Chapter 7. Life-Span Development of the Brain and Behavior
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
Mid-life stress may increase a woman's risk of developing dementia, according to researchers. In a study of 800 Swedish women, those who had to cope with events such as divorce or bereavement were more likely to get Alzheimer's decades later. The more stressful events there were, the higher the dementia risk became, BMJ Open reports. The study authors say stress hormones may be to blame, triggering harmful alterations in the brain. Stress hormones can cause a number of changes in the body and affect things such as blood pressure and blood sugar control. And they can remain at high levels many years after experiencing a traumatic event, Dr Lena Johansson and colleagues explain. But they say more work is needed to confirm their findings and ascertain whether the same stress and dementia link might also occur in men. In the study, the women underwent a battery of tests and examinations when they were in either their late 30s, mid-40s or 50s, and then again at regular intervals over the next four decades. At the start of the study, one in four women said they had experienced at least one stressful event, such as widowhood or unemployment. BBC © 2013
By DENISE GELLENE Dr. David Hubel, who was half of an enduring scientific team that won a Nobel Prize for explaining how the brain assembles information from the eye’s retina to produce detailed visual images of the world, died on Sunday in Lincoln, Mass. He was 87. The cause was kidney failure, his son Carl said. Dr. Hubel (pronounced HUGH-bull) and his collaborator, Dr. Torsten Wiesel, shared the 1981 Nobel in Physiology or Medicine with Roger Sperry for discovering ways that the brain processes information. Dr. Hubel and Dr. Wiesel concentrated on visual perception, initially experimenting on cats; Dr. Sperry described the functions of the brain’s left and right hemispheres. Dr. Hubel’s and Dr. Wiesel’s work further showed that sensory deprivation early in life can permanently alter the brain’s ability to process images. Their findings led to a better understanding of how to treat certain visual birth defects. Dr. Hubel and Dr. Wiesel collaborated for more than two decades, becoming, as they made their discoveries, one of the best-known partnerships in science. “Their names became such a brand name that H&W rolled off the tongue as easily in the lab as A&W root beer did at lunch,” Robert H. Wurtz, a neuroscientist, wrote in a review article about their work. Before Dr. Hubel and Dr. Wiesel started their research in the 1950s, scientists had long believed that the brain functioned like a movie screen — projecting images exactly as they were received from the eye. Dr. Hubel and Dr. Wiesel showed that the brain behaves more like a microprocessor, deconstructing and then reassembling details of an image to create a visual scene. © 2013 The New York Times Company
By KEN BELSON Football players as young as 7 sustain hits to the head comparable in magnitude to those absorbed by high school and adult players, and most of the hits are sustained in practices, not games, according to research to be released Wednesday. The findings, which may influence how youth football organizations handle training methods and rules, were included in four studies published by researchers at the Virginia Tech-Wake Forest University School of Biomedical Engineering and Sciences. The research, though limited, is considered by experts to be a step in the effort to address the relatively shallow understanding of the potential long-term effects of head trauma on young players. More than 25,000 football players from 8 to 19 years old are taken to emergency rooms seeking treatment for concussions every year, but most of the research on head injuries in football has focused on professional and college players. The new research, which was presented at the annual Biomedical Engineering Society conference this week, tracked about 120 players in Virginia and North Carolina from 7 to 18 over two seasons. Each young athlete wore six devices, known as accelerometers, in their helmets to measure the force, position and direction of the hits, and every practice and game was videotaped to determine how they occurred. To help determine any changes in brain structure and function, many of the players received magnetic resonance imaging brain scans before and after the season, and after they sustained a concussion. Some players also received magnetoencephalography scans, or MEG scans, to map their brain activity. © 2013 The New York Times Company
Virginia Hughes Enzymes called topoisomerases are crucial for the expression of extremely long genes in neurons, according to a study published 5 September in Nature1. More than one-quarter of these genes are known autism candidates, the study found. In the process of doing these analyses, the researchers stumbled on something surprising about autism genes in general: They're three to four times longer than the average gene expressed in neurons. "It's pretty remarkable that, at least to my knowledge, no one had noticed this before," notes Benjamin Philpot, associate professor of cell biology and physiology at the University of North Carolina, Chapel Hill, and one of the study's leaders. "But the genes are definitely much longer. It's very striking." The findings suggest that defects in topoisomerases — whether caused by genetic mutations or environmental influences — may contribute to some cases of autism and other developmental disorders, the researchers say. If it's true that long genes are preferentially affected in autism, "the implications are really quite fascinating," notes James Sutcliffe, associate professor of molecular physiology and biophysics at Vanderbilt University in Nashville, Tennessee, who was not involved in the research. In genetic sequencing studies, for example, mutations found in long genes tend to be discounted in statistical analyses. That’s because the longer a gene is, the more likely it is to harbor a mutation just by chance. But the new study suggests that mutations in long genes should be considered more carefully.
By Laura Geggel and SFARI.org Boredom, tiredness, hunger and stress can all set off a yawn. People can even 'catch' a bout of yawning when they see or hear another person in the throes of the involuntary gesture, a phenomenon known as social yawning. Researchers speculate that this shared behavior is a form of empathy that strengthens the bonds of a group: One drowsy person’s yawn that triggers others to do the same could lead to a unanimous call for bedtime, for example. Humans aren't the only species to yawn sympathetically: Dogs yawn in response to human yawns, and chimpanzees and baboons yawn in concert with one another. Children with autism apparently don’t respond to social yawning, however, prompting some researchers to blame their well-chronicled struggle with empathy. A new Japanese study suggests that, instead, children with the disorder miss facial cues, such as closed eyes, that make yawning contagious. The study was published 22 July in Autism Research and Treatment. The researchers say children with autism miss those cues because they avoid looking at people’s faces. But that may not entirely explain it. For example, a small 2009 study found that typically developing children yawn even when they’ve only heard another person do so, but children with autism do not. In the new study, the researchers set up two experiments to determine whether children with autism look at others’ faces enough to catch a social yawn. In the first test, 26 children with autism and 46 controls wore eye-tracking devices while watching video clips of people either yawning or remaining still. The researchers asked the children to count how many people in the clips were wearing glasses to make sure they looked at the people’s eyes. The video showed the person yawning only when the eye tracker verified that the children had fixed their gaze on the eyes. © 2013 Scientific American
By William Saletan In much of this country, over the last three years, pro-lifers have banned abortions 20 weeks after fertilization. They’ve justified these bans by asserting—contrary to the most authoritative studies—that fetuses at this stage of development can feel pain. Their assertions, in turn, are based on research by several doctors. But the doctors don’t buy the pro-lifers’ conclusions. They say their research doesn’t support the bans. The 12 state bans (several of which have been blocked or limited by courts) begin with legislative “findings.” The findings parrot a 33-page report posted by the National Right to Life Committee and other pro-life organizations. The report cites the work of a number of researchers. Pam Belluck, an enterprising New York Times correspondent, contacted the researchers and asked them about the abortion bans. It turns out there’s a big gap between the science and the legislation. The pro-life report cites Dr. Nicholas Fisk, a former president of the International Fetal Medicine and Surgery Society, 27 times. According to the report, Fisk’s work shows fetal “stress responses” that imply sensitivity to pain. But Fisk tells Belluck that he doesn’t buy the inference from stress hormones and cerebral blood flow to pain. Neural studies, he says, have persuaded him that until 24 weeks gestation—the current abortion limit in many states—fetal pain “is not possible at all.” The report also cites Dr. Mark Rosen, a fetal anesthesia pioneer, 16 times. Rosen’s work, the report suggests, shows that painkillers and anesthesia are common during fetal surgery because unborn children can feel pain. But Rosen tells Belluck that the real purpose of such drugs during fetal surgery is to minimize dangerous movement and harmful stress hormones, thereby facilitating recovery. The drugs don’t signify medical belief in fetal pain. Dr. Scott Adzick, another fetal surgery expert cited in the pro-life report, makes the same point. © 2013 The Slate Group, LLC
Billions of dollars have been spent on clinical trials of Alzheimer’s drugs that target amyloid plaques—the hallmark protein tangles that clog brain cells in people with the memory-robbing disease. So far, all have failed, leading some frustrated researchers to say it’s time to move on to other drug targets. Others say the drugs have not yet been fairly tested because they were administered too late, after brain damage is irreversible. Yesterday, the National Institutes of Health (NIH) announced that it is giving $33 million to a study that researchers hope will either revive the amyloid hypothesis, or put it to bed. The new trial—estimated to cost at least $100 million overall, with most of the remaining funds provided by partners in the pharmaceutical industry—will be part of the Alzheimer's Prevention Initiative, a large consortium of researchers attempting to identify biomarkers and treatments that can slow or stop the disease. Lead researchers Eric Reiman and Pierre Tariot of the Banner Alzheimer’s Institute in Phoenix plan to give a yet-to-be identified anti-amyloid drug, or placebo, to 650 people who carry two copies of the APOE4 gene—a genetic double whammy that confers a 10-fold increased risk of developing Alzheimer’s late in life. All participants will be between the ages of 60 and 75 and healthy, including free of recognized Alzheimer’s symptoms. Roughly a third will likely not have much amyloid in their brains yet, allowing the researchers to track whether the drug affects its accumulation, Reiman says. © 2012 American Association for the Advancement of Science
Link ID: 18677 - Posted: 09.21.2013
David Hilfiker knows what's coming. He was diagnosed with Alzheimer's so early that he's had time to tell his family what he wants to happen once forgetfulness turns incapacitating. "When it's time to put me in an institution, don't have me at home and destroy your own life," said the retired physician, who is still well enough that he blogs about the insidious progress of the disease. "Watching the Lights Go Out," it's titled. Nearly half of all seniors who need some form of long-term care -— from help at home to full-time care in a facility — have dementia, the World Alzheimer Report said Thursday. It's a staggering problem as the global population ages, placing enormous strain on families who provide the bulk of that care at least early on, and on national economies alike. Indeed, cognitive impairment is the strongest predictor of who will move into a care facility within the next two years, 7.5 times more likely than people with cancer, heart disease or other chronic ailments of older adults, the report found. "It's astonishing," said Marc Wortmann, executive director of Alzheimer's Disease International, which commissioned the report and focused on the problems of caregiving. "What many countries try to do is keep people away from care homes because they say that's cheaper. Yes it's cheaper for the government or the health system, but it's not always the best solution." And dropping birth rates mean there are fewer children in families to take care of aging parents, too, said Michael Hodin of the Global Coalition on Aging. © CBC 2013
Link ID: 18676 - Posted: 09.21.2013
by Andy Coghlan The two major brain abnormalities that underlie Alzheimer's disease can now be viewed simultaneously in brain scans while people are still alive, providing new insight into how the disease develops and whether drugs are working. The breakthrough comes from the development of a harmless tracer chemical that is injected into the bloodstream and accumulates exclusively in "tau tangles" – one type of abnormality that occurs in the brains of people with Alzheimer's and other kinds of dementia. Fluorescent light emitted from the chemical is picked up using positron emission tomography (PET), showing exactly where the tangles are. The tracer remains in the brain for a few hours before being broken down and expelled from the body. Similar tracers already exist for beta amyloid plaques, the other major anatomical feature of Alzheimer's, so the one for tau tangles completes the picture. "This is a big step forward," says John Hardy, an Alzheimer's researcher at University College London. "This is of critical significance, as tau lesions are known to be more intimately associated with neuronal loss than plaques," says Makoto Higuchi of the National Institute of Radiological Sciences in Chiba, Japan, and head of the team who developed the new tracer. The tracer could help researchers unravel exactly how Alzheimer's develops, and enable earlier diagnosis and monitoring of treatments. © Copyright Reed Business Information Ltd.
By PAM BELLUCK In the most significant sign yet of a broad shift in the focus of Alzheimer’s research from treating to preventing the disease, the federal government announced on Wednesday its largest grant so far to test an Alzheimer’s drug on healthy people at greatest risk for the most common form of the disease. The $33.2 million grant, and several other prevention studies awarded federal money in the last year, follow years of unsuccessful trials of treatments on people who already have dementia. Those failures have led to the realization that these drugs appear to be ineffective by the time memory and thinking problems have taken hold. At the same time, scientific advances have allowed researchers to identify people at risk for Alzheimer’s long before symptoms emerge. With five million Americans suffering from Alzheimer’s and their ranks projected to surge as baby boomers age, federal health officials consider the disease such a priority that Dr. Francis S. Collins, director of the National Institutes of Health, scraped money together when forced budget cuts slashed the Obama administration’s promise of $100 million in additional funding for Alzheimer’s for 2013. Dr. Collins said he dipped into the budgets of the 27 N.I.H. agencies to supply $40 million awarded Wednesday for several Alzheimer’s research projects. Another $5 million was provided by the National Institute on Aging. “The worst thing we could do would be to just hunker down and hold off tackling very important problems,” Dr. Collins said, adding, “Obviously, this is high-risk research, but goodness, the stakes are so high that we felt we had to go forward even in the face of the most difficult budget environment that anyone can remember in the N.I.H.” © 2013 The New York Times Company
Link ID: 18672 - Posted: 09.19.2013
By PAM BELLUCK It is a new frontier of the anti-abortion movement: laws banning abortion at 20 weeks after conception, contending that fetuses can feel pain then. Since 2010, a dozen states have enacted them, most recently Texas. Nationally, a bill passed the Republican-dominated House of Representatives in June. The science of fetal pain is highly complex. Most scientists who have expressed views on the issue have said they believe that if fetuses can feel pain, the neurological wiring is not in place until later, after the time when nearly all abortions occur. Several scientists have done research that abortion opponents say shows that fetuses can feel pain at 20 weeks after conception. One of those scientists said he believed fetuses could likely feel pain then, but he added that he believed the few abortions performed then could be done in ways to avoid pain. He and two other scientists said they did not think their work or current evidence provided scientific support for fetal-pain laws. Some scientists’ views have evolved as more research has been done. Dr. Nicholas Fisk, a senior maternal-fetal medicine specialist at Royal Brisbane and Women’s Hospital in Australia, said he once considered early fetal pain “a major possibility” after finding that fetuses receiving blood transfusions produced increased stress hormones and blood flow to the brain, and that painkillers lowered those levels. But Dr. Fisk, a former president of the International Fetal Medicine and Surgery Society, said neurological research has convinced him that pain “is not possible at all” before 24 weeks. © 2013 The New York Times Company
Drugs to treat Alzheimer's disease don't help patients with mild cognitive impairment and are linked to greater risk of harm, a Canadian review concludes. People with mild cognitive impairment show symptoms of memory problems that are not severe enough to be considered dementia or to interfere with day-to-day functioning. Each year, three to 17 per cent of people with mild cognitive impairment deteriorate to dementia, research suggests. It was hoped that "cognitive enhancers" used to treat dementia might delay progression to dementia. Dr. Sharon Straus of the department of geriatric medicine at the University of Toronto and her team reviewed clinical trials and reports on the effects of four cognitive enhancers. "Cognitive enhancers did not improve cognition or function among patients with mild cognitive impairment and were associated with a greater risk of gastrointestinal harms," the reviewers concluded in Monday's issue of the Canadian Medical Association Journal. "Our findings do not support the use of cognitive enhancers for mild cognitive impairment." The medications act on different neurotransmitters in the brain, such as acetylcholine. © CBC 2013
By CARL ZIMMER From biology class to “C.S.I.,” we are told again and again that our genome is at the heart of our identity. Read the sequences in the chromosomes of a single cell, and learn everything about a person’s genetic information — or, as 23andme, a prominent genetic testing company, says on its Web site, “The more you know about your DNA, the more you know about yourself.” But scientists are discovering that — to a surprising degree — we contain genetic multitudes. Not long ago, researchers had thought it was rare for the cells in a single healthy person to differ genetically in a significant way. But scientists are finding that it’s quite common for an individual to have multiple genomes. Some people, for example, have groups of cells with mutations that are not found in the rest of the body. Some have genomes that came from other people. “There have been whispers in the matrix about this for years, even decades, but only in a very hypothetical sense,” said Alexander Urban, a geneticist at Stanford University. Even three years ago, suggesting that there was widespread genetic variation in a single body would have been met with skepticism, he said. “You would have just run against the wall.” But a series of recent papers by Dr. Urban and others has demonstrated that those whispers were not just hypothetical. The variation in the genomes found in a single person is too large to be ignored. “We now know it’s there,” Dr. Urban said. “Now we’re mapping this new continent.” Dr. James R. Lupski, a leading expert on the human genome at Baylor College of Medicine, wrote in a recent review in the journal Science that the existence of multiple genomes in an individual could have a tremendous impact on the practice of medicine. “It’s changed the way I think,” he said in an interview. Scientists are finding links from multiple genomes to certain rare diseases, and now they’re beginning to investigate genetic variations to shed light on more common disorders. © 2013 The New York Times Company
Keyword: Genes & Behavior
Link ID: 18657 - Posted: 09.17.2013
Emily Underwood Jackie Murphy didn't worry that her son Fintan was a late talker, at least at first. Her other two children had been slow to say their first words, so it was only when the former California nurse noticed that her 20-month-old wasn't responding to his name, or even reacting to loud noises, that she became concerned. "One day, I dropped a toy xylophone behind him and he didn't even flinch," she says. "That's when I knew something was wrong." Fintan didn't have a hearing problem—he had autism, his mom finally learned after more than 6 months of searching for a diagnosis. A few months later, Murphy enrolled Fintan in the Autism Phenome Project at the MIND Institute at the University of California (UC), Davis, a long-term assessment of children, as many as 1800, aimed at teasing out subtypes of the complex disorder. Murphy also became a research subject, donating a blood sample. One of the project's researchers, Melissa Bauman, soon informed Murphy that her blood had tested positive for antibodies that react to fetal brain proteins. Bauman asked her to donate more blood for studies exploring the provocative idea that some of Murphy's antibodies had slipped through the placenta and into Fintan's developing brain, affecting its maturation. At that point, Murphy says, she and her husband made a big decision: Fearing that the immune proteins in her blood would harm another baby, they decided that she would not again get pregnant. Many more women could face a similarly difficult choice. In July, immunologist Judy Van de Water and her team at UC Davis, which includes Bauman and Daniel Braunschweig, bolstered the hypothesis that maternal antibodies cause some autism with two studies, including one showing autismlike symptoms in monkeys injected with such antibodies. And women may soon be able to check whether they have the suspect antibodies: California company Pediatric Bioscience announced that it is moving forward with a new diagnostic test, based on patented antibody screening techniques licensed from Van de Water and UC Davis. © 2013 American Association for the Advancement of Science
by Andy Coghlan Normal adult cells have been reprogrammed to become stem cells inside live mice for the first time. As stem cells can be coaxed into developing into almost any kind of cell, being able to prompt this behaviour in the body could one day be used to repair ailing organs including the heart, liver, spinal cord and pancreas. "By doing it in situ, the cells are already there in the tissue, in the right position," says Manuel Serrano at the Spanish National Cancer Research Centre in Madrid, and co-leader of the new work. The technique overcomes the difficulties inherent in making cells outside the body, grafting them into people, and then of potential rejection. It opens up new clinical opportunities, say the researchers. Since 2006, when Nobel-prizewinning researcher Shinya Yamanaka first made adult cells return to a stem-cell-like state of being pluripotent – able to turn into almost any cell type – all such induced pluripotent stem (iPS) cells have been made in vitro. This is done by taking a sample of adult cells, such as skin cells, and treating them with four proteins that rewind the cells back to an embryonic-like state. Serrano genetically altered mice to give them extra copies of the four genes that produce these proteins: Oct, Sox2, Klf4 and c-Myc. The genes were programmed to kick into action when exposed to doxycycline, an antibiotic. © Copyright Reed Business Information Ltd.
By Bruce Bower Babies have an ear for primeval dangers, a new study suggests. By age 9 months, infants pay special attention to sounds that have signaled threats to children’s safety and survival throughout human evolution, say psychologist Nicole Erlich of the University of Queensland, Australia, and her colleagues. Those sounds include a snake hissing, adults’ angry voices, a crackling fire, thunder claps and — as a possible indicator of a nearby but unseen danger — another infant’s cries. Noises denoting modern dangers, as well as pleasant sounds, failed to attract the same level of interest from 9-month-olds, Erlich and her colleagues report Aug. 27 in Developmental Science. People can learn to fear just about anything. But tens of thousands of years of evolution have primed infants’ brains to home in on longstanding perils, the scientists propose. “There is something special about evolutionarily threatening sounds that infants respond to,” Erlich says. Another study that supported that idea, by psychologist David Rakison of Carnegie Mellon University in Pittsburgh, found that 11-month-olds rapidly learn to associate fearful faces with images of snakes and spiders (SN: 9/26/09, p. 11). “There is now a coherent argument that infants are biologically prepared in at least two sensory systems to learn quickly which evolutionarily relevant objects to fear,” Rakison says. © Society for Science & the Public 2000 - 2013
Kelly Servick If keeping the brain spry were as simple as pumping iron, everyone would want to own the ultimate piece of cognitive exercise equipment. But designing activities to reverse the mental effects of aging is tricky. A new video game created by neuroscientists shows promise in reversing some signs of decline. Now, the researchers behind it aim to prove that video game training can be more than the latest workout craze. Games designed to keep the brain healthy as it ages have found an eager audience. “Many, many people have gotten into the business,” says neuropsychologist Glenn Smith of the Mayo Clinic in Rochester, Minnesota. The brain does appear to be capable of changing its structure and developing new skills over the course of a lifetime. But not all the products on the market are designed using scientific knowledge of the aging brain, and their ability to make meaningful, lasting changes hasn’t been proven, says Smith, who studies games as treatment for early signs of dementia. “There’s an awful lot of skepticism out there,” he says. The heart of the issue is whether practicing a video game can strengthen skills that are useful away from a computer. Early research showed that people could improve on computerized memory and speed tasks in the lab, Smith says. But it’s not clear whether these gains translate to everyday life. A recent trend puts more value in games that target the underlying problem—the decline in ability to remember and react as people age. © 2012 American Association for the Advancement of Science.
Scientists believe they have discovered a new reason why we need to sleep - it replenishes a type of brain cell. Sleep ramps up the production of cells that go on to make an insulating material known as myelin which protects our brain's circuitry. The findings, so far in mice, could lead to insights about sleep's role in brain repair and growth as well as the disease MS, says the Wisconsin team. The work is in the Journal of Neuroscience. Dr Chiara Cirelli and colleagues from the University of Wisconsin found that the production rate of the myelin making cells, immature oligodendrocytes, doubled as mice slept. The increase was most marked during the type of sleep that is associated with dreaming - REM or rapid eye movement sleep - and was driven by genes. In contrast, the genes involved in cell death and stress responses were turned on when the mice were forced to stay awake. Precisely why we need to sleep has baffled scientists for centuries. It's obvious that we need to sleep to feel rested and for our mind to function well - but the biological processes that go on as we slumber have only started to be uncovered relatively recently. Dr Cirelli said: "For a long time, sleep researchers focused on how the activity of nerve cells differs when animals are awake versus when they are asleep. "Now it is clear that the way other supporting cells in the nervous system operate also changes significantly depending on whether the animal is asleep or awake." The researchers say their findings suggest that sleep loss might aggravate some symptoms of multiple sclerosis (MS), a disease that damages myelin. BBC © 2013
Alison Abbott Like humans, Drosophila fruitflies become forgetful with age. But at least their memory deficits can be reversed by eating a diet rich in polyamines, according to a study published online today1 in Nature Neuroscience. “There’s a great need for cognitive enhancers to keep us healthy into old age — now polyamines are offering a new approach,” says learning and memory specialist Ronald Davis at the Scripps Research Institute Florida in Jupiter, who was not involved in the study. “There are reasons for optimism that this fly work will translate into human.” Polyamines — which include the graphically named putrescine, cadaverine and spermidine — are small molecules that are essential for cells to survive and grow. But their cellular levels decline with age. Some foods that are popularly considered to have health benefits — such as wheatgerm and fermented soya beans — contain high levels of polyamines. Japanese scientists have shown that natto, a fermented soya-bean product, raises the level of polyamines in the blood in humans2. But there is a long way to go before anyone can say that polyamines can help to stave off memory decline in ageing people, cautions Stephan Sigrist of the Free University of Berlin, one of the study's principal investigators. “Still, the polyamine system does offer a new target for those interested in developing therapies.” © 2013 Nature Publishing Group
Amanda Mascarelli It’s an inconvenient truth of aging: In our 30s and up, it gets increasingly harder for most of us to recall names, faces, and details from the past. Scientists have long debated whether this gradual decline is an early form of Alzheimer’s disease—a neurodegenerative condition that leads to severe dementia—or a distinct neurological process. Now, researchers have found a protein that distinguishes typical forgetfulness from Alzheimer’s and could lead to potential treatments for age-related memory loss. Previous studies have shown that Alzheimer’s disease and age-related memory loss involve different neural circuits in the hippocampus, a seahorse-shaped structure in the brain where memories are formed and organized. The hallmark signs of Alzheimer’s disease are well established—tangled proteins and plaques accumulate over time, and brain tissue atrophies. But little is known about what occurs when memory declines during normal aging, except that brain cells begin to malfunction, says Scott Small, a neurologist at Columbia University and senior author to the study. “At the molecular level, there’s been a lot of uncertainty about what is actually going wrong, and that’s what this paper isolates.” To tease apart the biological processes involved in memory loss in normal aging, Scott and other researchers from Columbia University in New York examined postmortem brain tissue from eight healthy people ranging in age from 33 to 86. They looked for differences in gene expression—the proteins or other products that a gene makes—between younger and older people. They also looked for age-related changes in the brains of mice. © 2012 American Association for the Advancement of Science