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Tero Toivanen

The eye contact effect: mechanisms and development - 0 views

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    The eye contact effect: mechanisms and development.
Tero Toivanen

Enhanced perception in savant syndrome: patterns, structure and creativity - Philosophi... - 1 views

  • utistic perception is characterized by: enhanced low-level operations; locally oriented processing as a default setting; greater activation of perceptual areas during a range of visuospatial, language, working memory or reasoning tasks; autonomy towards higher processes; and superior involvement in intelligence.
  • We now propose that enhanced detection of patterns, including similarity within and among patterns, is one of the mechanisms responsible for operations on human codes, a type of material with which savants show particular facility.
  • A second mechanism, related to but exceeding the existing concept of redintegration, involves completion, or filling-in, of missing information in memorized or perceived units or structures.
Tero Toivanen

Inside the Mind of a Savant: Scientific American - 0 views

  • Theory guides us in one respect. Kim’s brain shows abnormalities in the left hemisphere, a pattern found in many savants. What is more, left hemisphere damage has been invoked as an explanation of why males are much more likely than females to display not only savantism but also dyslexia, stuttering, delayed speech, and autism.
  • The proposed mechanism has two parts: male fetuses have a higher level of circulating testosterone, which can be toxic to developing brain tissue; and the left hemisphere develops more slowly than the right and therefore remains vulnerable for a longer period. Also supporting the role of left hemisphere damage are the many reported cases of “acquired savant syndrome,” in which older children and adults suddenly develop savant skills after damage to the left hemisphere.
  • although autism is more commonly linked with savantism than is any other single disorder, only about half of all savants are autistic.
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    Article about Kim Peek and mind of savant.
Tero Toivanen

The Mirror Neuron Revolution: Explaining What Makes Humans Social: Scientific American - 0 views

  • In recent years, Iacoboni has shown that mirror neurons may be an important element of social cognition and that defects in the mirror neuron system may underlie a variety of mental disorders, such as autism.
  • Mirror neurons are the only brain cells we know of that seem specialized to code the actions of other people and also our own actions. They are obviously essential brain cells for social interactions. Without them, we would likely be blind to the actions, intentions and emotions of other people.
  • The way mirror neurons likely let us understand others is by providing some kind of inner imitation of the actions of other people, which in turn leads us to “simulate” the intentions and emotions associated with those actions. When I see you smiling, my mirror neurons for smiling fire up, too, initiating a cascade of neural activity that evokes the feeling we typically associate with a smile.
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  • In 2006 your lab published a paper in Nature Neuroscience linking a mirror neuron dysfunction to autism. How might reduced mirror neuron activity explain the symptoms of autism?
  • Reduced mirror neuron activity obviously weakens the ability of these patients to experience immediately and effortlessly what other people are experiencing, thus making social interactions particularly difficult for these patients. Patients with autism have also often motor problems and language problems. It turns out that a deficit in mirror neurons can in principle explain also these other major symptoms. The motor deficits in autism can be easily explained because mirror neurons are just special types of premotor neurons, brain cells essential for planning and selecting actions. It has been also hypothesized that mirror neurons may be important in language evolution and language acquisition.
  • Thus, a deficit in mirror neurons can in principle account for three major symptoms of autism, the social, motor and language problems.
  • There is convincing behavioral evidence linking media violence with imitative violence. Mirror neurons provide a plausible neurobiological mechanism that explains why being exposed to media violence leads to imitative violence.
  • I think there are two key points to keep in mind. The first one is the one we started with: mirror neurons are brain cells specialized for actions. They are obviously critical cells for social interactions but they can’t explain non-social cognition. The second point to keep in mind is that every brain cell and every neural system does not operate in a vacuum. Everything in the brain is interconnected, so that the activity of each cell reflects the dynamic interactions with other brain cells and other neural systems.
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    In recent years, Marco Iacoboni, a neuroscientist at the University of California at Los Angeles, has shown that mirror neurons may be an important element of social cognition and that defects in the mirror neuron system may underlie a variety of mental disorders, such as autism.
Tero Toivanen

New Theory Of Autism Suggests Symptoms Or Disorder May Be Reversible - 0 views

  • the brains of people with autism are structurally normal but dysregulated, meaning symptoms of the disorder might be reversible.
  • autism is a developmental disorder caused by impaired regulation of the locus coeruleus, a bundle of neurons in the brain stem that processes sensory signals from all areas of the body.
  • The new theory stems from decades of anecdotal observations that some autistic children seem to improve when they have a fever, only to regress when the fever ebbs.
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  • This study documented that autistic children experience behavior changes during fever.
  • Einstein researchers contend that scientific evidence directly points to the locus coeruleus–noradrenergic (LC-NA) system as being involved in autism. "The LC-NA system is the only brain system involved both in producing fever and controlling behavior," says co-author Dominick P. Purpura, M.D., dean emeritus and distinguished professor of neuroscience at Einstein.
  • The locus coeruleus has widespread connections to brain regions that process sensory information. It secretes most of the brain's noradrenaline, a neurotransmitter that plays a key role in arousal mechanisms, such as the "fight or flight" response. It is also involved in a variety of complex behaviors, such as attentional focusing (the ability to concentrate attention on environmental cues relevant to the task in hand, or to switch attention from one task to another). Poor attentional focusing is a defining characteristic of autism.
  • "What is unique about the locus coeruleus is that it activates almost all higher-order brain centers that are involved in complex cognitive tasks," says Dr. Mehler.
  • autism, the LC-NA system is dysregulated by the interplay of environment, genetic, and epigenetic factors
  • They believe that stress plays a central role in dysregulation of the LC-NA system, especially in the latter stages of prenatal development when the fetal brain is particularly vulnerable.
  • a higher incidence of autism among children whose mothers had been exposed to hurricanes and tropical storms during pregnancy.
  • autistic children, fever stimulates the LC-NA system, temporarily restoring its normal regulatory function. "This could not happen if autism was caused by a lesion or some structural abnormality of the brain," says Dr. Purpura.
  • future of autism treatment probably lies in drugs that selectively target certain types of noradrenergic brain receptors or, more likely, in epigenetic therapies targeting genes of the LC-NA system.
  • If the locus coeruleus is impaired in autism, it is probably because tens or hundreds, maybe even thousands, of genes are dysregulated in subtle and complex ways," says Dr. Mehler. "The only way you can reverse this process is with epigenetic therapies, which, we are beginning to learn, have the ability to coordinate very large integrated gene networks."
  • "You can't take a complex neuropsychiatric disease that has escaped our understanding for 50 years and in one fell swoop have a therapy that is going to reverse it — that's folly. On the other hand, we now have clues to the neurobiology, the genetics, and the epigenetics of autism. To move forward, we need to invest more money in basic science to look at the genome and the epigenome in a more focused way."
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    the brains of people with autism are structurally normal but dysregulated, meaning symptoms of the disorder might be reversible.
Tero Toivanen

Researchers from the CHUM Research Centre (CRCHUM) have iden - 0 views

  • The results show for the first time the role of the SYN1 gene in autism, in addition to epilepsy, and strengthen the hypothesis that a deregulation of the function of synapse because of this mutation is the cause of both diseases
  • until now, no other genetic study of humans has made this demonstration.
  • The different forms of autism are often genetic in origin and nearly a third of people with autism also suffer from epilepsy.
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  • Although mutations in other genes involved in the development of synapses (the functional junction between two neurons) have previously been identified, this mechanism has never been proved in epilepsy in humans until the present study.
  • The results of the present study were published in the latest online edition of Human Molecular Genetics.
Tero Toivanen

NIMH · Our brains are made of the same stuff, despite DNA differences - 1 views

  • “Having at our fingertips detailed information about when and where specific gene products are expressed in the brain brings new hope for understanding how this process can go awry in schizophrenia, autism and other brain disorders,” said NIMH Director Thomas R. Insel, M.D.
  • Among key findings in the prefrontal cortex:Individual genetic variations are profoundly linked to expression patterns. The most similarity across individuals is detected early in development and again as we approach the end of life.Different types of related genes are expressed during prenatal development, infancy, and childhood, so that each of these stages shows a relatively distinct transcriptional identity. Three-fourths of genes reverse their direction of expression after birth, with most switching from on to off.Expression of genes involved in cell division declines prenatally and in infancy, while expression of genes important for making synapses, or connections between brain cells, increases. In contrast, genes required for neuronal projections decline after birth – likely as unused connections are pruned.By the time we reach our 50s, overall gene expression begins to increase, mirroring the sharp reversal of fetal expression changes that occur in infancy.Genetic variation in the genome as a whole showed no effect on variation in the transcriptome as a whole, despite how genetically distant individuals might be. Hence, human cortexes have a consistent molecular architecture, despite our diversity.
  • Among key findings:Over 90 percent of the genes expressed in the brain are differentially regulated across brain regions and/or over developmental time periods. There are also widespread differences across region and time periods in the combination of a gene’s exons that are expressed.Timing and location are far more influential in regulating gene expression than gender, ethnicity or individual variation.Among 29 modules of co-expressed genes identified, each had distinct expression patterns and represented different biological processes. Genetic variation in some of the most well-connected genes in these modules, called hub genes, has previously been linked to mental disorders, including schizophrenia and depression.Telltale similarities in expression profiles with genes previously implicated in schizophrenia and autism are providing leads to discovery of other genes potentially involved in those disorders.Sex differences in the risk for certain mental disorders may be traceable to transcriptional mechanisms. More than three-fourths of 159 genes expressed differentially between the sexes were male-biased, most prenatally. Some genes found to have such sex-biased expression had previously been associated with disorders that affect males more than females, such as schizophrenia, Williams syndrome, and autism.
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  • Our brains are all made of the same stuff. Despite individual and ethnic genetic diversity, our prefrontal cortex shows a consistent molecular architecture.
  • Males show more sex-biased gene expression. More genes differentially expressed (DEX) between the sexes were found in males than females, especially prenatally. Some genes found to have such sex-biased expression had previously been associated with disorders that affect males more than females, such as schizophrenia, Williams syndrome, and autism.
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    Our brains are all made of the same stuff. Despite individual and ethnic genetic diversity, our prefrontal cortex shows a consistent molecular architecture. 
Tero Toivanen

Developmental abnormalities in the mirror neuron system may - 1 views

  • Developmental abnormalities in the mirror neuron system may contribute to social deficits in autism.
  • Now, a new study published in Biological Psychiatry reports that the mirror system in individuals with autism is not actually broken, but simply delayed.
  • While most of us have their strongest mirror activity while they are young, autistic individuals seem to have a weak mirror system in their youth, but their mirror activity increases with age, is normal by about age 30 and unusually high thereafter.
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  • This increase in function of mirror neuron systems may be related to increased capacity for social function or responsiveness to rehabilitative treatments among individuals with autism.
  • One of the next steps in this line of research will be for researchers to examine how individuals with autism accomplish this improvement over time, and how therapeutic interventions targeting the same mechanism can help to support this important process.
Tero Toivanen

The Genetics of Autism (ActionBioscience) - 1 views

  • Despite this relatively high frequency, scientists do not understand the mechanism of this serious developmental problem. What they have discovered is that autism is one of the most heritable mental disorders known. In other words, autism appears to be largely genetic in origin, and most autistic children inherit the disorder from their parents.
  • In the case of PKU, geneticists have determined that retardation is due to genetics (a mutated phenylalanine hydroxylase gene) and the environment (a phenylalanine-containing diet).
  • In the case of autism, the likelihood that the sibling of an affected child also would be affected is between three and six percent.
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  • Nonetheless, this incidence is about 100 times greater than the rate at which autism affects unrelated people in the population.
  • One study showed that the likelihood that the identical twin of an autistic child also would be autistic was 82 percent, whereas the equivalent rate for fraternal twins was only 10 percent.
  • With sophisticated statistical techniques and numerous twin studies, behavioral geneticists now believe that as much as 90 percent of the behavioral phenotype of autism is related to inherited genes.
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    With sophisticated statistical techniques and numerous twin studies, behavioral geneticists now believe that as much as 90 percent of the behavioral phenotype of autism is related to inherited genes.
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