Targeting the mitochondrial electron transport chain in autism, a systematic review and synthesis of a novel therapeutic approach.
Autism is a complex developmental disorder with an unknown etiology and without any curative treatment. The mitochondrial electron transfer chains play a major role in the production of ATP, and the generation and management of reactive oxidative stress (ROS). This paper is a systematic review of the role of the mitochondrial electron transport chain in autism, and a consequent hypothesis for treating autism is synthesized. An electronic search with pre-specified inclusion criteria was conducted in order to retrieve all the published articles about the mitochondrial electron transport chain in autism. The two databases of PUBMED and Google Scholar were searched. From one hundred twenty five retrieved titles, 12 (three case control study and 9 case reports) articles met inclusion criteria. All of the included studies indicated dysfunction of electron transport chain in autism. The mitochondrial electron transfer chain seems impaired in some children with autism and ROS production is additionally enhanced. It is hypothesized that interventions involving alternative electron shuttling may improve autism through lowering the production of ROS. In addition, it is expected that this alternative electron shuttling to cytochrome c might enhance the production of ATP which is impaired in the disorder.
Research Center for Psychiatry and Behavioral Sciences, Shiraz University of Medical, Sciences, Hafez Hospital, Shiraz, Iran.
Ahmad
A
Ghanizadeh
Michael
M
Berk
Hassan
H
Farrashbandi
Ali
A
Alavi Shoushtari
Kristi-Ann
KA
Villagonzalo
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D001321:Autistic Disorder / Q000188:drug therapy*; D004579:Electron Transport / Q000187:drug effects*; D006801:Humans; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism
D017382:Reactive Oxygen Species; D000255:Adenosine Triphosphate