Current Neuropharmacological Interventions in Autism: Potential Drug Targets from Pre-clinical and Clinical Findings

Abstract

Autism spectrum disorder is the term used in the most recent edition of the diagnostic and statistical manual of neurodevelopmental disorders, which includes conditions such as autism. Etiological factors such as environmental toxins, food, genes, bacterial infections, and viruses are the reasons behind autism. In the lack of diagnostic criteria, early studies of the disorder reported differences in motor and cognitive abilities in persons with autism. Autism neuropathological features are correlated with different brain areas, such as the cerebral cortex, amygdala, and hippocampus. Autism is associated with mitochondrial dysfunction, oxidative stress, neuroinflammatory reactions, neuroexcitation, and abnormal synapse formation. Pre-clinically, the administration of propionic acid in the brains of rats by stereotaxic technique exacerbates autistic behavioral and neurochemical alterations. Prescription drugs to alleviate neurological disorders for autism are risperidone (Blocks D2 and 5HT2A receptors) and aripiprazole (D2 and 5HT1A partial agonist) approved by the US-FDA, which comes with limited therapeutic intervention. Findings suggest that malfunctions of propionic acid-disrupted neuronal mitochondrial coenzyme Q10 (CoQ10) and etc-complexes are the most pathogenic events for autism. As a result, the current review focused on the history of disease, clinical and pre-clinical drugs under investigation and suggested mediating neuroprotective intervention in autism with mitochondrial CoQ10 activation. Additionally, a greater understanding of the mitochondrial signaling pathway is an effort to improve successful treatment not only for Autism but also for other neurological disorders.