Chapter 7. Life-Span Development of the Brain and Behavior
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By Gretchen Reynolds Physical activity is good for our brains. A wealth of science supports that idea. But precisely how exercise alters and improves the brain remains somewhat mysterious. A new study with mice fills in one piece of that puzzle. It shows that, in rodents at least, strenuous exercise seems to beneficially change how certain genes work inside the brain. Though the study was in mice, and not people, there are encouraging hints that similar things may be going on inside our own skulls. For years, scientists have known that the brains of animals and people who regularly exercise are different than the brains of those who are sedentary. Experiments in animals show that, for instance, exercise induces the creation of many new cells in the hippocampus, which is a part of the brain essential for memory and learning, and also improves the survival of those fragile, newborn neurons. Researchers believe that exercise performs these feats at least in part by goosing the body’s production of a substance called brain-derived neurotropic factor, or B.D.N.F., which is a protein that scientists sometimes refer to as “Miracle-Gro” for the brain. B.D.N.F. helps neurons to grow and remain vigorous and also strengthens the synapses that connect neurons, allowing the brain to function better. Low levels of B.D.N.F. have been associated with cognitive decline in both people and animals. Exercise increases levels of B.D.N.F. in brain tissue. But scientists have not understood just what it is about exercise that prompts the brain to start pumping out additional B.D.N.F. So for the new study, which was published this month in the journal eLIFE, researchers with New York University’s Langone Medical Center and other institutions decided to microscopically examine and reverse engineer the steps that lead to a surge in B.D.N.F. after exercise. They began by gathering healthy mice. Half of the animals were put into cages that contained running wheels. The others were housed without wheels. For a month, all of the animals were allowed to get on with their lives. Those living with wheels ran often, generally covering several miles a day, since mice like to run. The others remained sedentary. © 2016 The New York Times Company
Megan Scudellari Shinya Yamanaka looked up in surprise at the postdoc who had spoken. “We have colonies,” Kazutoshi Takahashi said again. Yamanaka jumped from his desk and followed Takahashi to their tissue-culture room, at Kyoto University in Japan. Under a microscope, they saw tiny clusters of cells — the culmination of five years of work and an achievement that Yamanaka hadn't even been sure was possible. Two weeks earlier, Takahashi had taken skin cells from adult mice and infected them with a virus designed to introduce 24 carefully chosen genes. Now, the cells had been transformed. They looked and behaved like embryonic stem (ES) cells — 'pluripotent' cells, with the ability to develop into skin, nerve, muscle or practically any other cell type. Yamanaka gazed at the cellular alchemy before him. “At that moment, I thought, 'This must be some kind of mistake',” he recalls. He asked Takahashi to perform the experiment again — and again. Each time, it worked. Over the next two months, Takahashi narrowed down the genes to just four that were needed to wind back the developmental clock. In June 2006, Yamanaka presented the results to a stunned room of scientists at the annual meeting of the International Society for Stem Cell Research in Toronto, Canada. He called the cells 'ES-like cells', but would later refer to them as induced pluripotent stem cells, or iPS cells. “Many people just didn't believe it,” says Rudolf Jaenisch, a biologist at the Massachusetts Institute of Technology in Cambridge, who was in the room. But Jaenisch knew and trusted Yamanaka's work, and thought it was “ingenious”. © 2016 Macmillan Publishers Limited,
By Brady Dennis In one city after another, the tests showed startling numbers of children with unsafe blood lead levels: Poughkeepsie and Syracuse and Buffalo. Erie and Reading. Cleveland and Cincinnati. In those cities and others around the country, 14 percent of kids — and in some cases more — have troubling amounts of the toxic metal in their blood, according to new research published Wednesday. The findings underscore how despite long-running public health efforts to reduce lead exposure, many U.S. children still live in environments where they're likely to encounter a substance that can lead to lasting behavioral, mental and physical problems. "We've been making progress for decades, but we have a ways to go," said Harvey Kaufman, senior medical director at Quest Diagnostics and a co-author of the study, which was published in the Journal of Pediatrics. "With blood [lead] levels in kids, there is no safe level." Kaufman and two colleagues at Quest, the nation's largest lab testing provider, examined more than 5.2 million blood tests for infants and children under age 6 that were taken between 2009 and 2015. The results spanned every state and the District of Columbia. The researchers found that while blood lead levels declined nationally overall during that period, roughly 3 percent of children across the country had levels that exceed five micrograms per deciliter — the threshold that the Centers for Disease Control and Prevention considers cause for concern. But in some places and among particular demographics, those figures are much higher.
By Linda Marsa| Helen Epstein felt deeply isolated and alone. Haunted by her parents’ harrowing experiences in Nazi concentration camps in World War II, she was troubled as a child by images of piles of skeletons and barbed wire, and, in her words, “a floating sense of danger and incipient harm.” But her Czech-born parents’ defense against the horrific memories was to detach. “Their survival strategy in the war was denial and dissociation, and that carried into their behavior afterward,” recalls Epstein, who was born shortly after the war and grew up in Manhattan. “They believed in action over reflection. Introspection was not encouraged, but a full schedule of activities was.” It was only when she was a student at Israel’s Hebrew University in the late 1960s that she realized she was part of a community that shared a cultural and historical legacy that included both pain and fear. “I met dozens of kids of survivors,” she says, “one after the other who shared certain characteristics: preoccupation with a family past and Israel, and who spoke several middle European languages — just like me.” Epstein’s 1979 book about her observations, Children of the Holocaust, gave voice to that sense of alienation and free-floating anxiety. In the years since, mental health professionals have largely attributed the second generation’s moodiness, hypervigilance and depression to learned behavior. It is only now, more than three decades later, that science has the tools to see that this legacy of trauma becomes etched in our DNA — a process known as epigenetics, in which environmental factors trigger genetic changes that may be passed on, just as surely as blue eyes and crooked smiles.
By Esther Landhuis About 100 times rarer than Parkinson’s, and often mistaken for it, progressive supranuclear palsy afflicts fewer than 20,000 people in the U.S.—and two thirds do not even know they have it. Yet this little-known brain disorder that killed comic actor Dudley Moore in 2002 is quietly becoming a gateway for research that could lead to powerful therapies for a range of intractable neurodegenerative conditions including Alzheimer’s and chronic traumatic encephalopathy, a disorder linked to concussions and head trauma. All these diseases share a common feature: abnormal buildup of a protein called tau in the brains of patients. Progressive supranuclear palsy has no cure and is hard to diagnose. Although doctors may have heard of the disease, many know little about it. It was not described in medical literature until 1964 but some experts believe one of the earliest accounts of the debilitating illness appeared in an 1857 short story by Charles Dickens and his friend Wilke Collins: “A cadaverous man of measured speech. A man who seemed as unable to wink, as if his eyelids had been nailed to his forehead. A man whose eyes—two spots of fire—had no more motion than if they had been connected with the back of his skull by screws driven through them, and riveted and bolted outside among his gray hair. He had come in and shut the door, and he now sat down. He did not bend himself to sit as other people do, but seemed to sink bolt upright, as if in water, until the chair stopped him.” © 2016 Scientific American
Most available antidepressants do not help children and teenagers with serious mental health problems and some may be unsafe, experts have warned. A review of clinical trial evidence found that of 14 antidepressant drugs, only one, fluoxetine – marketed as Prozac – was better than a placebo at relieving the symptoms of young people with major depression. Another drug, venlafaxine, was associated with an increased risk of suicidal thoughts and suicide attempts. Blood test could identify people who will respond to antidepressants Read more But the authors stressed that the true effectiveness and safety of antidepressants taken by children and teenagers remained unclear because of the poor design and selective reporting of trials, which were mostly funded by drug companies. They recommended close monitoring of young people on antidepressants, regardless of what drugs they were prescribed, especially at the start of treatment. Professor Peng Xie, a member of the team from Chongqing Medical University in China, said: “The balance of risks and benefits of antidepressants for the treatment of major depression does not seem to offer a clear advantage in children and teenagers, with probably only the exception of fluoxetine.” Major depressive disorder affects around 3% of children aged six to 12 and 6% of teenagers aged 13 to 18. In 2004 the US Food and Drug Administration (FDA) issued a warning against the use of antidepressants in young people up to the age of 24 because of concerns about suicide risk. Yet the number of young people taking the drugs increased between 2005 and 2012, both in the US and UK, said the study authors writing in the Lancet medical journal. In the UK the proportion of children and teenagers aged 19 and under taking antidepressants rose from 0.7% to 1.1%. © 2016 Guardian News and Media Limited
By Amina Zafar, When Susan Robertson's fingers and left arm felt funny while she was Christmas shopping, they were signs of a stroke she experienced at age 36. The stroke survivor is now concerned about her increased risk of dementia. The link between stroke and dementia is stronger than many Canadians realize, the Heart and Stroke Foundation says. The group's annual report, released Thursday, is titled "Mind the connection: preventing stroke and dementia." Stroke happens when blood stops flowing to parts of the brain. Robertson, 41, of Windsor, Ont., said her short-term memory, word-finding and organizational skills were impaired after her 2011 stroke. She's extremely grateful to have recovered the ability to speak and walk after doctors found clots had damaged her brain's left parietal lobe. "I knew what was happening, but I couldn't say it," the occupational nurse recalled. Dementia risk A stroke more than doubles the risk of dementia, said Dr. Rick Swartz, a spokesman for the foundation and a stroke neurologist in Toronto. Raising awareness about the link is not to scare people, but to show how controlling blood pressure, not smoking or quitting if you do, eating a balanced diet and being physically active reduce the risk to individuals and could make a difference at a society level, Swartz said. While aging is a common risk factor in stroke and dementia, evidence in Canada and other developed countries shows younger people are also increasingly affected. ©2016 CBC/Radio-Canada.
By BENEDICT CAREY Jerome S. Bruner, whose theories about perception, child development and learning informed education policy for generations and helped launch the modern study of creative problem solving, known as the cognitive revolution, died on Sunday at his home in Manhattan. He was 100. His death was confirmed by his partner, Eleanor M. Fox. Dr. Bruner was a researcher at Harvard in the 1940s when he became impatient with behaviorism, then a widely held theory, which viewed learning in terms of stimulus and response: the chime of a bell before mealtime and salivation, in Ivan Pavlov’s famous dog experiments. Dr. Bruner believed that behaviorism, rooted in animal experiments, ignored many dimensions of human mental experience. In one 1947 experiment, he found that children from low-income households perceived a coin to be larger than it actually was — their desires apparently shaping not only their thinking but also the physical dimensions of what they saw. In subsequent work, he argued that the mind is not a passive learner — not a stimulus-response machine — but an active one, bringing a full complement of motives, instincts and intentions to shape comprehension, as well as perception. His writings — in particular the book “A Study of Thinking” (1956), written with Jacqueline J. Goodnow and George A. Austin — inspired a generation of psychologists and helped break the hold of behaviorism on the field. To build a more complete theory, he and the experimentalist George A. Miller, a Harvard colleague, founded the Center for Cognitive Studies, which supported investigation into the inner workings of human thought. Much later, this shift in focus from behavior to information processing came to be known as the cognitive revolution. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 22300 - Posted: 06.09.2016
By Sandra G. Boodman Richard McGhee and his family believed the worst was behind them. McGhee, a retired case officer at the Defense Intelligence Agency who lives near Annapolis, had spent six months battling leukemia as part of a clinical trial at MD Anderson Cancer Center in Houston. The experimental chemotherapy regimen he was given had worked spectacularly, driving his blood cancer into a complete remission. But less than nine months after his treatment ended, McGhee abruptly fell apart. He became moody, confused and delusional — even childish — a jarring contrast with the even-keeled, highly competent person he had been. He developed tremors in his arms, had trouble walking and became incontinent. “I was really a mess,” he recalled. Doctors suspected he had developed a rapidly progressive and fatal dementia, possibly a particularly aggressive form of Alzheimer’s disease. If that was the case, his family was told, his life span would be measured in months. Luckily, the cause of McGhee’s precipitous decline proved to be much more treatable — and prosaic — than doctors initially feared. “It’s really a pleasure to see somebody get better so rapidly,” said Michael A. Williams, a professor of neurology and neurosurgery at the University of Washington School of Medicine in Seattle. Until recently, Williams was affiliated with Baltimore’s Sinai Hospital, where he treated McGhee in 2010. “This was a diagnosis waiting to be found.”
By Jordana Cepelewicz Colors exist on a seamless spectrum, yet we assign hues to discrete categories such as “red” and “orange.” Past studies have found that a person's native language can influence the way colors are categorized and even perceived. In Russian, for example, light blue and dark blue are named as different colors, and studies find that Russian speakers can more readily distinguish between the shades. Yet scientists have wondered about the extent of such verbal influence. Are color categories purely a construct of language, or is there a physiological basis for the distinction between green and blue? A new study in infants suggests that even before acquiring language, our brain already sorts colors into the familiar groups. A team of researchers in Japan tracked neural activity in 12 prelinguistic infants as they looked at a series of geometric figures. When the shapes' color switched between green and blue, activity increased in the occipitotemporal region of the brain, an area known to process visual stimuli. When the color changed within a category, such as between two shades of green, brain activity remained steady. The team found the same pattern in six adult participants. The infants used both brain hemispheres to process color changes. Language areas are usually in the left hemisphere, so the finding provides further evidence that color categorization is not entirely dependent on language. At some point as a child grows, language must start playing a role—just ask a Russian whether a cloudless sky is the same color as the deep sea. The researchers hope to study that developmental process next. “Our results imply that the categorical color distinctions arise before the development of linguistic abilities,” says Jiale Yang, a psychologist at Chuo University and lead author of the study, published in February in PNAS. “But maybe they are later shaped by language learning.” © 2016 Scientific American
James Gorman Fruit flies are far from human, but not as far as you might think. They do many of the same things people do, like seek food, fight and woo mates. And their brains, although tiny and not set up like those of humans or other mammals, do many of the same things that all brains do — make and use memories, integrate information from the senses, and allow the creature to navigate both the physical and the social world. Consequently, scientists who study how all brains work like to use flies because it’s easier for them to do invasive research that isn’t allowed on humans. The technology of neuroscience is sophisticated enough to genetically engineer fly brains, and to then use fluorescent chemicals to indicate which neurons are active. But there are some remaining problems, like how to watch the brain of a fly that is moving around freely. It is one thing to record what is going on in a fly’s brain if the insect’s movement is restricted, but quite another to try to catch the light flash of brain cells from a fly that is walking around. Takeo Katsuki, an assistant project scientist at the Kavli Institute at the University of California, San Diego, is interested in courtship. And, he said, fruit flies simply won’t engage in courtship when they are tethered. So he and Dhruv Grover, another assistant project scientist, and Ralph J. Greenspan, in whose lab they both work, set out to develop a method for recording the brain activity of a walking fly. One challenge was to track the fly as it moved. They solved that problem with three cameras to follow the fly and a laser to activate the fluorescent chemicals in the brain. © 2016 The New York Times Company
By Andy Coghlan People once dependent on wheelchairs after having a stroke are walking again since receiving injections of stem cells into their brains. Participants in the small trial also saw improvements in their speech and arm movements. “One 71-year-old woman could only move her left thumb at the start of the trial,” says Gary Steinberg, a neurosurgeon at Stanford University who performed the procedure on some of the 18 participants. “She can now walk and lift her arm above her head.” Run by SanBio of Mountain View, California, this trial is the second to test whether stem cell injections into patients’ brains can help ease disabilities resulting from stroke. Patients in the first, carried out by UK company ReNeuron, also showed measurable reductions in disability a year after receiving their injections and beyond. All patients in the latest trial showed improvements. Their scores on a 100-point scale for evaluating mobility – with 100 being completely mobile – improved on average by 11.4 points, a margin considered to be clinically meaningful for patients. “The most dramatic improvements were in strength, coordination, ability to walk, the ability to use hands and the ability to communicate, especially in those whose speech had been damaged by the stroke,” says Steinberg. In both trials, improvements in patients’ mobility had plateaued since having had strokes between six months and three years previously. © Copyright Reed Business Information Ltd
By NICHOLAS ST. FLEUR Nine scientists have won this year’s Kavli Prizes for work that detected the echoes of colliding black holes, revealed how adaptable the nervous system is, and created a technique for sculpting structures on the nanoscale. The announcement was made on Thursday by the Norwegian Academy of Science Letters in Oslo, and was live-streamed to a watching party in New York as a part of the World Science Festival. The three prizes, each worth $1 million and split among the recipients, are awarded in astrophysics, nanoscience and neuroscience every two years. They are named for Fred Kavli, a Norwegian-American inventor, businessman and philanthropist who started the awards in 2008 and died in 2013. Eve Marder of Brandeis University, Michael M. Merzenich of the University of California, San Francisco, and Carla J. Shatz of Stanford won the neuroscience prize. Dr. Marder illuminated the flexibility and stability of the nervous system through her work studying crabs and lobsters and the neurons that control their digestion. Dr. Merzenich was a pioneer in the study of neural plasticity, demonstrating that parts of the adult brain, like those of children, can be reorganized by experience. Dr. Shatz showed that “neurons that fire together wire together,” by investigating how patterns of activity sculpt the synapses in the developing brain. The winners will receive their prizes in September at a ceremony in Oslo. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 22279 - Posted: 06.04.2016
By Simon Makin Other species are capable of displaying dazzling feats of intelligence. Crows can solve multistep problems. Apes display numerical skills and empathy. Yet, neither species has the capacity to conduct scientific investigations into other species' cognitive abilities. This type of behavior provides solid evidence that humans are by far the smartest species on the planet. Besides just elevated IQs, however, humans set themselves apart in another way: Their offspring are among the most helpless of any species. A new study, published recently in Proceedings of the National Academy of Sciences (PNAS), draws a link between human smarts and an infant’s dependency, suggesting one thing led to the other in a spiraling evolutionary feedback loop. The study, from psychologists Celeste Kidd and Steven Piantadosi at the University of Rochester, represents a new theory about how humans came to possess such extraordinary smarts. Like a lot of evolutionary theories, this one can be couched in the form of a story—and like a lot of evolutionary stories, this one is contested by some scientists. Kidd and Piantadosi note that, according to a previous theory, early humans faced selection pressures for both large brains and the capacity to walk upright as they moved from forest to grassland. Larger brains require a wider pelvis to give birth whereas being bipedal limits the size of the pelvis. These opposing pressures—biological anthropologists call them the “obstetric dilemma”—could have led to giving birth earlier when infants’ skulls were still small. Thus, newborns arrive more immature and helpless than those of most other species. Kidd and Piantadosi propose that, as a consequence, the cognitive demands of child care increased and created evolutionary pressure to develop higher intelligence. © 2016 Scientific American
By Gary Stix Scientists will never find a single gene for depression—nor two, nor 20. But among the 20,000 human genes and the hundreds of thousands of proteins and molecules that switch on those genes or regulate their activity in some way, there are clues that point to the roots of depression. Tools to identify biological pathways that are instrumental in either inducing depression or protecting against it have recently debuted—and hold the promise of providing leads for new drug therapies for psychiatric and neurological diseases. A recent paper in the journal Neuron illustrates both the dazzling complexity of this approach and the ability of these techniques to pinpoint key genes that may play a role in governing depression. Scientific American talked with the senior author on the paper—neuroscientist Eric Nestler from the Icahn School of Medicine at Mt. Sinai in New York. Nestler spoke about the potential of this research to break the logjam in pharmaceutical research that has impeded development of drugs to treat brain disorders. Scientific American: The first years in the war on cancer met with a tremendous amount of frustration. Things look like they're improving somewhat now for cancer. Do you anticipate a similar trajectory may occur in neuroscience for psychiatric disorders? Eric Nestler: I do. I just think it will take longer. I was in medical school 35 years ago when the idea that identifying a person's specific pathophysiology was put forward as a means of directing treatment of cancer. We're now three decades later finally seeing the day when that’s happening. I definitely think the same will occur for major brain disorders. The brain is just more complicated and the disorders are more complicated so it will take longer. © 2016 Scientific American
By Anil Ananthaswamy and Alice Klein Our brain’s defence against invading microbes could cause Alzheimer’s disease – which suggests that vaccination could prevent the condition. Alzheimer’s disease has long been linked to the accumulation of sticky plaques of beta-amyloid proteins in the brain, but the function of plaques has remained unclear. “Does it play a role in the brain, or is it just garbage that accumulates,” asks Rudolph Tanzi of Harvard Medical School. Now he has shown that these plaques could be defences for trapping invading pathogens. Working with Robert Moir at the Massachusetts General Hospital in Boston, Tanzi’s team has shown that beta-amyloid can act as an anti-microbial compound, and may form part of our immune system. .. To test whether beta-amyloid defends us against microbes that manage to get into the brain, the team injected bacteria into the brains of mice that had been bred to develop plaques like humans do. Plaques formed straight away. “When you look in the plaques, each one had a single bacterium in it,” says Tanzi. “A single bacterium can induce an entire plaque overnight.” Double-edged sword This suggests that infections could be triggering the formation of plaques. These sticky plaques may trap and kill bacteria, viruses or other pathogens, but if they aren’t cleared away fast enough, they may lead to inflammation and tangles of another protein, called tau, causing neurons to die and the progression towards © Copyright Reed Business Information Ltd.
Robert Plomin, Scientists have investigated this question for more than a century, and the answer is clear: the differences between people on intelligence tests are substantially the result of genetic differences. But let's unpack that sentence. We are talking about average differences among people and not about individuals. Any one person's intelligence might be blown off course from its genetic potential by, for example, an illness in childhood. By genetic, we mean differences passed from one generation to the next via DNA. But we all share 99.5 percent of our three billion DNA base pairs, so only 15 million DNA differences separate us genetically. And we should note that intelligence tests include diverse examinations of cognitive ability and skills learned in school. Intelligence, more appropriately called general cognitive ability, reflects someone's performance across a broad range of varying tests. Genes make a substantial difference, but they are not the whole story. They account for about half of all differences in intelligence among people, so half is not caused by genetic differences, which provides strong support for the importance of environmental factors. This estimate of 50 percent reflects the results of twin, adoption and DNA studies. From them, we know, for example, that later in life, children adopted away from their biological parents at birth are just as similar to their biological parents as are children reared by their biological parents. Similarly, we know that adoptive parents and their adopted children do not typically resemble one another in intelligence. © 2016 Scientific American
By Roland Pease BBC Radio Science Unit Researchers have invented a DNA "tape recorder" that can trace the family history of every cell in an organism. The technique is being hailed as a breakthrough in understanding how the trillions of complex cells in a body are descended from a single egg. "It has the potential to provide profound insights into how normal, diseased or damaged tissues are constructed and maintained," one UK biologist told the BBC. The work appears in Science journal. The human body has around 40 trillion cells, each with a highly specialised function. Yet each can trace its history back to the same starting point - a fertilised egg. Developmental biology is the business of unravelling how the genetic code unfolds at each cycle of cell division, how the body plan develops, and how tissues become specialised. But much of what it has revealed has depended on inference rather than a complete cell-by-cell history. "I actually started working on this problem as a graduate student in 2000," confessed Jay Shendure, lead researcher on the new scientific paper. "Could we find a way to record these relationships between cells in some compact form we could later read out in adult organisms?" The project failed then because there was no mechanism to record events in a cell's history. That changed with recent developments in so called CRISPR gene editing, a technique that allows researchers to make much more precise alterations to the DNA in living organisms. The molecular tape recorder developed by Prof Shendure's team at the University of Washington in Seattle, US, is a length of DNA inserted into the genome that contains a series of edit points which can be changed throughout an organism's life. © 2016 BBC.
By Jordana Cepelewicz General consensus among Alzheimer’s researchers has it that the disease’s main culprit, a protein called amyloid beta, is an unfortunate waste product that is not known to play any useful role in the body—and one that can have devastating consequences. When not properly cleared from the brain it builds up into plaques that destroy synapses, the junctions between nerve cells, resulting in cognitive decline and memory loss. The protein has thus become a major drug target in the search for a cure to Alzheimer’s. Now a team of researchers at Harvard Medical School and Massachusetts General Hospital are proposing a very different story. In a study published this week in Science Translational Medicine, neurologists Rudolph Tanzi and Robert Moir report evidence that amyloid beta serves a crucial purpose: protecting the brain from invading microbes. “The original idea goes back to 2010 or so when Rob had a few too many Coronas,” Tanzi jokes. Moir had come across surprising similarities between amyloid beta and LL37, a protein that acts as a foot soldier in the brain’s innate immune system, killing potentially harmful bugs and alerting other cells to their presence. “These types of proteins, although small, are very sophisticated in what they do,” Moir says. “And they’re very ancient, going back to the dawn of multicellular life.” © 2016 Scientific American,
By GINA KOLATA Could it be that Alzheimer’s disease stems from the toxic remnants of the brain’s attempt to fight off infection? Provocative new research by a team of investigators at Harvard leads to this startling hypothesis, which could explain the origins of plaque, the mysterious hard little balls that pockmark the brains of people with Alzheimer’s. It is still early days, but Alzheimer’s experts not associated with the work are captivated by the idea that infections, including ones that are too mild to elicit symptoms, may produce a fierce reaction that leaves debris in the brain, causing Alzheimer’s. The idea is surprising, but it makes sense, and the Harvard group’s data, published Wednesday in the journal Science Translational Medicine, supports it. If it holds up, the hypothesis has major implications for preventing and treating this degenerative brain disease. The Harvard researchers report a scenario seemingly out of science fiction. A virus, fungus or bacterium gets into the brain, passing through a membrane — the blood-brain barrier — that becomes leaky as people age. The brain’s defense system rushes in to stop the invader by making a sticky cage out of proteins, called beta amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage and dies. What is left behind is the cage — a plaque that is the hallmark of Alzheimer’s. So far, the group has confirmed this hypothesis in neurons growing in petri dishes as well as in yeast, roundworms, fruit flies and mice. There is much more work to be done to determine if a similar sequence happens in humans, but plans — and funding — are in place to start those studies, involving a multicenter project that will examine human brains. “It’s interesting and provocative,” said Dr. Michael W. Weiner, a radiology professor at the University of California, San Francisco, and a principal investigator of the Alzheimer’s Disease Neuroimaging Initiative, a large national effort to track the progression of the disease and look for biomarkers like blood proteins and brain imaging to signal the disease’s presence. © 2016 The New York Times Company