Chapter 13. Memory, Learning, and Development
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A high-resolution map of the human brain in utero is providing hints about the origins of brain disorders including schizophrenia and autism. The map shows where genes are turned on and off throughout the entire brain at about the midpoint of pregnancy, a time when critical structures are taking shape, researchers Wednesday in the journal Nature. "It's a pretty big leap," says , an investigator at the in Seattle who played a central role in creating the map. "Basically, there was no information of this sort prior to this project." Having a map like this is important because many psychiatric and behavioral problems appear to begin before birth, "even though they may not manifest until teenage years or even the early 20s," says , director of the . The human brain is often called the most complex object in the universe. Yet its basic architecture is created in just nine months, when it grows from a single cell to more than 80 billion cells organized in a way that will eventually let us think and feel and remember. "We're talking about a remarkable process," a process controlled by our genes, Lein says. So he and a large team of researchers decided to use genetic techniques to create a map that would help reveal this process. Funding came from the 2009 federal stimulus package. The massive effort required tens of thousands of brain tissue samples so small that they had to be cut out with a laser. Researchers used brain tissue from aborted fetuses, which the Obama administration has authorized over the objections of abortion opponents. ©2014 NPR
He was known in his many appearances in the scientific literature as simply K.C., an amnesiac who was unable to form new memories. But to the people who knew him, and the scientists who studied him for decades, he was Kent Cochrane, or just Kent. Cochrane, who suffered a traumatic brain injury in a motorcycle accident when he was 30 years old, helped to rewrite the understanding of how the brain forms new memories and whether learning can occur without that capacity. "From a scientific point of view, we've really learned a lot [from him], not just about memory itself but how memory contributes to other abilities," said Shayna Rosenbaum, a cognitive neuropsychologist at York University who started working with Cochrane in 1998 when she was a graduate student. Cochrane was 62 when he died late last week. The exact cause of death is unknown, but his sister, Karen Casswell, said it is believed he had a heart attack or stroke. He died in his room at an assisted living facility where he lived and the family opted not to authorize an autopsy. Few in the general public would know about Cochrane, though some may have seen or read media reports on the man whose life was like that of the lead character of the 2000 movie Memento. But anyone who works on the science of human memory would know K.C. Casswell and her mother, Ruth Cochrane, said the family was proud of the contribution Kent Cochrane made to science. Casswell noted her eldest daughter was in a psychology class at university when the professor started to lecture about the man the scientific literature knows as K.C. © CBC 2014
Keyword: Learning & Memory
Link ID: 19442 - Posted: 04.03.2014
by Bob Holmes People instinctively organise a new language according to a logical hierarchy, not simply by learning which words go together, as computer translation programs do. The finding may add further support to the notion that humans possess a "universal grammar", or innate capacity for language. The existence of a universal grammar has been in hot dispute among linguists ever since Noam Chomsky first proposed the idea half a century ago. If the theory is correct, this innate structure should leave some trace in the way people learn languages. To test the idea, Jennifer Culbertson, a linguist at George Mason University in Fairfax, Virginia, and her colleague David Adger of Queen Mary University of London, constructed an artificial "nanolanguage". They presented English-speaking volunteers with two-word phrases, such as "shoes blue" and "shoes two", which were supposed to belong to a new language somewhat like English. They then asked the volunteers to choose whether "shoes two blue" or "shoes blue two" would be the correct three-word phrase. In making this choice, the volunteers – who hadn't been exposed to any three-word phrases – would reveal their innate bias in language-learning. Would they rely on familiarity ("two" usually precedes "blue" in English), or would they follow a semantic hierarchy and put "blue" next to "shoe" (because it modifies the noun more tightly than "two", which merely counts how many)? © Copyright Reed Business Information Ltd.
by Aviva Rutkin Don't blame baby for trying to eat that Lego piece. Humans may have a brain circuit dedicated to grabbing stuff and putting it in our mouths, and it probably develops in the womb. Researchers and parents alike have long known that babies stick all manner of things in their mouths from very early on. Some fetuses even suck their thumbs. As putting something in the mouth seems advanced compared to the other, limited actions of newborns, Angela Sirigu of the Institute of Cognitive Sciences in Bron, France, and colleagues wondered whether the behaviour is encoded in the brain from birth. To investigate, they studied 26 people of different ages while they were undergoing brain surgery. The researchers found that they were able to make nine of the unconscious patients bring their hands up and open their mouths, just by stimulating a part of the brain we know is linked to those actions in non-human primates. Brain pudding Because this behaviour is encoded in the same region as in other primates, it may be there from birth or earlier, the researchers say. If it was learned, you would expect it to involve multiple brain areas, and those could vary between individuals. Newborn kangaroos are able to climb into their mother's pouch and baby wildebeests can run away from lions, but our babies appear helpless and have to learn most complex actions. The new work suggests that the way our brain develops is more like what happens in other animals than previously thought. © Copyright Reed Business Information Ltd.
Keyword: Development of the Brain
Link ID: 19431 - Posted: 04.01.2014
By SAM WANG A STUDY published last week found that the brains of autistic children show abnormalities that are likely to have arisen before birth, which is consistent with a large body of previous evidence. Yet most media coverage focuses on vaccines, which do not cause autism and are given after birth. How can we help people separate real risks from false rumors? Over the last few years, we’ve seen an explosion of studies linking autism to a wide variety of genetic and environmental factors. Putting these studies in perspective is an enormous challenge. In a database search of more than 34,000 scientific publications mentioning autism since its first description in 1943, over half have come since 2008. As a statistically minded neuroscientist, I suggest a different approach that relies on a concept we are familiar with: relative odds. As a single common measuring stick to compare odds, I have chosen the “risk ratio,” a measure that allows the bigger picture to come into focus. For a variety of studies I asked the same question: How large is the increased risk for autism? My standard for comparison was the likelihood in the general population of autism spectrum disorder. Here’s an example. Start from the fact that the recorded rate of autism is now 1 in 68, according to a report released last week by the Centers for Disease Control and Prevention. If babies born in purple farmhouses have a rate of autism of 2 in 68, this doubling means that the purple farmhouse carries a risk ratio of 2. However, correlation is not causation, and there is no need to repaint that farmhouse just yet. © 2014 The New York Times Company
Link ID: 19429 - Posted: 03.31.2014
By SABRINA TAVERNISE In 1972, researchers in North Carolina started following two groups of babies from poor families. In the first group, the children were given full-time day care up to age 5 that included most of their daily meals, talking, games and other stimulating activities. The other group, aside from baby formula, got nothing. The scientists were testing whether the special treatment would lead to better cognitive abilities in the long run. Forty-two years later, the researchers found something that they had not expected to see: The group that got care was far healthier, with sharply lower rates of high blood pressure and obesity, and higher levels of so-called good cholesterol. The study, which was published in the journal Science on Thursday, is part of a growing body of scientific evidence that hardship in early childhood has lifelong health implications. But it goes further than outlining the problem, offering evidence that a particular policy might prevent it. “This tells us that adversity matters and it does affect adult health,” said James Heckman, a professor of economics at the University of Chicago who led the data analysis. “But it also shows us that we can do something about it, that poverty is not just a hopeless condition.” The findings come amid a political push by the Obama administration for government-funded preschool for 4-year-olds. But a growing number of experts, Professor Heckman among them, say they believe that more effective public programs would start far earlier — in infancy, for example, because that is when many of the skills needed to take control of one’s life and become a successful adult are acquired. © 2014 The New York Times Company
by Laura Sanders Ever-increasing numbers of autism diagnoses have parents worried about a skyrocketing epidemic, and this week’s news may only drive alarm higher. Perhaps it shouldn’t. In 2010, 1 in 68 (or 14.7 per 1,000) 8-year-olds had an autism spectrum disorder, the Centers for Disease Control and Prevention now estimates. That number is a substantial increase from 2008, which had an estimate of 1 in 88 (or 11.3 per 1,000). But the numbers might not reflect a spike in actual cases. Instead, the rise might be driven, at least in part, by an increase in diagnoses. The estimates are drawn from a collection of organizations that provide services to children with autism, including doctors, schools and social service agencies. As awareness builds and more people look for signs of autism, these numbers will keep going up. Regional spottiness suggests that better autism detection is feeding the increase. The autism rate in Alabama is just one in 175, while the rate in New Jersey is one in 45, the CDC reports. It would be surprising, and scientifically really important, if children in Alabama were truly much more protected from the disorder. Instead, differences in diagnosis rates are probably at play. If these alarmingly high numbers are driven by professionals and parents better spotting autism, that’s nothing to be alarmed at. On the contrary: This is good news. The earlier therapies begin, the better kids with autism do. That’s the idea behind CDC’s “Learn the Signs: Act Early” program to educate people about signs that something might be amiss with a child. So our best move is to find the kids who need help, and find them when they’re young. Most kids, including the ones in the new CDC survey, aren’t diagnosed with autism until about age 4 1/2. But whatever goes wrong happens long before then. © Society for Science & the Public 2000 - 2013.
Link ID: 19424 - Posted: 03.29.2014
Ewen Callaway An equine oddity with the head of a zebra and the rump of a donkey, the last quagga (Equus quagga quagga) died in 1883. A century later, researchers published1 around 200 nucleotides sequenced from a 140-year-old piece of quagga muscle. Those scraps of DNA — the first genetic secrets pulled from a long-dead organism — revealed that the quagga was distinct from the mountain zebra (Equus zebra). More significantly, the research showed that from then on, examining fossils would no longer be the only way to probe extinct life. “If the long-term survival of DNA proves to be a general phenomenon,” geneticists Russell Higuchi and Allan Wilson of the University of California, Berkeley, and their colleagues noted in their quagga paper1, “several fields including palaeontology, evolutionary biology, archaeology and forensic science may benefit.” At first, progress was fitful. Concerns over the authenticity of ancient-DNA research fuelled schisms in the field and deep scepticism outside it. But this has faded, thanks to laboratory rigour that borders on paranoia and sequencing techniques that help researchers to identify and exclude contaminating modern DNA. These advances have fostered an ancient-genomics boom. In the past year, researchers have unveiled the two oldest genomes on record: those of a horse that had been buried in Canadian permafrost for around 700,000 years2, and of a roughly 400,000-year-old human relative from a Spanish cavern3. A Neanderthal sequence every bit as complete and accurate as a contemporary human genome has been released4, as has the genome of a Siberian child connecting Native Americans to Europeans5. © 2014 Nature Publishing Group
By Greg Miller Nobody knows what causes autism, a condition that varies so widely in severity that some people on the spectrum achieve enviable fame and success while others require lifelong assistance due to severe problems with communication, cognition, and behavior. Scientists have found countless clues, but so far they don’t quite add up. The genetics is complicated. The neuroscience is conflicted. Now, a new study adds an intriguing, unexpected, and sure-to-be controversial finding to the mix: It suggests the brains of children with autism contain small patches where the normally ordered arrangement of neurons in the cerebral cortex is disrupted. “We’ve found locations where there appears to be a failure of normal development,” said Eric Courchesne, a neuroscientist at the University of California, San Diego and an author of the study, which appears today in the New England Journal of Medicine. “It’s been really difficult to identify a lesion or anything in the brain that’s specific and diagnostic of autism,” said Thomas Insel, director of the National Institute of Mental Health, one of several agencies that funded the project. The new study is notable because it applies sophisticated molecular labeling methods to postmortem tissue from people with autism who died as children, which is incredibly hard to come by, Insel says. “If it’s real, if it’s replicated and it’s a consistent finding, it’s more evidence that autism starts prenatally and only manifests itself when kids start to have trouble with language or social behavior around age two or three,” Insel said. “These kinds of changes in cellular architecture would happen during brain development, probably around the first part of the second trimester.” © 2014 Condé Nast
James Hamblin Forty-one million IQ points. That’s what Dr. David Bellinger determined Americans have collectively forfeited as a result of exposure to lead, mercury, and organophosphate pesticides. In a 2012 paper published by the National Institutes of Health, Bellinger, a professor of neurology at Harvard Medical School, compared intelligence quotients among children whose mothers had been exposed to these neurotoxins while pregnant to those who had not. Bellinger calculates a total loss of 16.9 million IQ points due to exposure to organophosphates, the most common pesticides used in agriculture. Last month, more research brought concerns about chemical exposure and brain health to a heightened pitch. Philippe Grandjean, Bellinger’s Harvard colleague, and Philip Landrigan, dean for global health at Mount Sinai School of Medicine in Manhattan, announced to some controversy in the pages of a prestigious medical journal that a “silent pandemic” of toxins has been damaging the brains of unborn children. The experts named 12 chemicals—substances found in both the environment and everyday items like furniture and clothing—that they believed to be causing not just lower IQs but ADHD and autism spectrum disorder. Pesticides were among the toxins they identified. “So you recommend that pregnant women eat organic produce?” I asked Grandjean, a Danish-born researcher who travels around the world studying delayed effects of chemical exposure on children. “That’s what I advise people who ask me, yes. It’s the best way of preventing exposure to pesticides.” Grandjean estimates that there are about 45 organophosphate pesticides on the market, and “most have the potential to damage a developing nervous system.” © 2014 by The Atlantic Monthly Group.
By Jennifer Richler A few days ago, an old friend sent me a panicked email. She had just finished reading Ron Suskind’s beautiful essay in the New York Times Magazine about raising a son with autism: “Reaching My Autistic Son Through Disney.” Suskind describes how, at almost 3 years of age, his son Owen “disappeared.” The child was once “engaged, chatty, full of typical speech,” but then he stopped talking, lost eye contact, even struggled to use a sippy cup. Owen was eventually diagnosed with a regressive form of autism, which Suskind says affects about a third of children with the disorder. “Unlike the kids born with it,” he continues, “this group seems typical until somewhere between 18 and 36 months—then they vanish.” That was the line that alarmed my friend, whose son is nearing his third birthday. “What is this ‘regressive autism?’ ” she asked me, the resident autism expert in her peer group. (I conducted research on autism and regression in autism before becoming a freelance writer.) “I thought we were out of the woods!” I’m sure many parents of young children who read the piece had the same reaction, and it’s completely understandable. It’s also unwarranted. The claim that many kids with autism develop typically for almost three years and then experience a near-complete loss of language, social skills, and motor ability—a claim I’ve read many times before—simply isn’t true. It’s time to set the record straight. © 2014 The Slate Group LLC.
Link ID: 19409 - Posted: 03.26.2014
Claudia Dreifus The biochemist Ricardo E. Dolmetsch has pioneered a major shift in autism research, largely putting aside behavioral questions to focus on cell biology and biochemistry. Dr. Dolmetsch, 45, has done most of his work at Stanford. Since our interviews — a condensed and edited version of which follows — he has taken a leave to join Novartis, where his mission is to organize an international team to develop autism therapies. “Pharmaceutical companies have financial and organizational resources permitting you to do things you might not be able to do as an academic,” he said. “I really want to find a drug.” Q. Did you start out your professional life studying the biochemistry of autism? A. No. In graduate school and as a postdoc, I’d done basic research on the ion channels on the membranes of cells. By my mid-20s, I had my name on some high-profile papers. Then, around 2006, my son who was then 4 was diagnosed with autism. We had suspected it. He didn’t talk much, was hyperactive, very moody. He assembled huge towers based on the color spectrum. He did all sorts of things that were very unusual. Given the signs, why did you wait that long to seek a diagnosis? I’m from Latin America [Cali, Colombia], and my Latin thing was, “This is the way boys are.” But he would just scream for hours and hours, uncontrollable. He didn’t sleep. We didn’t understand it. After a while, his teachers said, “You probably ought to have him seen.” So we went to a psychiatrist and neurologist and ultimately we got differing diagnoses. © 2014 The New York Times Company
Link ID: 19404 - Posted: 03.25.2014
by Barbara J. King Why do little boys tend to behave differently from little girls? Why do boys and girls play differently, for instance, choosing different toys as their favorites? Ask these questions and you invite a firestorm — of more questions. Is the premise behind these queries even accurate? Aren't our sons and daughters really more similar than different, after all? And when behavioral sex differences do occur, aren't parents who inflict sex-stereotypical expectations on their children largely responsible? Seven experts on chimpanzee behavior, led by of Franklin and Marshall College and including the world-famous primatologist , have in Animal Behaviour that speaks, they say, to these issues. Their data on wild chimpanzees from , Tanzania, indicate that human sex differences in childhood are primarily the result of biological, evolutionary mechanisms. The scientists analyzed data on the behavior of 12 male and eight female chimpanzee youngsters, ages 30-36 months. At that age, chimpanzees, who develop quite slowly compared with many other mammals, are still considered infants. As a rule, chimpanzees spend most of their day in close proximity to their mothers clear through their ninth year of life. In the Gombe study, male infants were found to be more gregarious than female chimpanzees; they interacted with significantly more individuals outside the immediate family, including more adult males, than did females. This result held even when the number of the mothers' social partners was controlled. ©2014 NPR
by Simon Makin How much can environmental factors explain the apparent rise in autism spectrum disorders? Roughly 1 per cent of children in the US population are affected by autism spectrum disorder (ASD). Rates in many countries, including the US, have risen sharply in recent years but no one is sure why. It is still not clear whether this is prompted by something in the environment, increased awareness of the condition and changes in diagnoses, or a result of people having children later. The environmental case is hotly debated. There is some evidence that maternal infections during pregnancy can increase the risk. Other studies have pointed to a possible link with antidepressants while others have looked at elevated levels of mercury. But determining prenatal exposure to any substance is difficult because it is hard to know what substances people have been exposed to and when. To get around this, Andrey Rzhetsky and colleagues at the University of Chicago analysed US health insurance claims containing over 100 million patient records – a third of the population – dating from 2003 to 2010. They used rates of genital malformations in newborn boys as a proxy of parents' exposure to environmental risk factors. This is based on research linking a proportion of these malformations to toxins in the environment, including pesticides, lead and medicines. Toxic environment? The team compared the rates of these malformations to rates of ASD county by county. After adjusting for gender, income, ethnicity and socio-economic status, they found that a 1 per cent increase in birth defects – their measure for environmental effects - was associated with an average increase of 283 per cent in cases of ASD. © Copyright Reed Business Information Ltd.
Link ID: 19393 - Posted: 03.21.2014
By Shelly Fan One of the tragedies of aging is the slow but steady decline in memory. Phone numbers slipping your mind? Forgetting crucial items on your grocery list? Opening the door but can’t remember why? Up to 50 percent of adults aged 64 years or older report memory complaints. For many of us, senile moments are the result of normal changes in brain structure and function instead of a sign of dementia, and will inevitably haunt us all. Rather than taking it lying down, scientists are devising interventions to help keep the elderly mind sharp. One popular approach—borrowed from the training of memory experts—is to teach the elderly mnemonics, or little tricks to help encode and recall new information using rhythm, imagery or spatial navigation. By far the most widely used mnemonic device is the method of loci (MoL), a technique devised in ancient Greece. In a 2002 study looking at the neural correlates of superior human memory, nine of 10 memory masters employed the method spontaneously. It involves picturing highly familiar routes through a building (your childhood home) or a town (your way to work). Walk down the route and imagine placing to-be-remembered items at attention-grabbing spots along the way; the more surreal or bizarre you make these images, the better they can help you remember. To recall these stored items, simply retrace your steps. Like fishing lines, the loci are hooked to the memory and help you pull them to the surface. Although generally used to remember objects, numbers or names, the MoL has also been used in people with depression to successfully store bits and pieces of happy autobiographical memories that they can easily retrieve in times of stress. © 2014 Scientific American,
Want to live a long, dementia-free life? Stress your cells out. That’s the conclusion of a new study, which finds that heightened cellular stress causes brain cells to produce a protein that staves off Alzheimer’s disease and other forms of dementia. The work could lead to new ways to diagnose or treat such diseases. “This paper is very impressive,” says neuroscientist Li-Huei Tsai of the Massachusetts Institute of Technology in Cambridge, who was not involved in the new work. “It puts a finger on a particular pathway that can provide some explanation as to why some people are more susceptible to Alzheimer’s.” Alzheimer’s disease, characterized by a progressive loss of memory and cognition, affects an estimated 44.4 million people worldwide, mostly over the age of 65. The illness has been linked to the accumulation of certain proteins in the brain, but what causes symptoms has been unclear. That’s because the brains of some elderly people without dementia have the same clumps of so-called amyloid β and τ proteins typically associated with Alzheimer’s. The new study deals with a protein called repressor element 1-silencing transcription factor (REST), which turns genes and off. Scientists knew that REST played a key role in fetal brain development by controlling the activity of certain genes, but they thought it was absent in adult brains. However, when Bruce Yankner, a neurologist at Harvard Medical School in Boston, looked at all the genes and proteins that change in brains as people age, he found that REST levels begin increasing again when a person hits their 30s. Stumped as to why, he and his colleagues isolated human and mouse brain cells and probed what factors altered REST levels and what consequences those levels had. © 2014 American Association for the Advancement of Science
By Maggie Fox and Erika Edwards Women are carrying the bigger burden of Alzheimer’s disease in the U.S., according to a new report — making up not only most of the cases, but paying more of the cost of caring for the growing population of people with the mind-destroying illness. The new report from the Alzheimer’s Association paints Alzheimer’s as a disease that disproportionately affects women, both as patients and as caregivers. It points out that women in their 60s are about twice as likely to develop Alzheimer’s over the rest of their lives as they are to develop breast cancer. “So women are at the epicenter of Alzheimer's disease today, not only by being most likely to be diagnosed with Alzheimer's, but also by being the caregiver most of the time,” said Maria Carrillo, vice president of the advocacy group. Alzheimer’s affects more than 5 million Americans, a number projected to soar to 13 million over the next 35 years. A study published earlier this year suggested it’s a big killer, taking down more than 500,000 Americans every year. Three out of five of those living with Alzheimer’s are women, the report finds. “The surprising statistic we pulled out of this report actually is that women over 65 have a one in six chance of developing Alzheimer's disease, in comparison to one out of 11 in men,” Carrillo said. And that compares to a one in eight lifetime risk for developing breast cancer.
The cancer gene BRCA1, which keeps tumors in the breast and ovaries at bay by producing proteins that repair damaged DNA, may also regulate brain size. Mice carrying a mutated copy of the gene have 10-fold fewer neurons and other brain abnormalities, a new study suggests. Such dramatic effects on brain size and function are unlikely in human carriers of BRCA1 mutations, the authors of the study note, but they propose the findings could shed light on the gene's role in brain evolution. Scientists have known for a long time that the BRCA1 gene is an important sentinel against DNA damage that can lead to ovarian and breast cancers. More than half of women with a mutated copy of the BRCA1 gene will develop breast cancer, a statistic that has led some who carry the mutation to get preventative mastectomies. But its roles outside the breast and ovaries are less clear, says Inder Verma, a geneticist and molecular biologist at the Salk Institute for Biological Studies in San Diego, California, who headed the new study. Mice bred without BRCA1 die soon after birth, so it’s clear that the gene is necessary to sustain life, but scientists are just starting to unravel its many functions, he says. Several years ago, one of the students in Verma’s lab noticed that BRCA1 is very active in the neuroectoderm, a sliver of embryonic tissue containing neural stem cells that divide and differentiate into the brain’s vast assortment of cell types and structures. Verma and his colleagues wondered why the gene was expressed at such high levels in that region, and what would happen if it were eliminated. They created a strain of mice in which BRCA1 was knocked out only in neural stem cells. As the mice developed, Verma’s team found that the rodents’ brains were only a third of their normal size, with particularly striking reductions in brain areas involved in learning and memory. The grown mice also had a wobbly, drunken gait—a telltale symptom of ataxia, a neurological disorder that affects muscle control and balance, the researchers report online today in the Proceedings of the National Academy of Sciences. © 2014 American Association for the Advancement of Science.
Keyword: Development of the Brain
Link ID: 19378 - Posted: 03.18.2014
by Laura Sanders Candy and sweets make your kid hyper, the common lore goes. But science says that's not true. 1. Sugar makes kids hyper. Lots of parents swear that a single hit of birthday cake holds the power to morph their well-behaved, polite youngster into a sticky hot mess that careens around a room while emitting eardrum-piercing shrieks. Anyone who has had the pleasure to attend a 5-year-old’s birthday party knows that the hypothesis sounds reasonable, except that science has found that it’s not true. Sugar doesn’t change kids’ behavior, a double-blind research study found way back in 1994. A sugary diet didn’t affect behavior or cognitive skills, the researchers report. Sugar does change one important thing, though: parents’ expectations. After hearing that their children had just consumed a big sugar fix, parents were more likely to say their child was hyperactive, even when the big sugar fix was a placebo, another study found. Of course, there are plenty of good reasons not to feed your kids a bunch of sugar, but fear of a little crazed sugar monster isn’t one of them. © Society for Science & the Public 2000 - 2013.
Keyword: Development of the Brain
Link ID: 19376 - Posted: 03.18.2014
by Colin Barras Amyloid plaques, a hallmark of diseases like Alzheimer's, are bad news for humans – but they could have been drivers of the earliest life on Earth. A new study shows that these amyloid clusters can behave as catalysts, backing a theory that they helped trigger the reactions that sustain life, long before modern enzymes appeared. Without enzymes, life's metabolic reactions simply wouldn't occur. But making enzymes from scratch isn't easy. They are normally large, complicated proteins folded into a specific three-dimensional shape. It's difficult to see how these large proteins could have popped out of the primordial soup fully formed. Even if they did, nature faced another problem. There are 20 naturally occurring amino acids, which are the building blocks for all proteins, and each enzyme is made up of a unique sequence of at least 100 amino acids. This means there is a mind-bogglingly vast number – 20100 – of possible enzymes, each with a different amino acid sequence and a slightly different 3D structure. But very few of these 3D structures will work effectively as enzymes because they have to be an exact fit for the substrate they react with – in the same way that a lock can only be opened by one particular key. Even with millions of years to work at the problem, says Ivan Korendovych at Syracuse University in New York, nature would have struggled to build and test all possible enzyme molecules to identify the relatively few that catalyse today's metabolic reactions. © Copyright Reed Business Information Ltd.
Link ID: 19372 - Posted: 03.17.2014