Links for Keyword: Genes & Behavior

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Heidi Ledford Networks of genes linked to obesity have been uncovered.GettyResearchers have used a new technique to identify networks of genes linked to obesity in both mice and humans. The procedure is more comprehensive than the traditional method of hunting for genes associated with disease, and is already being used to identify new drug targets. Over the past year, a flurry of studies have revealed genetic variations associated with disease. These ‘genome-wide association studies’ have been used to find variants associated with everything from heart disease to diabetes (See Genome studies: Genetics by numbers). Traditionally, single genes are linked with particular diseases by locating genetic variants present in people who have the disease and identifying the part of a chromosome associated with that disease. Then researchers have to track down the gene on the chromosome, without knowing what it does or why it would be involved. Eric Schadt of Rosetta Inpharmatics, a subsidiary of Merck Pharmaceuticals in Seattle, Washington, lead one of the research teams involved in the new work. He likens the traditional approach to finding a simple light switch for a disease: flipping this single gene switch on or off may produce a higher or lower risk of disease. The new approach looks at changes in expression of already-known genes, and finds networks of genes associated with disease, rather than single switches. “Instead of the simple ‘turn the light on or off’ analogy, we would view this as a network of these switches,” says Schadt. © 2008 Nature Publishing Group

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 11421 - Posted: 06.24.2010

— By studying gene mutations in patients with the complex set of behavioral and neurological symptoms that accompany Rett syndrome, Howard Hughes Medical Institute investigator Huda Zoghbi and her colleagues at Baylor College of Medicine have designed a mouse model that faithfully recapitulates the disease down to its distinctive hand-wringing behavior. The development of the mouse, reported in the July 18, 2002 issue of the journal Neuron, provides a springboard into the study of Rett syndrome, the leading cause of mental retardation in girls. First recognized as a syndrome in the 1980s, the disorder affects one in 10,000-15,000 girls. It is particularly devastating for families with affected children because infants are seemingly normal at birth and achieve the usual developmental milestones for the first few months of life. Then, as the infant reaches toddlerhood, a sudden and dramatic decline in physical and mental capabilities takes hold, accompanied by onset of seizures, irregular breathing, awkward gait, and hand-wringing. “I know of no other neurological disease that gives this distinctive stereotypic behavior — this hand-wringing these girls do basically all the time they are awake,” said Zoghbi. “With this mouse model we can now ask, ‘Why is that?’” ©2002 Howard Hughes Medical Institute

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: 2332 - Posted: 06.24.2010

First fruits of the genome project identify genes in flies bred for a behavioral preference SAN DIEGO – From Triple Crown winner Seattle Slew to Yorkshire ‘lowfat' pigs, people have been breeding animals and plants for desirable traits since prehistoric times. But there has been no easy way of telling which genes have been favored by the selective breeding. Until now. By making use of the new technique of DNA microarrays ("chips"), a team of scientists lead by Ralph J. Greenspan at The Neurosciences Institute has discovered a way of solving the conundrum of identifying which genes have changed when breeding for a particular trait. In their study of two strains of the common fruit fly (Drosophila melanogaster), selected for differences in their response to gravity ("geotaxis”), they have found that the difference is due to small contributions from many genes, and they have identified several of the genes, two of which have human genetic counterparts.

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: 2196 - Posted: 06.24.2010

Ewen Callaway A handful of genes could mark the difference between high-strung Chihuahuas and unflappable basset hounds. A comparison of 148 dog breeds has uncovered genes for size, lifespan, and even complex behaviours such as pointing and herding. Geneticists have previously uncovered genes for dog traits such as coat colour and narcolepsy, but these searches tended to focus on a single breed, comparing pooches with variations in a single trait – for example, boxers with and without white spots. This strategy does not work for rooting out the genetic basis of behaviours because certain breeds either display these behaviours or they don't, says Gordon Lark at the University of Utah in Salt Lake City, US. So with the help of a dog show judge, Lark's team scored dogs from 148 breeds for traits including herding, pointing, boldness, excitability and trainability. Then they scoured their genomes for similarities and differences. Dogs were also scored for size, body proportions and longevity. The search implicated several genes in stereotypical dog behaviours. For example, herding behaviour typical of collies and shepherds may be linked to a gene that is similar to one associated with schizophrenia in humans. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 11729 - Posted: 06.24.2010

BETHESDA, Md. – Researchers have identified a novel gene mutation that causes X-linked mental retardation for which there was no previously known molecular diagnosis, according to an article to be published electronically on Tuesday, March 20, 2007 in The American Journal of Human Genetics. Investigators F. Lucy Raymond (Cambridge Institute of Medical Research, University of Cambridge, Cambridge, UK) and Patrick S. Tarpey (Wellcome Trust Sanger Institute, Hixton, UK) describe the ZDHHC9 gene found in those with severe retardation as being mutated to the point of entirely losing function. "ZDHHC9 is a novel gene," explains Dr. Raymond. "This gene would not have been predicted to play a role in mental retardation based on the previous genetics work. It was found only because we were systematically looking at all the genes on the X chromosome irrespective of what they do." X-linked mental retardation is severe. Some patients require total care and may not have language ability. The condition runs in families and only affects the male offspring. So far only a few of these genes have been identified. Working through a large, international collaboration, the researchers collected genetic samples from 250 families in which at least two boys have mental retardation to help identify novel genes that cause X-linked mental retardation. The investigators systematically analyzed the X chromosome for gene mutations.

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: 10116 - Posted: 06.24.2010

By comparing foxes selected for tameness with others that have not been selected in this way, researchers have found evidence that dramatic behavioral and physiological changes accompanying tameness may be associated with only limited changes in gene activity in the brain. The work is reported by Elena Jazin and colleagues at Uppsala University, the Swedish University of Agricultural Sciences, and the Norwegian University of Life Science. The first step in the process of domestication in mammals is the selection for tame individuals that can adapt to life with humans and to frequent handling. To investigate the changes in gene activity that accompany tameness, in the present study the authors compared two groups of farm-raised silver foxes (Vulpes vulpes). One group derived from a long-standing domestication process in which farm-raised silver foxes have been selected for more than 40 generations for non-aggressive behavior toward men (see the related work of Brian Hare and colleagues, Current Biology 15:226–230). Another group of foxes was also farm raised but was not selected for tameness. The foxes selected for tameness were docile and friendly and showed developmental, morphological, and neurochemical changes similar to those observed in other domestic animals.

Related chapters from BP7e: Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 0:
Link ID: 8212 - Posted: 06.24.2010

SEATTLE – One teenager likes to snowboard off a cliff. Another prefers to read a book and wouldn't think of trading places. Why these differences exist is a mystery, but for the first time researchers have identified a possible genetic explanation behind risk-seeking behavior. Scientists at Fred Hutchinson Cancer Research Center have found that a specific neurodevelopmental gene, called neuroD2, is related to the development of an almond-shaped area of the brain called the amygdala, the brain's emotional seat. This gene also controls emotional-memory formation and development of the fear response, according to research led by James Olson, M.D., Ph.D., associate member of the Clinical Research Division at the Hutchinson Center. The findings will be published in the early online edition of the Proceedings of the National Academy of Sciences the week of Sept. 26. Olson and colleagues studied mice with a single copy of the neuroD2 gene and found they had an impaired ability to form emotional memories and conditioned fear. "Most of us are familiar with the fact that we can remember things better if those memories are formed at a time when there is a strong emotional impact – times when we are frightened, angry or falling in love," he said. "That's called emotional-memory formation. The amygdala is the part of the brain that is responsible for formation of emotional memory."

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 7956 - Posted: 06.24.2010

Antwerp, Belgium – Neuralgic Amyotrophy is a painful disorder of the peripheral nervous system. This heritable disease causes prolonged acute attacks of pain in the shoulder or arm, followed by temporary paralysis. Researchers from the Flanders Interuniversity Institute for Biotechnology (VIB) connected to the University of Antwerp, have uncovered a small piece of the molecular puzzle of this disease by identifying the defects in the gene responsible for this disorder. Hereditary Neuralgic Amyotrophy (HNA) is characterized by repeated attacks of pain in a shoulder, arm, and/or hand, followed by total or partial paralysis of the affected area. The pain and the loss of movement usually disappear within a couple of weeks, but sometimes recovery can take months or even several years. Many HNA patients also have particular facial features, such as eyes that are somewhat closer together, a fold in the upper eyelid that covers the inside corner of the eye, and sometimes a cleft palate. HNA is a relatively rare disorder: the disease appears in some 200 families worldwide. There is also a non-hereditary form of HNA, called the Parsonage-Turner Syndrome. The clinical picture of this more frequently occurring form - 2 to 4 cases per 100,000 persons - is not distinguishable from that of the heritable form. The attacks of pain are usually provoked by external factors such as vaccination, infection, operation, and even pregnancy or childbirth. By virtue of their genetic predisposition, carriers of the hereditary form of HNA run greater risk of having an attack.

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 7947 - Posted: 06.24.2010

CAMBRIDGE, Mass., –- Scientists working with salmon have found that gene expression in the brain can differ significantly among members of a species with different life histories. Their study indicates that roughly 15 percent of Atlantic salmon genes show differential expression in males who migrate from their freshwater birthplaces to mature in oceans versus those who do not leave the freshwater environment to mature. The researchers, at Harvard University, the University of Massachusetts and the US Geological Survey, report the finding in the current issue of Proceedings of the Royal Society B. They compared female salmon, male salmon that will eventually undertake the well-known journey from their river birthplaces to oceans –- and then migrate heroically back upstream one to three years later to spawn –- and males of the same age known as "sneakers" that mature at greatly reduced size without leaving freshwater. "The finding that hundreds of the nearly 3,000 genes we studied were expressed differently in the brains of sneakers and other male salmon came as a surprise," says Nadia Aubin-Horth, a postdoctoral researcher in the Bauer Center for Genomics Research in Harvard's Faculty of Arts and Sciences. "Since these males of the same species in the same wild environment differed only in their life history, we did not expect the expression of so many of their genes to differ." Aubin-Horth and her colleagues were also surprised by some of the 17 separate classes of genes demonstrating differing activity levels.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 7667 - Posted: 06.24.2010

Durham, N.C. – A gene that plays many fundamental roles in cells throughout the body has, for the first time, been implicated in human disease, according to researchers at the Duke Center for Human Genetics. A defect in the ubiquitous gene dynamin 2 underlies one form of the prevalent, familial nerve disorder, known as Charcot-Marie-Tooth disease (CMT). The disorder affects approximately 1 in every 2,500 people, making it one of the most common of all hereditary disorders, said the researchers. Their findings also reveal a previously unknown link between CMT and a deficiency of white blood cells, suggesting that defects in dynamin 2 might underlie both conditions, the researchers reported in the Jan. 30, 2005, issue of Nature Genetics. The discovery -- together with earlier findings of genes that can also cause the genetically heterogeneous and debilitating disease -- is providing new insight into the nervous system, said first author of the study Stephan Züchner, M.D., assistant professor of psychiatry and member of the Duke Center for Human Genetics. Also, he said, the findings bring a better understanding of the types of defects that might, in general, lead to peripheral nerve disorders. © 2001-2005 Duke University Medical Center

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: 6791 - Posted: 06.24.2010

BOSTON- Researchers at Dana-Farber Cancer Institute have compiled the first atlas showing the locations of crucial gene regulators, or switches that determine how different parts of the brain develop – and, in some cases, develop abnormally or malfunction. The scientists say the map will accelerate research on brain tumors and neurological diseases that result from mutations in these switch genes – called "transcription factors." When these genes are altered, the genes they control can go awry, causing abnormalities in the development or function of nerves and related structures. Although the gene regulators were pinpointed using mouse brains, the map applies to the human brain as well. "This is the first systematic mapping of all of the major brain areas that shows what regulatory genes are expressed in those specific locations," said Quifu Ma, PhD, of Dana-Farber's Cancer Biology Department. He is senior author of a paper appearing in today's online issue of the journal Science, along with Charles D. Stiles, PhD, also of Dana-Farber. Transcription factors are genes that control the expression, or activity, of "target" genes. These factors play a pivotal role in brain development by direction the formation of neurons and supporting cells called glia from uncommitted progenitor cells. Until now, brain transcription factors had not been systematically isolated and their locations within different parts of the brain pinned down.

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: 6617 - Posted: 06.24.2010

Female mice that are abnormally small due to gene "knockout" technology are also bad mothers whose poor parenting skills cause their young to die within a day or two of birth, scientists report this week in the on-line edition of the Proceedings of the National Academy of Sciences. Since Chawnshang Chang, Ph.D., cloned the gene for testicular orphan receptor 4 (TR4) 10 years ago, he and other scientists have tried to learn its function – scientists call it an "orphan" receptor because they don't know what protein links up with it. So a team led by Chang, director of George Whipple Laboratory for Cancer Research at the University of Rochester Medical Center, knocked out the gene in mice, then watched what happened. They found that many of the mice died before birth. Those that lived are markedly smaller than their normal counterparts: They're born far smaller and then make up some of the difference as they grow, but generally they are about 20 to 30 percent smaller by the time they reach adulthood. The miniature mice are not as fertile as normal mice, having only about half the offspring as other mice. Most visibly, the females have very bad parenting skills: They don't build nests, nurse their young, or tend to their offspring, which die within a day or two as a result.

Related chapters from BP7e: Chapter 5: Hormones and the Brain; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 8: Hormones and Sex
Link ID: 6255 - Posted: 06.24.2010

Honeybees can precisely regulate the temperature of their nest – and they do it thanks to genetically determined variations in their individual thermostats. The new research has revealed one of the few known benefits of the high genetic diversity found in honeybee colonies. Maintaining a nest temperature of between about 32°C and 36°C is vital during spring and summer, when eggs are developing and hatching. “If they don’t keep the nest at this temperature, the brood won’t develop properly,” says Julia Jones of the University of Sydney, Australia, who led the work. If the temperature drops too low, the worker bees huddle together around the brood to keep it warm. If it gets too high, they stand at the nest entrance and use their wings to fan out hot air. The new work shows that bees with different fathers start fanning at slightly different temperatures. This stops sudden colony-wide shifts between warming and cooling behaviours, and keeps the temperature in the nest more constant. “It’s been shown before that honeybees with different genotypes have different thresholds for certain things – for instance, they’re attracted to different concentrations of nectar," says Jones. "But this is the first time any benefit has been shown from different behaviour thresholds based on genotype in the bees.” © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 5706 - Posted: 06.24.2010

– Adrian Bird and Skirmantas Kriaucionis of the University of Edinburgh have discovered a novel form of the protein MeCP2. This alternate form, coined MeCP2 alpha, differs from the original only in the first 19 amino acids. Interestingly, Adrian Bird, Director of the Welcome Trust Centre for Cell Biology at Edinburgh University, found that MeCP2 alpha, is ten times more prevalent not only in the brain but also in other tissues. These findings are currently reported online in Nucleic Acids Research. Similar findings were reported yesterday in Nature Genetics online by Berge Minassian, a neurologist and scientist at Toronto's Hospital for Sick Children. Adrian Bird originally cloned the MECP2 gene in 1992 while in Vienna, Austria at the Institute for Molecular Pathology. In October of 1999 Huda Zoghbi of Baylor College of Medicine and the Howard Hughes Medical Institute announced that mutations in the MECP2 gene were the leading cause of Rett Syndrome (RTT). RTT is a severe neurological disorder diagnosed almost exclusively in girls. Children with RTT appear to develop normally until 6 to 18 months of age, when they enter a period of regression, losing speech and motor skills. Most develop repetitive hand movements, irregular breathing patterns, seizures and extreme motor control problems. RTT leaves its victims profoundly disabled, requiring maximum assistance with every aspect of daily living. There is no cure.

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: 5166 - Posted: 06.24.2010

– 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