Inflammation and mitochondrial dysfunction in autism spectrum disorder
Version 2 2024-06-13, 16:55Version 2 2024-06-13, 16:55
Version 1 2023-10-23, 02:40Version 1 2023-10-23, 02:40
journal contribution
posted on 2024-06-13, 16:55authored byM Gevezova, V Sarafian, G Anderson, M Maes
Autism Spectrum Disorders (ASD) is a severe childhood psychiatric condition with an array
of cognitive, language and social impairments that can significantly impact family life. ASD is
classically characterized by reduced communication skills and social interactions, with limitations imposed
by repetitive patterns of behavior, interests, and activities. The pathophysiology of ASD is
thought to arise from complex interactions between environmental and genetic factors within the context
of individual development. A growing body of research has raised the possibility of identifying
the aetiological causes of the disorder. This review highlights the roles of immune-inflammatory
pathways, nitro-oxidative stress and mitochondrial dysfunctions in ASD pathogenesis and symptom
severity. The role of NK-cells, T helper, T regulatory and B-cells, coupled with increased inflammatory
cytokines, lowered levels of immune-regulatory cytokines, and increased autoantibodies and microglial
activation is elucidated. It is proposed that alterations in mitochondrial activity and nitrooxidative
stress are intimately associated with activated immune-inflammatory pathways. Future research
should determine as to whether the mitochondria, immune-inflammatory activity and nitrooxidative
stress changes in ASD affect the development of amygdala-frontal cortex interactions. A
number of treatment implications may arise, including prevention-orientated prenatal interventions,
treatment of pregnant women with vitamin D, and sodium butyrate. Treatments of ASD children and
adults with probiotics, sodium butyrate and butyrate-inducing diets, antipurinergic therapy with suramin,
melatonin, oxytocin and taurine are also discussed.