much about human physiology because they are much simpler and easier to understand. In this case, researchers chose Caenorhabditis elegans (C. elegans), because it has only 302 neurons, 222 of which form while the worm is still an embryo. While some of these neurons go to the worm nerve ring (brain) they also spread along the ventral nerve cord, which is broadly analogous to the spinal cord in humans. The worm even has its own versions of many of the same proteins used to direct brain formation in more complex organisms such as flies, mice, or humans.
Carl Zimmer In 2013, an obese man went to Hvidovre Hospital in Denmark to have his stomach stapled. All in all, it was ordinary bariatric surgery — with one big exception. A week before the operation, the man provided a sperm sample to Danish scientists. A week after the procedure, he did so again. A year later, he donated a third sample. Scientists were investigating a tantalizing but controversial hypothesis: that a man’s experiences can alter his sperm, and that those changes in turn may alter his children. That idea runs counter to standard thinking about heredity: that parents pass down only genes to their children. People inherit genes that predispose them to obesity, or stress, or cancer — or they don’t. Whether one’s parents actually were obese or constantly anxious doesn’t rewrite those genes. Yet a number of animal experiments in recent years have challenged conventional thinking on heredity, suggesting that something more is at work. In 2010, for example, Dr. Romain Barres of the University of Copenhagen and his colleagues fed male rats a high-fat diet and then mated them with females. Compared with male rats fed a regular diet, those on the high-fat diet fathered offspring that tended to gain more weight, develop more fat and have more trouble regulating insulin levels. Eating high-fat food is just one of several experiences a father can have that can change his offspring. Stress is another. Male rats exposed to stressful experiences — like smelling the odor of a fox — will father pups that have a dampened response to stress. © 2015 The New York Times Company
Some people may have a get-out clause when it comes to giving up cigarettes. A third of white people who smoke have gene variations that make it harder for them to kick the habit. A gene called ANKK1 regulates the release of dopamine – a chemical involved in the brain’s reward centres. Ming Li and colleagues at the Zhejiang University School of Medicine in Hangzhou, China, wondered whether variations of this gene might affect people’s ability to give up cigarettes. So his team analysed 23 studies that have linked ANKK1 to smoking, involving more than 11,000 participants in total. Across the board, there was no significant link between successful quitting and the gene variants. But when they looked at just the studies that analysed white people, the results were striking. About two-thirds of white smokers carried a variation of the gene called A2/A2. These people were about 22 per cent more likely to be able to quit smoking than those who carried an alternative version of the gene, either A1/A1 or A1/A2. The A1/A1 and A1/A2 gene variations have previously been linked to obesity and drug addiction, which suggests they may predispose people to addictive behaviours. People carrying these versions of ANKK1 may need more aggressive strategies to fight their addiction to cigarettes, says Li. It is not clear whether the gene has the same effect for non-white people, he says. More studies that involve non-white people will be necessary to investigate this. © Copyright Reed Business Information Ltd.
Tina Hesman Saey Genies are said to have the power to grant three wishes. But genies recently released from laboratory flasks promise to fulfill nearly any wish a biologist can dream up. End the scourge of insect-borne diseases? Check. Inoculate endangered amphibians against killer fungi? Yes. Pluck invasive species from environments where they don’t belong? As you wish. These genies aren’t magical; they are research tools known as gene drives — clever bits of engineered DNA designed to propel themselves into the DNA of a pesky or troubled organism. A gene drive is a targeted contagion intended to spread within species, forever altering the offspring. Gene drive enthusiasts say these genies could wipe out malaria, saving more than half a million lives each year. Invasive species, herbicide-resistant weeds and pesticide-resistant bugs could be driven out of existence. Animals that carry harmful viruses could be immunized with ease. Scientists have sought the power of gene drives for decades. But only with the emergence of a genetic tool called CRISPR/Cas9 — the bottle opener that unleashed the genie — has gene drive technology offered the prospect of providing a speedy means to end some of the world’s greatest health and ecological scourges. “Everything is possible with CRISPR,” says geneticist Hugo Bellen. “I’m not kidding.” © Society for Science & the Public 2000 - 2015.
Keyword: Genes & Behavior
Link ID: 21671 - Posted: 12.03.2015
By Kelli Whitlock Burton Evolutionarily speaking, we are born to make babies. Our bodies—and brains—don’t fall apart until we come to the end of our child-bearing years. So why are grandmothers, who don’t reproduce and who contribute little to food production, still around and still mentally sound? A new study offers an intriguing genetic explanation. Scientists have proposed several explanations for why our species lives as long and as healthily as it does. One idea is that grandmothers help out with child rearing. A 1998 study found, for example, that a Hadza group of hunter-gatherers in Tanzania had more babies if grandmothers helped feed their newly-weaned young grandchildren. The researchers speculated this kind of care freed up young mothers to reproduce, and ensured that the caregiver grandmother’s genes were passed on to more young. They called their theory the “grandmother hypothesis.” But grandmothers need to have all their wits about them to help out in this way, and the new study may explain how this happens. Physician-scientist Ajit Varki and evolutionary biologist Pascal Gagneux of the University of California, San Diego, arrived at the findings accidentally. The pair was studying a gene that helps control the body’s inflammatory and immune response to injury or infection. Previous studies have linked two forms of the gene—CD33—to Alzheimer’s disease. While one CD33 variant, or allele, predisposes a person to the disease, the other appears to protect against it by preventing the formation of protein clumps in the brain. © 2015 American Association for the Advancement of Science.
In Greek mythology, the Hydra was a gigantic, snake-like monster with nine heads and poisonous blood and breath, which lurked in the swamps of Lerna. Heracles was sent to destroy the beast as one of his twelve labours, but when he decapitated one of its heads, two more grew back in its place. He eventually defeated it with the help of his trusty nephew Iolaus, however, by burning out the severed roots with firebrands to prevent the regrowth, then decapitating its one immortal head and burying it under a heavy rock. The real Hydra has regenerative capacities that surpass those of its mythological namesake. When it is dismembered, any fragment of its body can regenerate to form a completely new individual, and it can even remain alive after its entire nervous system has been lost. Researchers in Switzerland now report that it does so by adapting its skin cells to make them behave more like neurons. Their findings provide clues about how nerve cells first evolved, billions of years ago. Hydra is a small freshwater polyp with a tubular body consisting of just two layers of cells, and a network of nerves that controls its movements, feeding, and its light-sensitive stinging tentacles. The central region of its body contains specialized, multi-purpose skin cells which can contract and detect mechanical stimuli. These so-called ‘i-cells’ also act as stem cells, continuously renewing themselves, while also producing immature nerve cells that migrate out to the extremities, where they differentiate to form the dense nerve net. © 2015 Guardian News and Media Limited
Keyword: Development of the Brain
Link ID: 21663 - Posted: 11.28.2015
Human DNA is 1 to 2% Neandertal, or more, depending on where your ancestors lived. Svante Pääbo, founder of the field of paleogenetics and winner of a 2016 Breakthrough Prize, explains why that matters © 2015 Scientific American
The town of Yarumal in Colombia is famous for all the wrong reasons: it has the world’s largest population of people with Alzheimer’s disease. In Yarumal and the surrounding state of Antioquia, 5000 people carry a gene mutation which causes early-onset Alzheimer’s – half of them will be diagnosed by the age of 45, and the other half will succumb by the time they are 65. Locals call the disease La Bobera, “the foolishness”, and the village bears uncanny parallels with the fictional Macondo in Gabriel Garcia Marquez’s novel One Hundred Years of Solitude, where people suffer memory disorders and hallucinations. But while Yarumal’s “curse” is well known, no one knew how the mutation first appeared. Now researchers have traced the ancestry of the mutation, concluding that it was probably introduced by a Spanish conquistador early in the 17th century. Ken Kosik at the University of California, Santa Barbara, and colleagues collected blood samples from 102 people in Antioquia and sequenced their genomes. The mutation causing this form of early-onset Alzheimer’s is called E280A and is found in a gene on chromosome 14 – 74 people had the mutation. Because Kosik’s team had information on the genome sequence around the mutation, they could use something called identity-by-descent analysis to determine how the people in the study were related. The analysis suggested the mutation arose from a common ancestor around 375 years ago. © Copyright Reed Business Information Ltd.
By Gretchen Reynolds Sturdy legs could mean healthy brains, according to a new study of British twins. As I frequently have written in this column, exercise may cause robust improvements in brain health and slow age-related declines in memory and thinking. Study after study has shown correlations between physical activity, muscular health and mental acuity, even among people who are quite old. But these studies have limitations and one of them is that some people may be luckier than others. They may have been born to have a more robust brain than someone else. Their genes and early home environment might have influenced their brain health as much as or more than their exercise habits. Their genes and early home environment also might have influenced those exercise habits, as well as how their bodies and brains responded to exercise. In other words, genes and environment can seriously confound experimental results. That problem makes twins so valuable for scientific purposes. (Full disclosure, I am a twin, although not an identical one.) Twins typically share the same early home environment and many of the same genes, and if they are identical, all their genes are the same. So if one twin’s body, brain and thinking abilities begin to differ substantially over the years from their twin’s, the cause is less likely to be solely genetic or the early environment, and more likely to be attributable to lifestyle, including exercise habits. It was that possibility that recently prompted Claire Steves, a senior lecturer in twin research at King’s College London, to consider twins and their thighs. © 2015 The New York Times Company
Link ID: 21641 - Posted: 11.18.2015
Laura Sanders In an unexpected twist, two antibodies designed to fight Alzheimer’s disease instead made nerve cells in mice misbehave more. The results, published online November 9 in Nature Neuroscience, highlight how little is known about how these drugs actually work, says study coauthor Marc Aurel Busche of Technical University Munich. “We need to understand what these antibodies do in the brains of patients better,” he says. The treatment approach relies on antibodies that target amyloid-beta, a protein that builds up in the brains of people with Alzheimer’s. One of the antibodies used in the new study, bapineuzumab, failed to show benefits in much-anticipated trials described in the New England Journal of Medicine in 2014. Despite that setback, some researchers say antibodies are still the best option to halt Alzheimer’s. The bapineuzumab trial was flawed, says neurologist Dennis Selkoe of Harvard Medical School and Brigham and Women’s Hospital. And the new results, which come from mice, have little relevance for ongoing tests of other antibodies in people, he says. “A-beta immunotherapy is the most promising approach right now, and nothing in their paper undercuts that,” he says. Several other antibodies have recently shown modest benefits in people with Alzheimer’s, he adds. Representatives from Eli Lilly and Biogen, pharmaceutical companies that are developing antibody treatments, declined to comment on the new study. © Society for Science & the Public 2000 - 2015
By Michelle Roberts Health editor, BBC News online An increasingly warped sense of humour could be an early warning sign of impending dementia, say UK experts. The University College London study involved patients with frontotemporal dementia, with the results appearing in the Journal of Alzheimer's Disease. Questionnaires from the friends and family of the 48 patients revealed many had noticed a change in humour years before the dementia had been diagnosed. This included laughing inappropriately at tragic events. Experts say more studies are now needed to understand how and when changes in humour could act as a red flag for dementia. There are many different types of dementia and frontotemporal dementia is one of the rarer ones. The area of the brain it affects is involved with personality and behaviour, and people who develop this form of dementia can lose their inhibition, become more impulsive and struggle with social situations. Dr Camilla Clark and colleagues recruited 48 patients from their dementia clinic at University College London. And they asked the friends or relatives of the patients to rate their loved one's liking for different kinds of comedy - slapstick comedy such as Mr Bean, satirical comedy such as Yes, Minister or absurdist comedy such as Monty Python - as well as any examples of inappropriate humour. Nearly all of the respondents said, with hindsight, that they had noticed a shift in the nine years before the dementia had been diagnosed. Many of the patients had developed a dark sense of humour - for example, laughing at tragic events in the news or in their personal lives. The dementia patients also tended to prefer slapstick to satirical humour, when compared with 21 healthy people of a similar age. © 2015 BBC.
Link ID: 21617 - Posted: 11.10.2015
by Laura Sanders Babies’ minds are mysterious. Thoughts might be totally different in a brain that lacks words, and sensations might feel alien in a body so new. Are babies’ perceptions like ours, or are they completely different? Even if babies could talk, words would surely fail to convey what it’s like to experience, oh, every single thing for the first time. A recent paper offers a sliver of insight into young babies’ inner lives. The study, published October 19 in Current Biology, finds an example in which 4-month-old babies are happily oblivious to the external world. The research focuses on a perceptual trick that suckers adults and 6-month-old babies alike. When the hands are crossed, people often mistake which hand feels a touch. Let’s say your left hand (now crossed over to the right side of your body) gets a tickle. Your eyes would see a hand on the right side of your body get touched — a place usually claimed by your right hand, but now occupied by your left. Those mismatches between sight, touch and expectation can thwart you from quickly and correctly saying which hand was touched. Here’s the twist: 4-month-old babies don’t fall for this trick, Andrew Bremner of Goldsmiths, University of London and his colleagues found. In the experiment, a researcher would hold infants’ legs in either a crossed position or straight, while one of two remote-controlled buzzers taped to their feet tickled one foot. The researchers then watched which foot or leg wiggled as a result. If the buzzed foot moved, that meant that the baby got it right. © Society for Science & the Public 2000 - 2015.
By DAVE ITZKOFF and BENEDICT CAREY For the first time in more than a year, the widow of the actor Robin Williams is speaking publicly about the circumstances that preceded Mr. Williams’s death, and sharing details about a disease he had when he died. Stories from Our Advertisers In interviews with People magazine and with ABC News, the widow, Susan Schneider Williams, laid the blame for her husband’s suicide in 2014 not on depression but on diffuse Lewy body dementia. “It was not depression that killed Robin,” Mrs. Williams said in the People magazine interview. “Depression was one of let’s call it 50 symptoms and it was a small one.” She added: “This was a very unique case and I pray to God that it will shed some light on Lewy bodies for the millions of people and their loved ones who are suffering with it. Because we didn’t know. He didn’t know.” Parts of an interview with Mrs. Williams were shown Tuesday on ABC’s “Good Morning America,” with further segments scheduled for that evening on the network’s “World News Tonight” and “Nightline” programs, and Friday on its morning talk show “The View.” Robin Williams was one of the most explosively, exhaustingly, prodigiously verbal comedians who ever lived, says film critic A. O. Scott. And the only thing faster than Williams’s mouth was his mind. By Adam Freelander on Publish Date August 12, 2014. Photo by ABC, via Associated Press. Watch in Times Video » Mr. Williams, the stand-up comic and star of “Mork & Mindy,” “Good Morning, Vietnam,” “Good Will Hunting” (for which he won an Oscar) and “Dead Poets Society,” killed himself on Aug. 11, 2014, in the home he shared with Mrs. Williams in Tiburon, Calif. He was 63. © 2015 The New York Times Company
By Michelle Roberts Health editor, BBC News online Brain training - playing online games that give memory and reasoning skills a workout - is beneficial for older people, a large-scale study has concluded. Researchers at King's College London found the mental exercises kept minds sharp and helped people with everyday skills such as shopping and cooking. Nearly 7,000 people aged 50 and over signed up for the six-month experiment, launched by BBC TV's Bang Goes The Theory. Longer studies are now beginning. The volunteers were recruited from the general population by a partnership between the BBC, the Alzheimer's Society and the Medical Research Council. As far as the investigators were aware, none had any problems with memory or cognition when they signed up to the experiment. Some of the volunteers were encouraged to play online brain training games for 10 minutes at a time, as often as they wished. The others - the control group - were asked to do simple internet searches. The researchers tested the subjects on a series of medically recognised cognitive tests at baseline and then again at three months and six months to see if there was any detectable difference between the groups. The researchers found after six months, those who played "brain training" games for reasoning and problem-solving kept their broader cognitive skills better than those who did not. The benefit appeared to kick in when people played the games at least five times a week. And people over 60 who played these games reported better scores for carrying out essential everyday tasks, the Journal of Post-acute and Long Term Care Medicine reports. © 2015 BBC