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LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
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We are analyzing https://link.springer.com/chapter/10.1007/7854_2010_109.

Title:
When the Serotonin Transporter Gene Meets Adversity: The Contribution of Animal Models to Understanding Epigenetic Mechanisms in Affective Disorders and Resilience | SpringerLink
Description:
Although converging epidemiological evidence links exposure to stressful life events with increased risk for affective spectrum disorders, there is extraordinary interindividual variability in vulnerability to adversity. The environmentally moderated penetrance of...
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Family & Parenting
  • Non-Profit & Charity

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We're unsure how the site profits.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com has a secret sauce for making money, but we can't detect it yet.

Keywords {🔍}

google, scholar, pubmed, article, cas, serotonin, transporter, lesch, gene, neurosci, psychiatry, social, disorders, brain, polymorphism, murphy, epigenetic, stress, mice, genetic, variation, htt, behav, mol, depression, neural, rhesus, suomi, higley, models, adversity, early, sci, knockout, molecular, mechanisms, life, interaction, emotional, region, nat, meaney, chapter, affective, effects, environmental, httlpr, maternal, acad, processing,

Topics {✒️}

low-anxiety phenotype linked hypothalamic–pituitary–adrenal mri serotonin transporter-deficient mice serotonin transporter exhibit 5-ht event-related fmri study replicable gene-disorder associations csf monoamine metabolite google scholar serotonin transporter knockout serotonin transporter gene long-evans rats results barr cs common snps explain privacy choices/manage cookies murine serotonin transporter klaus-peter lesch serotonin transporter genotype serotonin transporter knock vesicular monoamine release stressful life events serotonin transporter polymorphism 5-ht transporter confers high-affinity binding ren-patterson 5-ht transporter knock functional serotonin transporter serotonin transporter inactivation specific gene effects gene–environment interactions behav brain res boyce-rustay jm gimenez-amaya jm frontoparietal “mirror” network intermediate brain phenotypes cellular serotonin systems increases stress abnormalities alternative biallelic variation dell’acqua ml major psychiatric disorders identifying molecular substrates rhesus monkey neonates altering epigenetic marking european economic area extraordinary interindividual variability environmentally moderated penetrance unfavourable outcomes resembling gamma-aminobutyric acid watson kk von economo neurons medial frontal cortex

Questions {❓}

  • Anisman H, Zaharia MD, Meaney MJ, Merali Z (1998) Do early-life events permanently alter behavioral and hormonal responses to stressors?

Schema {🗺️}

ScholarlyArticle:
      headline:When the Serotonin Transporter Gene Meets Adversity: The Contribution of Animal Models to Understanding Epigenetic Mechanisms in Affective Disorders and Resilience
      pageEnd:280
      pageStart:251
      image:https://media.springernature.com/w153/springer-static/cover/book/978-3-642-19703-1.jpg
      genre:
         Biomedical and Life Sciences
         Biomedical and Life Sciences (R0)
      isPartOf:
         name:Molecular and Functional Models in Neuropsychiatry
         isbn:
            978-3-642-19703-1
            978-3-642-19702-4
         type:Book
      publisher:
         name:Springer Berlin Heidelberg
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Klaus-Peter Lesch
            affiliation:
                  name:University of Wuerzburg
                  address:
                     name:Molecular Psychiatry, ADHD Clinical Research Network, Laboratory of Translational Neuroscience, Department of Psychiatry, Psychosomatics and Psychotherapy, University of Wuerzburg, Wuerzburg, Germany
                     type:PostalAddress
                  type:Organization
                  name:Maastricht University
                  address:
                     name:Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, European Graduate School for Neuroscience (EURON), Maastricht University, Maastricht, The Netherlands
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      keywords:Cognition, Depression, Emotion, Environment, Epigenetics, Gene, Mouse, Primate, Resilience, Serotonin transporter
      description:Although converging epidemiological evidence links exposure to stressful life events with increased risk for affective spectrum disorders, there is extraordinary interindividual variability in vulnerability to adversity. The environmentally moderated penetrance of genetic variation is thought to play a major role in determining who will either develop disease or remain resilient. Research on genetic factors in the aetiology of disorders of emotion regulation has, nevertheless, been complicated by a mysterious discrepancy between high heritability estimates and a scarcity of replicable gene-disorder associations. One explanation for this incongruity is that at least some specific gene effects are conditional on environmental cues, i.e. gene-by-environment interaction (G × E) is present. For example, a remarkable number of studies reported an association of variation in the human serotonin (5-HT) transporter gene (SLC6A4, 5-HTT, SERT) with emotional and cognitive traits as well as increased risk for depression in interaction with psychosocial adversity. The results from investigations in non-human primate and mouse support the occurrence of G × E interaction by showing that variation of 5-HTT function is associated with a vulnerability to adversity across the lifespan leading to unfavourable outcomes resembling various neuropsychiatric disorders. The neural and molecular mechanisms by which environmental adversity in early life increases disease risk in adulthood are not known but may include epigenetic programming of gene expression during development. Epigenetic mechanisms, such as DNA methylation and chromatin modification, are dynamic and reversible and may also provide targets for intervention strategies (see Bountra et al., Curr Top Behav Neurosci, 2011). Animal models amenable to genetic manipulation are useful in the identification of molecular mechanisms underlying epigenetic programming by adverse environments and individual differences in resilience to stress. Therefore, deeper insight into the role of epigenetic regulation in the process of neurodevelopmental programmes is likely to result in early diagnosis of affective spectrum disorders and will contribute to the design of innovative treatments targeting neural pathways that foster resilience.
      datePublished:2011
      isAccessibleForFree:
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Book:
      name:Molecular and Functional Models in Neuropsychiatry
      isbn:
         978-3-642-19703-1
         978-3-642-19702-4
Organization:
      name:Springer Berlin Heidelberg
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Wuerzburg
      address:
         name:Molecular Psychiatry, ADHD Clinical Research Network, Laboratory of Translational Neuroscience, Department of Psychiatry, Psychosomatics and Psychotherapy, University of Wuerzburg, Wuerzburg, Germany
         type:PostalAddress
      name:Maastricht University
      address:
         name:Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, European Graduate School for Neuroscience (EURON), Maastricht University, Maastricht, The Netherlands
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Klaus-Peter Lesch
      affiliation:
            name:University of Wuerzburg
            address:
               name:Molecular Psychiatry, ADHD Clinical Research Network, Laboratory of Translational Neuroscience, Department of Psychiatry, Psychosomatics and Psychotherapy, University of Wuerzburg, Wuerzburg, Germany
               type:PostalAddress
            type:Organization
            name:Maastricht University
            address:
               name:Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, European Graduate School for Neuroscience (EURON), Maastricht University, Maastricht, The Netherlands
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Molecular Psychiatry, ADHD Clinical Research Network, Laboratory of Translational Neuroscience, Department of Psychiatry, Psychosomatics and Psychotherapy, University of Wuerzburg, Wuerzburg, Germany
      name:Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience, European Graduate School for Neuroscience (EURON), Maastricht University, Maastricht, The Netherlands
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(288)

Analytics and Tracking {📊}

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Libraries {📚}

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