Treatment of Autism Spectrum Disorders by Mitochondrial-targeted Drug: Future of Neurological Diseases Therapeutics.

This review looks at how problems with mitochondria (tiny parts of cells that make energy) might be involved in autism. Since mitochondria are passed down from mothers and are important during early development, researchers think they might play a role in autism. The paper discusses new treatments that target these mitochondria and could help children with autism in the future.

This 2023 review examines the potential role of mitochondrial dysfunction in autism spectrum disorders and explores mitochondrial-targeted therapeutic approaches. The authors discuss how mitochondria, the cellular powerhouses inherited maternally, may be involved in autism development through oxidative damage and metabolic dysfunction. The review covers risk factors, genetic determinants, pathogenic pathways, and current therapeutic regimens for ASD. Emphasis is placed on emerging mitochondrial-targeted treatments currently under investigation at various clinical trial stages.

The authors suggest that mitochondrial dysfunction's role in autism may be greater than previously recognized, based on accumulating evidence from cellular and sub-cellular studies.

Mitochondrial dysfunction represents an emerging therapeutic target for autism treatment. Clinicians should be aware of potential mitochondrial-targeted interventions under development. However, these approaches remain experimental and require further clinical validation before implementation in practice.

This is a narrative review without systematic methodology. No sample size or specific studies are detailed. The evidence quality and clinical trial stages of mentioned therapeutic regimens are not specified. Limited quantitative data provided.

Autism is a neurodevelopmental disorder with a complex etiology that might involve environmental and genetic variables. Recently, some epidemiological studies conducted in various parts of the world have estimated a significant increase in the prevalence of autism, with 1 in every 59 children having some degree of autism. Since autism has been associated with other clinical abnormalities, there is every possibility that a sub-cellular component may be involved in the progression of autism. The organelle remains a focus based on mitochondria's functionality and metabolic role in cells.

Furthermore, the mitochondrial genome is inherited maternally and has its DNA and organelle that remain actively involved during embryonic development; these characteristics have linked mitochondrial dysfunction to autism. Although rapid stride has been made in autism research, there are limited studies that have made particular emphasis on mitochondrial dysfunction and autism. Accumulating evidence from studies conducted at cellular and sub-cellular levels has indicated that mitochondrial dysfunction's role in autism is more than expected. The present review has attempted to describe the risk factors of autism, the role of mitochondria in the progression of the disease, oxidative damage as a trigger point to initiate mitochondrial damage, genetic determinants of the disease, possible pathogenic pathways and therapeutic regimen in vogue and the developmental stage.

Furthermore, in the present review, an attempt has been made to include the novel therapeutic regimens under investigation at different clinical trial stages and their potential possibility to emerge as promising drugs against ASD.