Links for Keyword: Genes & Behavior

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 81 - 100 of 265

– BETHESDA, MD – As the US population ages, there is an increasing effort to understand the underlying mechanisms that contribute to learning and memory. This effort could be of critical importance to scientists trying to decipher how the molecular genetic mechanisms of learning and memory are disrupted or impaired. The results of a new study provide evidence that individual differences in some cognitive functions may have a genetic basis. A New Study The authors of the study are Nelson Ruiz-Opazo, of the Section of Molecular Medicine, Boston University School of Medicine, Boston, MA, and John Tonkiss, from the Center for Behavioral Development and Mental Retardation, Boston University School of Medicine, Boston, MA. Their study, entitled "X-Linked Loci Influence Spatial Navigation Performance in Dahl Rats," now appears in the Articles in Press section of Physiological Genomics, one of one of 14 scientific journals published monthly by the American Physiological Society (APS) (www.the-aps.org).

Related chapters from BP7e: Chapter 18: Attention and Higher Cognition; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 14: Attention and Consciousness; Chapter 13: Memory, Learning, and Development
Link ID: 4919 - Posted: 06.24.2010

SACRAMENTO, Calif.) – A team of researchers, led by physicians at the UC Davis M.I.N.D Institute, have discovered a new, progressive neurodegenerative disorder that predominantly affects men over age 50 and results in tremors, balance problems and dementia that become increasingly more severe with age. A significant but currently unknown number of adults with these tremor and balance problems are being diagnosed as normal aging, Parkinson's disease, senile dementia and Alzheimer's disease when their condition may be accurately and easily identified with a standard DNA blood test ordered by their doctor. The discovery is published in the Jan. 28 issue of the Journal of the American Medical Association. Known as fragile X-associated tremor/ataxia syndrome, or FXTAS (pronounced fax-tass), the disorder affects older men who are carriers of a small mutation (premutation) in the same gene that causes fragile X syndrome, the most common cause of inherited mental retardation. Nearly 1 in 800 men in the general population carries this premutation in the fragile X gene, and UC Davis research suggests that as many as 30 percent of carriers -- roughly 1 in 3,000 men -- may develop FXTAS later in life.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 4871 - Posted: 06.24.2010

St. Louis, -- For some brain tumors, the key to success is not just what you know but who you know, according to researchers at Washington University School of Medicine in St. Louis. In trying to develop a mouse model of neurofibromatosis 1 (NF1), a genetic disorder that predisposes children to certain types of brain tumors, the team discovered that tumors only developed when all brain cells were genetically abnormal, not just the cell type that becomes cancerous. The study is featured on the cover of the Dec. 15 issue of the journal Cancer Research. "We are quite excited about this report as it represents the first model of this type of tumor," says principal investigator David H. Gutmann, M.D., Ph.D., the Donald O. Schnuck Family Professor of Neurology. "We've always assumed that cancer results from the loss of specific genes in a particular cell, but apparently that isn't always the case. Our findings suggest that as in real estate, location is everything – a permissive environment may be the key to whether a tumor cell becomes cancerous or just sits dormant for a person's entire life."

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 4696 - Posted: 06.24.2010

Discovery shows power of mouse genome to identify human genes for rare genetic diseases ANN ARBOR, MI – In a small town on Grand Cayman Island in the Caribbean, people are living with a serious neurological disorder, called Cayman ataxia, found nowhere else in the world. People born with this rare, inherited condition have poor muscle coordination, some degree of mental retardation, uncontrollable head and eye movements and difficulty speaking or walking. Now, in a discovery that reinforces the importance of the mouse to human genetics, scientists at the University of Michigan Medical School have discovered two mutations in a gene called ATCAY, which appear to be responsible for Cayman ataxia in humans and for similar neurological disorders in mice.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 4376 - Posted: 06.24.2010

When a plane arrives late to an airport, it affects more than just the frustrated passengers on the tardy plane – the ripple effects could throw the entire day’s timetable off schedule. Similarly, in a new study, North Carolina State University geneticists have found that changes to genes regulating olfactory behavior in the fruit fly Drosophila melanogaster, a popular insect model for genetics, have far greater implications than previously appreciated. The study is presented in a paper published in the Sept. 7 online edition of Nature Genetics. Dr. Robert Anholt, professor of zoology and genetics, director of NC State’s Keck Center for Behavioral Biology and the paper’s lead author, said that in the study of how genes affect behavior, the days of thinking about genes in a linear fashion are over.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 4235 - Posted: 06.24.2010

HONOLULU, HI – Researchers have recently discovered a progressive neurodegenerative condition -- resulting in tremor, balance problems, and dementia -- which may affect as many as one in 3,000 men. This condition has now been associated with the same gene that causes fragile X syndrome, the most common heritable form of mental retardation. Findings of this study are being presented at the American Academy of Neurology Annual Meeting in Honolulu, March 29-April 5, 2003. Remarkably, the same gene has been found to cause these two different and independent syndromes, affecting different groups of individuals. Fragile X syndrome is a developmental disorder beginning in childhood, while the newly identified neurological syndrome (Fragile X Associated Tremor/Ataxia Syndrome, or FXTAS) affects mainly male carriers who were not affected by fragile X syndrome retardation, and who displayed no symptoms prior to age 50. "We discovered that FXTAS-affected individuals have numerous inclusions, or spherical particles, in their brain cells," noted study author Paul Hagerman, MD, PhD, professor of Biological Chemistry at the University of California Davis School of Medicine. Through this study, the researchers are determining what is in the inclusions and why they form. "We believe this finding is an important clue as to the cause of the disorder, one that may ultimately help with development of therapies for both the tremor disorder and fragile X syndrome."

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 3644 - Posted: 06.24.2010

COLLEGE STATION, – Inside a drawer in Luis Rene Garcia's biology lab, tens of thousands of roundworms are bumping into one another, slithering together and breeding. For the tiny worms, known to science as C. elegans, it's all just another day on a laboratory petri dish. But somewhere in the writhing masses, Dr. Garcia suspects, lie clues to a mystery with large implications: Is some behavior hereditary? Garcia, an assistant professor of biology at Texas A&M University, is an expert in the sexual habits of C. elegans and the genes that apparently control the behaviors. Although the premise that heredity influences human behavior is controversial, it is more generally accepted in animals, Garcia says, especially when it involves base behaviors such as mating. He straddles the familiar nature-nurture debate, theorizing that genes set basic tendencies and the environment shapes the behaviors further. To begin testing his hypothesis, Garcia is deconstructing some of the most elemental of all behaviors in one of the world's simplest organisms.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 3573 - Posted: 06.24.2010

COLLEGE STATION – They behaved just like pigs. Or at least, that's what a study of cloned pigs found at Texas A&M University. The behavior of cloned pigs, produced last year at Texas A&M, were compared to pigs bred normally. The recent study was completed by master's of science student Greg Archer, under the supervision of Dr. Ted Friend, professor of applied ethology in the department of animal science. "We found the variation within a litter of clones to be as variable or greater (than the normal litters) at least 80 percent of the time for all the tests that we did," Archer said.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 3249 - Posted: 06.24.2010

Philadelphia, PA) –While type 1 Neurofibromatosis (NF1) is primarily known to cause tumors of the nervous system, scientists were puzzled as to why patients with NF1 are also prone to cardiovascular problems such as hypertension and congenital heart disease. Researchers from the University of Pennsylvania School of Medicine have solved this particular part of the puzzle by showing how the Nf1 gene – which is mutated in those suffering from Neurofibromatosis – is also essential in endothelial cells, the cells that make up blood vessels. Type 1 Neurofibromatosis affects many children, occurring in one in every 4,000 births. The researchers believe their findings may result in new therapeutics for NF1, as well as provide validation of an animal model for the disease. Their findings will appear online today in advance of publication in the January issue of the journal Nature Genetics.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 3145 - Posted: 06.24.2010

Most people find caffeine stimulating – Americans alone consume about 350 million cups of coffee daily. But some people find that it makes them anxious instead. A recently completed study sheds new light on the likely reason for this difference. Individuals who have two linked genetic variations are far more likely to end up biting their nails following a jolt of caffeine than those who don't, reported Harriet de Wit of the University of Chicago on Sunday, Dec. 8 at the annual meeting of the American College of Neuropsychopharmacology held in San Juan, Puerto Rico. "This is the first time that anyone has identified why people have different behavioral reactions to the same drug," said de Wit.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 3135 - Posted: 06.24.2010

Rehovot, Israel---How do 30,000 genes in our DNA work together to form a large part of who we are? How do one hundred billion neurons operate in our brain? The huge number of factors involved makes such complex networks hard to crack. Now, a study published in the October 25 issue of Science uncovers a strategy for finding the organizing principles of virtually any network – from neural networks to ecological food webs or the Internet. A team headed by Dr. Uri Alon, of the Weizmann Institute of Science's Molecular Cell Biology Department has found several such organizational patterns – which they call "network motifs" – underlying genetic, neural, technological, and food networks. The mathematical technique was first proposed by Alon earlier this year (published in Nature Genetics) and has now been shown to be applicable in a wide range of systems. In developing the technique, Alon surmised that patterns serving an important function in nature might recur more often than in randomized networks. This in mind, he devised an algorithm that enabled him to analyze the plentiful scientific findings examining key networks in some well-researched organisms. Alon noticed that some patterns in the networks were inexplicably more repetitive than they would be in randomized networks. This handful of patterns was singled out as a potential bundle of network motifs.

Related chapters from BP7e: Chapter 1: Biological Psychology: Scope and Outlook; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 1: An Introduction to Brain and Behavior; Chapter 13: Memory, Learning, and Development
Link ID: 2951 - Posted: 06.24.2010

– Two research teams have converged on a novel gene that appears to regulate key aspects of communication between nerve and muscle cells. Knowing the identity and function of these regulatory signals, which have remained largely mysterious until now, will allow researchers to better understand how the nervous system forges important connections during development. The two research teams – one led by Howard Hughes Medical Institute investigator Michael O' Connor and his colleagues -- reported the discovery and characterization of the gene in fruit flies in articles in the February 15, 2002, issue of Neuron. The other team, led by former HHMI investigator Corey Goodman, discovered the same gene via a different route. Both research teams identified the gene, wishful thinking (wit), by studying the larval neuromuscular junction (NMJ) in the fruit fly Drosophila. The Drosophila NMJ consists of 30 muscle fibers that are attached to 35 neurons. The well-characterized system is a prime model for exploring how muscle growth triggers the growth of its innervating motor neurons that drive muscle contraction.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 1555 - Posted: 06.24.2010

By JUDITH SHULEVITZ How is a church like a can opener? Among the pleasures of using evolutionary logic to think about matters nonbiological, one is getting to ask questions like that. The evolutionary take on a cultural fact like religion or warfare can cut through the fog of judgment and show how a social institution solves some mechanical problem of human co-existence. What function did intergroup violence serve? What are gods good for? Nicholas Wade’s book “The Faith Instinct” is at its best when putting us through such exercises and sidelining the by-now tiresome debates about religion as a force for good or evil. According to Wade, a New York Times science writer, religions are machines for manufacturing social solidarity. They bind us into groups. Long ago, codes requiring altruistic behavior, and the gods who enforced them, helped human society expand from families to bands of people who were not necessarily related. We didn’t become religious creatures because we became social; we became social creatures because we became religious. Or, to put it in Darwinian terms, being willing to live and die for their coreligionists gave our ancestors an advantage in the struggle for resources. Wade holds that natural selection can operate on groups, not just on individuals, a contentious position among evolutionary thinkers. He does not see religion as what Stephen Jay Gould and Richard Lewontin called a spandrel — a happy side effect of evolution (or, if you’re a dyspeptic atheist, an unhappy one). He does not agree with the cognitive anthropologist Pascal Boyer that religion is a byproduct of our overactive brains and their need to attribute meaning and intention to a random world. He doesn’t perceive religious ideas as memes — that is to say, the objects of a strictly cultural or mental process of evolution. He thinks we have a God gene. Copyright 2009 The New York Times Company

Related chapters from BP7e: Chapter 6: Evolution of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 0: ; Chapter 11: Emotions, Aggression, and Stress
Link ID: 13607 - Posted: 06.24.2010

By Emily Anthes We take it for granted that certain aspects of our social behavior—whether we chat easily with strangers at a party, for instance, or prefer to be a wallflower—are influenced by genetics. But now researchers at the University of California, San Diego, and Harvard University have shown that genes have a much broader sway, affecting the kinds of social networks people form and the positions they occupy in them. James Fowler, a political scientist at U.C.S.D., and his colleagues studied the social networks of 1,110 adolescent fraternal and identical twins. They found that three aspects of the twins’ social networks appeared to be shaped by genetics. How many times each teen was named by others as a friend and how likely each youth’s friends were to know one another were both approximately 50 percent related to genetic factors. Whether a teen was located at the center of a network or toward the edge was about 30 percent genetic. “We have innate characteristics that give us a tendency to gravitate toward one part of a network,” Fowler explains. “We vary in the tendency with which we’ll attract people as friends, and we vary in our tendency to introduce our friends to one another.” The genetic foundation uncovered in the study, he posits, is probably a broad combination of genes that are mostly linked to personality traits such as humor, generosity or extroversion. © 1996-2009 Scientific American Inc.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 13037 - Posted: 06.24.2010

By Tina Hesman Saey Whether you like it or not, you’re a little different. If it makes you feel any better, so is everybody else. In fact, everybody is far more different than anybody had imagined. Scientists are only beginning to discover just how different humans are from each other at the genetic level and what those personal genetic attributes mean for health, history and the human evolutionary future. It’s true that people are 99.9 percent alike, if only minor spelling variations in the genetic instruction book are taken into account. In each person, about one in every 1,000 DNA bases — the chemical letters of the genetic alphabet — differs from the generic human construction and operating manual. So, on average, one person will differ from another at about 3 million of the 3 billion letters in the human genome. Researchers have recently mapped many of these single letter variations, called single 
nucleotide polymorphisms or SNPs, looking for variants that might play a role in complex diseases such as heart disease, diabetes and high blood pressure (SN: 6/21/08, p. 20). So far, SNPs have been associated with many diseases, but SNPs can also be protective. And those little spelling differences may contain information about a person’s geographic ancestry — just as whether people write color or colour is a clue about whether they hail from the United States or Great Britain. © Society for Science & the Public 2000 - 2009

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 12744 - Posted: 06.24.2010

By Tina Hesman Saey Tattoos on the skin can say a lot about person. On a deeper level, chemical tattoos on a person’s DNA are just as distinctive and individual — and say far more about a person’s life history. A pair of reports published online January 18 in Nature Genetics show just how important one type of DNA tattoo, called methylation, can be. Researchers at Johns Hopkins University report the unexpected finding that most DNA methylation — a chemical alteration that turns off genes — occurs most often near, but not precisely within, the DNA regions on which scientists have typically focused their studies. The other report, from researchers at the Universityof Toronto and collaborators, suggests that identical twins owe their similarity not only to having the same genetic make-up, but also to certain methylation patterns established in the fertilized egg. Methylation is just one of many epigenetic signals — chemical changes to DNA and its associated proteins — that modify gene activity without altering the genetic information in the genes. Methylation and other epigenetic signals help guide stem cells as they develop into other type of cells. Scientists have long suspected that mishandling methylation and other epigenetic flags could lead to cancer. The Johns Hopkins group has now shown that DNA methylation is more common at what they call “CpG island shores” instead of at the CpG islands that most researchers have been studying. CpG islands are short stretches of DNA rich in the bases cytosine and guanine, also known as C and G in the genetic alphabet. (Adenine (A) and thymine (T) are the other DNA bases.) CpG islands are located near the start site of genes and help control a gene’s activity. Planting a chemical flag called a methyl group on an island declares the gene off-limits, blocking activity. © Society for Science & the Public 2000 - 2009

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 12457 - Posted: 06.24.2010

By Victoria Stern Spinal cord injuries and disorders afflict millions worldwide, from disabled veterans to people with neurodegenerative disorders such as Lou Gehrig’s disease, yet there is currently no way to repair a damaged spine. Geneticists at the Allen Institute for Brain Science in Seattle are hoping to change that by developing the first genetic encyclopedia of the spinal cord. The Allen Spinal Cord Atlas, which will be available online for free in early 2009, will map out which genes are active in which locations along the spine in mice, which share 90 percent of their genetic material with humans. Researchers are looking forward to using the new tool, based on the success of the Allen Institute’s 2006 Brain Atlas. That genetic map led to key insights, such as the link between glioblastoma, the deadliest type of brain tumor, and a gene called BEX1. Gregory Foltz of Swedish Medical Center in Seattle saw that BEX1 was turned off in the brains of his tumor patients, and using the Brain Atlas, he confirmed that the gene is usually active in healthy brains, as reported in Cancer Research in 2006. Foltz realized that when BEX1 is inhibited, cells grow uncontrollably and can form tumors—and researchers hope to develop treatments that target the malfunctioning gene. © 1996-2008 Scientific American Inc.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 12122 - Posted: 06.24.2010

By Karen Schrock Have you ever emerged from a matinee movie, squinted into the sudden burst of sunlight and sneezed uncontrollably? Up to a third of the population will answer this question with an emphatic "Yes!" (whereas nearly everyone else scratches their head in confusion). Sneezing as the result of being exposed to a bright light—known as the photic sneeze reflex—is a genetic quirk that is still unexplained by science, even though it has intrigued some of history's greatest minds. Aristotle mused about why one sneezes more after looking at the sun in The Book of Problems: "Why does the heat of the sun provoke sneezing?" He surmised that the heat of the sun on the nose was probably responsible. Some 2 ,000 years later, in the early 17th century, English philosopher Francis Bacon neatly refuted that idea by stepping into the sun with his eyes closed—the heat was still there, but the sneeze was not (a compact demonstration of the fledgling scientific method). Bacon's best guess was that the sun's light made the eyes water, and then that moisture ("braine humour," literally) seeped into and irritated the nose. Humours aside, Bacon's moisture hypothesis seemed quite reasonable until our modern understanding of physiology made it clear that the sneeze happens too quickly after light exposure to be the result of the comparatively sluggish tear ducts. So neurology steps in: Most experts now agree that crossed wires in the brain are probably responsible for the photic sneeze reflex. © 1996-2007 Scientific American Inc.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 11198 - Posted: 06.24.2010

By RICHARD E. NISBETT JAMES WATSON, the 1962 Nobel laureate, recently asserted that he was “inherently gloomy about the prospect of Africa” and its citizens because “all our social policies are based on the fact that their intelligence is the same as ours — whereas all the testing says not really.” Dr. Watson’s remarks created a huge stir because they implied that blacks were genetically inferior to whites, and the controversy resulted in his resignation as chancellor of Cold Spring Harbor Laboratory. But was he right? Is there a genetic difference between blacks and whites that condemns blacks in perpetuity to be less intelligent? The first notable public airing of the scientific question came in a 1969 article in The Harvard Educational Review by Arthur Jensen, a psychologist at the University of California, Berkeley. Dr. Jensen maintained that a 15-point difference in I.Q. between blacks and whites was mostly due to a genetic difference between the races that could never be erased. But his argument gave a misleading account of the evidence. And others who later made the same argument — Richard Herrnstein and Charles Murray in “The Bell Curve,” in 1994, for example, and just recently, William Saletan in a series of articles on Slate — have made the same mistake. In fact, the evidence heavily favors the view that race differences in I.Q. are environmental in origin, not genetic. Copyright 2007 The New York Times Company

Related chapters from BP7e: Chapter 1: Biological Psychology: Scope and Outlook; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 1: An Introduction to Brain and Behavior; Chapter 13: Memory, Learning, and Development
Link ID: 11070 - Posted: 06.24.2010

Ewen Callaway Spit might have helped human evolution by enabling our ancestors to harvest more energy from starch than their primate cousins. Compared with chimpanzees, humans boast many more copies of the gene that makes salivary amylase — a saliva enzyme that breaks down starch into digestible sugars. And carbohydrate-loving societies carry more copies of the gene than those that follow low-carbohydrate diets, claims a new study in Nature Genetics1. This strongly implies that people have adapted to their local environment. "High starch foods and a high starch diet have been an important evolutionary force for humans," says George Perry, an anthropologist at Arizona State University in Tempe, who led the new analysis. The change could possibly have supported the growth in hominin brains that occurred some two million years ago, says Nate Dominy, an anthropologist at the University of California in Santa Cruz involved in the study. "Our diet must have had some shift to feed that brain," says Dominy, who thinks root vegetables like African tubers allowed large-brained humans to flourish. Starch, which helps to make a baked potato mushy, is an important source of food for modern humans. But without amylase in the saliva, man can make little use of such complex carbohydrates - enzymes elsewhere in the body are not as good at breaking the compounds down. ©2007 Nature Publishing Group

Related chapters from BP7e: Chapter 6: Evolution of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 0: ; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 10704 - Posted: 06.24.2010