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Probing the Brain in Autism Using fMRI and Diffusion Tensor Imaging
Published on: September 12, 2011
Focal brain inflammation and autism.
Theoharis C Theoharides1, Shahrzad Asadi, Arti B Patel
1Molecular Immunopharmacology and Drug Discovery Laboratory, Department of Molecular Physiology and Pharmacology, Tufts University School of Medicine, Suite J304, 136 Harrison Avenue, Boston, MA 02111, USA. theoharis.theoharides@tufts.edu
Journal of Neuroinflammation
|April 11, 2013
Summary
Brain inflammation is implicated in autism spectrum disorder (ASD) pathogenesis. The flavonoid luteolin may benefit ASD by inhibiting key inflammatory pathways involving corticotropin-releasing hormone and neurotensin.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Autism spectrum disorder (ASD) lacks definitive pathogenesis and reliable biomarkers, hindering effective therapies.
- ASD is associated with social and learning disabilities, regression around age 3, and heightened stress/allergy responses.
- Brain inflammation is increasingly recognized as a factor in neuropsychiatric disease development.
Purpose of the Study:
- To explore the role of corticotropin-releasing hormone (CRH) and neurotensin (NT) in ASD-related brain inflammation.
- To investigate the link between neurotensin, mitochondrial DNA (mtDNA), and auto-inflammatory responses in ASD.
- To evaluate the potential therapeutic benefit of the flavonoid luteolin in ASD.
Main Methods:
- Analysis of CRH and NT pathways in stress response and mast cell/microglia activation.
- Examination of elevated NT and mtDNA levels in ASD children's serum.
- Assessment of the PTEN/mTOR signaling pathway's role in ASD pathogenesis.
- In vitro evaluation of luteolin's inhibitory effects on mTOR, mast cells, and microglia.
Main Results:
- CRH and NT stimulate mast cells and microglia, leading to focal brain inflammation and neurotoxicity in ASD.
- Increased NT and mtDNA in ASD children suggest an auto-inflammatory response triggered by misconstrued innate pathogens.
- PTEN mutations and hyperactive mTOR signaling are implicated in ASD.
- Luteolin demonstrated inhibitory effects on mTOR, mast cells, and microglia.
Conclusions:
- CRH, NT, and environmental factors may exacerbate mTOR hyperactivity and neuroinflammation in ASD.
- Luteolin shows promise as a therapeutic agent for ASD by modulating key inflammatory pathways.
- Targeting neuroinflammation and specific signaling pathways presents a viable strategy for ASD treatment development.
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