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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

BBC NEWS | Health | Genes 'have key role in autism' - 0 views

  • The changes influence genes which help form and maintain connections between brain cells.
  • The Nature study highlighted one common genetic variant which, if corrected would cut cases of autism by 15%.
  • Previously, other genetic variants have been linked to autism, but they are all relatively rare.
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  • It found several genetic variants commonly associated with ASD, all of them pointing two specific genes found on chromosome 5 which control production of proteins which help cells stick to each other, and make nervous connections.
  • One variant, linked to a gene called CDH10, was so common - present in over 65% of cases of autism - that the researchers calculated that fixing it would cut the number of autism cases by 15%.
  • They also linked ASD rather less strongly to a group of about 30 genes which produce proteins that play a key role in enabling brain cells to migrate to correct places, and to connect to neighbouring cells.
  • Professor Simon Baron-Cohen, an autism expert at the University of Cambridge, said 133 genes had now been linked to the condition, and much work was needed to piece together how they interacted with each other and the environment.
  • The National Autistic Society said the exact causes of autism were unknown. In a statement, the society said: "There is evidence to suggest that genetic factors are responsible for some forms of autism. "However, the difficulty of establishing gene involvement is compounded by the interaction of genes and by their interaction with environmental factors. "Various studies over many years have sought to identify candidate genes but so far inconclusively."
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    Scientists have produced the most compelling evidence to date that genetics play a key role in autism.
Tero Toivanen

New Study: Autism has Multiple Genetic Roots | Suite101 - 3 views

  • The study’s major finding was that children with ASD have significantly more CNVs affecting their genes than children without ASD. Children with ASD have 20 percent more CNVs in general, and 70 percent more CNVs impacting genes known to be associated with ASD or cognitive problems. Significantly, many of the genes that are affected control important functions such as cell proliferation and cell-to-cell communication.
  • Some of the newly discovered genetic variants are inherited, and are found in parents or siblings of children with them. Others, however, seem to have originated spontaneously in the affected child, and do not appear in other family members.
  • While these findings add significantly to the scientific understanding of the genetic and biological underpinnings of ASD, the immediate usefulness is limited. That’s because there are a very large number of CNVs, and each child shows a different pattern of genetic changes. Each of these changes is rare; no CNV showed up in more than one percent of the children studied.
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  • “This will lead to a paradigm shift in understanding the etiology of autism,” says Stephen Scherer, a senior scientist at The Hospital for Sick Children in Toronto, Canada. “Until now, most scientists thought individuals with autism shared common genes. We now think each person has his own rare variations.”
  • If significant CNVs show up, behavioral treatment can be started early. That has been shown to improve children’s outcomes significantly. “If we provide stimulation early, while the brain is still plastic, we can improve cognitive development, social interaction and communication,” says Geri Dawson, Chief Science Officer of Autism Speaks, the major sponsor of the research project.
  • What this new research suggests is that autism and ASD probably result from the interaction between many different genes and a child’s environment. Rather than search for one single cause and one “magic bullet,” researchers will try to find as many significant genetic variants as possible, link them to the biological functions and pathways they control, and then search for medications that can improve or normalize the functioning of damaged pathways.
Tero Toivanen

Scientists have shown how a single protein may trigger autis - 1 views

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    Scientists have shown how a single protein may trigger autistic spectrum disorders by stopping effective communication between brain cells. While hundreds of genes linked to the condition have been found, the precise combination of genetics, biochemistry and other environmental factors which produce autism is still unclear.
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. 
Graeme Wadlow

Cultural Confusions Show that Facial Expressions Are Not Universal - 0 views

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    Current Biology - Cultural Confusions Show that Facial Expressions Are Not Universal
Tero Toivanen

Neuronal Circuits In Autism Can Be Reversed - 0 views

  • When the production of neuroligin-3 in the mice was reactivated, the nerve cells reduced the production of the glutamate receptors to a normal level and the structural defects in the brain typical for autism were gone. Consequently, these glutamate receptors could be targeted in the development of drugs that could stop autism from developing or even reverse it.
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    "A specific dysfunction in neuronal circuits has been identified, by Professors Peter Scheiffele and Kaspar Vogt at the Biozentrum of the University of Basel, that results from autism. The researchers also discovered a way to reverse these neuronal changes. They believe that their findings, published in the journal Science, will have a great effect in drug development for treating autism."
Tero Toivanen

Facing Autism in New Brunswick: Evidence of Common Genes Linking Autism Spectrum Disord... - 0 views

  • genetic mutations in the SHANK2 gene, partially responsible for linking nerve cells,  and variants in the number of gene copies that were common to patients with autism and patients with mental retardation.
  • the same mutation can be present in an autistic patient with normal intelligence and in a mentally impaired patient
  • Our findings further link common genes between ASD and intellectual disability.
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    Link between Autism and intellectual disability?
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