Rafie Hamidpour, Soheila Hamidpour, Mohsen Hamidpour, Marriam Zarabi, Mahnaz Sohraby, Mina Shalari
This review article discusses the opportunities and possibilities of antipurinergic therapy (APT) with suramin on mice models with ASD and fragile X syndrome. Suramin is an APT mediator that triggers the mechanism linked to mitochondria, influences immunity, and has the ability to stabilize locomotor function and coordination, social behavior, normalize brain synapse structure, cell-tocell signaling, and recover mitochondrial metabolism in mice with autistic-like behaviors and genetics. Suramin may provide new therapeutic strategies for ASD subtypes. Many clinical studies have explored the scope
of APT with suramin to assist with the genetic, metabolic, and environmental risk factors of ASD. The pharmacological components of suramin allow binding against purinergic receptors without release, serving as an antagonist of extracellular APT, and other nucleotides. In recent studies, APT and suramin have been investigated to help correct behavior, genetic irregularities, and metabolism stemmed from neurodevelopmental disorders. This review article looks at APT with suramin under the following conditions in animal models:
• Gene-environment interaction
• APT with poly(I:C) mouse model
• Fragile X mental retardation syndrome 1 (Fmr1)
knockout mouse model This review article investigates studies by Naviaux et al.and the influence of suramin and APT in relation to ASD and fragile X syndrome. It was concluded that APT with suramin assists in correcting genetic abnormalities and environmental predispositions that may impact social
behavior related to ASD.
