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Focal brain inflammation and autism

Journal of Neuroinflammation, ISSN: 1742-2094, Vol: 10, Issue: 1, Page: 46
2013
  • 140
    Citations
  • 0
    Usage
  • 295
    Captures
  • 3
    Mentions
  • 128
    Social Media
Metric Options:   Counts1 Year3 Year

Metrics Details

  • Citations
    140
  • Captures
    295
  • Mentions
    3
    • News Mentions
      3
      • 3
  • Social Media
    128
    • Shares, Likes & Comments
      128
      • Facebook
        128

Most Recent News

Scientists Find Chronic Brain Inflammation in Children With Autism

by The Vaccine Reaction A recent small study out of Tufts University Medical Center in Boston, Massachusetts has concluded that, “inflammation may be the main

Review Description

Increasing evidence indicates that brain inflammation is involved in the pathogenesis of neuropsychiatric diseases. Autism spectrum disorders (ASD) are characterized by social and learning disabilities that affect as many as 1/80 children in the USA. There is still no definitive pathogenesis or reliable biomarkers for ASD, thus significantly curtailing the development of effective therapies. Many children with ASD regress at about age 3 years, often after a specific event such as reaction to vaccination, infection, stress or trauma implying some epigenetic triggers, and may constitute a distinct phenotype. ASD children respond disproportionally to stress and are also affected by food and skin allergies. Corticotropin-releasing hormone (CRH) is secreted under stress and together with neurotensin (NT) stimulates mast cells and microglia resulting in focal brain inflammation and neurotoxicity. NT is significantly increased in serum of ASD children along with mitochondrial DNA (mtDNA). NT stimulates mast cell secretion of mtDNA that is misconstrued as an innate pathogen triggering an auto-inflammatory response. The phosphatase and tensin homolog (PTEN) gene mutation, associated with the higher risk of ASD, which leads to hyper-active mammalian target of rapamycin (mTOR) signalling that is crucial for cellular homeostasis. CRH, NT and environmental triggers could hyperstimulate the already activated mTOR, as well as stimulate mast cell and microglia activation and proliferation. The natural flavonoid luteolin inhibits mTOR, mast cells and microglia and could have a significant benefit in ASD. © 2013 Theoharides et al.; licensee BioMed Central Ltd.

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