Autism spectrum disorder: Current progress in therapeutic options for mitochondrial dysfunction and ongoing management possibilities with a multifariousness: A critical overview

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by persistent deficits in interactions, social skills and communications. It consists of an inability to acquire social and emotional skills during early developmental age that to one to two years of the age which progressively results in variable degrees of social adaptation incapacity. Over the last 20 years, the frequency of ASD has progressively increased, with a recent estimate about 1 in 36 children and with boys 4 times more susceptible to the development of ASD than girls. The etiology of ASD is multifactorial and includes functional and structural neurological abnormalities. There is an alarming lack of knowledge in the subject among health care professionals. Hence it is needed to be aware of the people and manages aggressive behavior, hyperactivity, and irritability. Past two decades many efforts have focused on the determination of genes associated with autism, immune dysfunction and free radicles contributing to ASD. The present article aims to highlight the current state knowledge regarding the role of mitochondrial DNA (mtDNA) in the etiology of ASD, core symptoms, diagnosis, therapeutic aspects (meditational and non-meditational) and the prediction of clinical outcomes in the future.