Focal brain inflammation and autism
Journal of Neuroinflammation, ISSN: 1742-2094, Vol: 10, Issue: 1, Page: 46
2013
- 140Citations
- 295Captures
- 3Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations140
- Citation Indexes140
- 140
- CrossRef120
- Captures295
- Readers295
- 295
- Mentions3
- News Mentions3
- 3
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.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84875891902&origin=inward; http://dx.doi.org/10.1186/1742-2094-10-46; http://www.ncbi.nlm.nih.gov/pubmed/23570274; http://jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-10-46; https://dx.doi.org/10.1186/1742-2094-10-46; https://jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-10-46
Springer Science and Business Media LLC
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