Redox Regulation and the Autistic Spectrum: Role of Tryptophan Catabolites, Immuno-inflammation, Autoimmunity and the Amygdala
The autistic spectrum disorders (ASD) form a set of multi-faceted disorders with significant genetic, epigenetic
and environmental determinants. Oxidative and nitrosative stress (O&NS), immuno-inflammatory pathways,
mitochondrial dysfunction and dysregulation of the tryptophan catabolite (TRYCATs) pathway play significant
interactive roles in driving the early developmental etiology and course of ASD. O&NS interactions with immunoinflammatory
pathways mediate their effects centrally via the regulation of astrocyte and microglia responses, including
regional variations in TRYCATs produced. Here we review the nature of these interactions and propose an early
developmental model whereby different ASD genetic susceptibilities interact with environmental and epigenetic
processes, resulting in glia biasing the patterning of central interarea interactions. A role for decreased local melatonin and
N-acetylserotonin production by immune and glia cells may be a significant treatment target.
Keywords: Autism, glia, immuno-inflammation, melatonin, nitrosative stress, oxidative stress, tryptophan.
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