Chapter 13. Memory, Learning, and Development

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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

Keyword: Autism
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

Keyword: Alzheimers; Development of the Brain
Link ID: 21688 - Posted: 12.10.2015

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.

Keyword: Alzheimers; Vision
Link ID: 21686 - Posted: 12.09.2015

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

Keyword: Alzheimers
Link ID: 21685 - Posted: 12.09.2015

By Michael M. Torrice, We learn from experience: It sounds like a trite sentiment posted by a friend on Facebook, but neuroscientists would agree. Our interactions with the world around us strengthen and weaken the connections between our neurons, a process that neuroscientists consider to be the cellular mechanism of learning. Now researchers report that boosting signaling of a certain receptor in the brain with a small molecule can enhance these cellular changes and improve learning in people. The findings could lead to new treatments for patients with disorders associated with deficits in learning, such as Alzheimer’s disease and schizophrenia. Through decades of research on how synapses change in animal brains, scientists have found that the N-methyl-d-aspartate receptor (NMDAR) plays a critical role in strengthening synapses during learning. Compounds that increase NMDAR signaling can drive such changes and, as a result, help animals learn new tasks. Robert F. Asarnow at UCLA and colleagues wanted to test whether one such compound, d-cycloserine, would act similarly in people. But neuroscientists measure synapse changes in animals by sticking electrodes into slices of brain tissue to record electrical signals. “Obviously, we don’t do that to our friends,” Asarnow says. So his team used electroencephalography (EEG) to record electrical activity through electrodes stuck to the scalps of its subjects. The team monitored this activity as the subjects watched a certain pattern flash on a screen at high frequency for a couple minutes. Afterward, the subjects showed a spike in EEG activity in their visual cortex when they viewed the pattern at a later time. This suggested a population of neurons had wired themselves together by strengthening their synapses. © 2015 Scientific American

Keyword: Learning & Memory
Link ID: 21684 - Posted: 12.09.2015

by Laura Sanders There’s only so much brainpower to go around, and when the eyes hog it all, the ears suffer. When challenged with a tough visual task, people are less likely to perceive a tone, scientists report in the Dec. 9 Journal of Neuroscience. The results help explain what parents of screen-obsessed teenagers already know. For the study, people heard a tone while searching for a letter on a computer screen. When the letter was easy to find, participants were pretty good at identifying a tone. But when the search got harder, people were less likely to report hearing the sound, a phenomenon called inattentional deafness. Neural responses to the tone were blunted when people worked on a hard visual task, but not when the visual task was easy, researchers found. By showing that a demanding visual job can siphon resources away from hearing, the results suggest that perceptual overload can jump between senses. © Society for Science & the Public 2000 - 2015

Keyword: Attention; Hearing
Link ID: 21682 - 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.

Keyword: Development of the Brain; Brain imaging
Link ID: 21678 - Posted: 12.08.2015

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

Keyword: Epigenetics; Obesity
Link ID: 21676 - Posted: 12.05.2015

By Nicholas Bakalar Watching television may be bad for your brain, a new study suggests. Researchers followed 3,274 people whose average age was 25 at the start of the study for 25 years, using questionnaires every five years to collect data on their physical activity and TV watching habits. At year 25, they administered three tests that measured various aspects of mental acuity. The highest level of TV watching — more than three hours a day most days — was associated with poor performance on all three tests. Compared with those who watched TV the least, those who watched the most had between one-and-a-half and two times the odds of poor performance on the tests, even after adjusting for age, sex, race, educational level, body mass index, smoking, alcohol use, hypertension and diabetes. Those with the lowest levels of physical activity and the highest levels of TV watching were the most likely to have poor test results. The authors acknowledge that their findings, published in JAMA Psychiatry, depend on self-reports, and that they had no baseline tests of cognitive function for comparison. “We can’t separate out what is going on with the TV watching,” said the lead author, Dr. Kristine Yaffe, a professor of psychiatry and neurology at the University of California, San Francisco. “Is it just the inactivity, or is there something about watching TV that’s the opposite of cognitive stimulation?” © 2015 The New York Times Company

Keyword: Intelligence
Link ID: 21675 - Posted: 12.05.2015

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.

Keyword: Drug Abuse; Genes & Behavior
Link ID: 21672 - Posted: 12.03.2015

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.

Keyword: Alzheimers; Genes & Behavior
Link ID: 21669 - Posted: 12.01.2015

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

By Nala Rogers If you travel with a group of friends, you might delegate navigation to the person with the best sense of direction. But among homing pigeons, the leader is whoever flies the fastest—even if that pigeon has to pick up navigation skills on the job, according to a new study. To find out how the skills of individual pigeons influence flock direction, researchers tested four flocks on journeys from three different locations, each about 5 kilometers from their home loft near Oxford, U.K. At each site, the researchers tracked the pigeons during solo flights before releasing them together for several group journeys. The fastest birds surged to the front during group flights and determined when the flock turned, despite the fact that these leaders were often poor navigators during their initial solo expeditions. But on a final set of solo flights—made after the group journeys—these same leaders chose straighter routes than followers, the researchers report today in Current Biology. Apparently, being responsible for group decisions helped pigeons learn the route, say scientists, raising questions about the two-way interplay between skills and leadership. © 2015 American Association for the Advancement of Science

Keyword: Animal Migration; Learning & Memory
Link ID: 21661 - Posted: 11.28.2015

By John Bohannon It may sound like a bird-brained idea, but scientists have trained pigeons to spot cancer in images of biopsied tissue. Individually, the avian analysts can't quite match the accuracy of professional pathologists. But as a flock, they did as well as trained humans, according to a new study appearing this week in PLOS ONE. Cancer diagnosis often begins as a visual challenge: Does this lumpy spot in a mammogram image justify a biopsy? And do cells in biopsy slides look malignant or benign? Training doctors and medical technicians to tell the difference is expensive and time-consuming, and computers aren't yet up to the task. To see whether a different type of trainee could do better, a team led by Richard Levenson, a pathologist and technologist at the University of California, Davis, and Edward Wasserman, a psychologist at the University of Iowa, in Iowa City, turned to pigeons. In spite of their limited intellect, the bobble-headed birds have certain advantages. They have excellent visual systems, similar to, if not better than, a human's. They sense five different colors as opposed to our three, and they don’t “fill in” the gaps like we do when expected shapes are missing. However, training animals to do a sophisticated task is tricky. Animals can pick up on unintentional cues from their trainers and other humans that may help them correctly solve problems. For example, a famous 20th century horse named Clever Hans was purportedly able to do simple arithmetic, but was later shown to be observing the reactions of his human audience. And although animals can perform extremely well on tasks that are confined to limited circumstances, overtraining on one set of materials can lead to total inaccuracy when the same information is conveyed slightly differently. © 2015 American Association for the Advancement of Science

Keyword: Vision; Learning & Memory
Link ID: 21652 - Posted: 11.21.2015

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

Keyword: Evolution; Genes & Behavior
Link ID: 21650 - Posted: 11.21.2015

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.

Keyword: Alzheimers; Genes & Behavior
Link ID: 21647 - Posted: 11.20.2015

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

Keyword: Alzheimers
Link ID: 21641 - Posted: 11.18.2015

By Emilie Reas What makes for a long-lasting memory? Research has shown that emotional or important events take root deeply, whereas neutral or mundane happenings create weak impressions that easily fade. But what about an experience that initially seemed forgettable but was later shown to be important? Animal research suggested that these types of older memories could be strengthened, but scientists had not been able to replicate this finding in humans—until now. New evidence suggests that our initially weak memories are maintained by the brain for a period, during which they can be enhanced. In the recent study published in Nature, psychologists at New York University showed 119 participants a series of images of tools and animals. A few minutes later the subjects saw a new set of images, with an electric shock paired with either the tools or the animals, to increase the salience of just one of those categories. The participants' memories for both sets of images were then tested either immediately, six hours later or the next day. Participants remembered images from the first neutral series better if they belonged to the same category (tool or animal) that was later paired with the shock. The findings suggest that even if an event does not seem meaningful when it occurs, a later cue that the experience was important can enhance the old memory. Although research has not yet demonstrated this effect outside the laboratory, the scientists speculate it happens often in daily life. For example, imagine you meet several new people at a networking event. During a job interview days later, you discover that one of those acquaintances is on the hiring committee, and suddenly the details of your conversation at the networking event become vivid and memorable—whereas the conversations you had with others at the event fade with time. © 2015 Scientific American

Keyword: Learning & Memory
Link ID: 21629 - Posted: 11.12.2015

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

Keyword: Alzheimers; Neuroimmunology
Link ID: 21622 - Posted: 11.10.2015