Source of evidence | Key findings | References |
---|---|---|
Brain tissues obtained from autopsy | Neuroinflammation observed in cerebral cortex and white matter, and cerebellum of ASD patients by immunocytochemical methods and cytokine profiling | [56] |
CSF of living ASD patients | Cytokine profiling showed neuroinflammation | [56] |
Brain tissues from the dorsolateral prefrontal cortex of ASD individuals | Microglia activation reported in individuals as young as < 6 years of age with morphological changes in microglia | [57] |
PET scans using brain microglia radiotracer | Findings suggest an increased microglia activation in multiple regions of the brain of subjects with ASD | [58] |
PET scan for TSPO | Lower expression of TSPO in several brain regions of patients with ASD when compared with control | [59] |
MR–PET scan of [18F]FEPPA (specific ligand for TSPO) | Significantly lower [18F]FEPPA total volume of distribution in ASD patients when compared to the control | [60] |
Brain tissues/blood hormone level of mice | Mice showed increased blood cortisone levels, increased microglia in hippocampus and increased proinflammatory cytokines in cerebellum when compared with control group | [61] |
Brain of MIA mice and offspring of MIA mice | MIA in pregnant mice led to abnormal cortical development in offspring and increased IL-17a mRNA expression in foetal brain mediated via maternal IL-17a pathway | [62] |
Serum, plasma, CSF and brain of patients with ASD | Increased levels of proinflammatory substances like interleukins, chemokines and osteopontin, TNF-α, IF- γ and growth factors | [63] |