Cell therapies for autism spectrum disorder: a systematic review of clinical applications

Abstract Purpose Autism spectrum disorder (ASD) is a neurodevelopmental condition that affects patients’ ability to communicate, engage with others, and behave in certain ways. Despite the existence of several therapy possibilities, an effective treatment for ASD has not yet been identified. Cell therapies have been becoming increasingly recognized in recent years as a potential therapeutic approach for the management of ASD. Different types of cellular products are transplanted using different delivery methods as part of cell therapy, which has the ability to regulate the immune system, demonstrate paracrine, neuro-regenerative, anti-inflammatory, and anti-oxidative stress effects, as well as transfer healthy mitochondria. We have compared the results and findings of completed cell therapy clinical trials for the treatment of ASD in this systematic review. Methods A total of 547 studies were identified, in which 11 studies were found to be eligible to be included in this review as they were completed cell therapy clinical trials or clinical applications with quantitative results for the treatment of ASD patients. Results This systematic review provides an overview of clinical trials conducted with different types of cell therapy strategies for the treatment of ASD and their potential mechanisms of action. The limitations and future possibilities for this field of study, as well as the safety and efficacy of cell treatments in ASD, were reviewed. Conclusion Overall, the evidence suggests that various cell therapy methods may offer a novel and effective treatment option for individuals with ASD, although further research is needed to fully understand the optimal treatment strategy and therapeutic potential

Bronchopulmonary dysplasia and wnt pathway-associated single nucleotide polymorphisms.

AIM: Genetic variants contribute to the pathogenesis of bronchopulmonary dysplasia (BPD). The aim of this study is to evaluate the association of 45 SNPs with BPD susceptibility in a Turkish premature infant cohort. METHODS: Infants with gestational age <32 weeks were included. Patients were divided into BPD or no-BPD groups according to oxygen need at 28 days of life, and stratified according to the severity of BPD. We genotyped 45 SNPs, previously identified as BPD risk factors, in 192 infants. RESULTS: A total of eight SNPs were associated with BPD risk at allele level, two of which (rs4883955 on KLF12 and rs9953270 on CHST9) were also associated at the genotype level. Functional relationship maps suggested an interaction between five of these genes, converging on WNT5A, a member of the WNT pathway known to be implicated in BPD pathogenesis. Dysfunctional CHST9 and KLF12 variants may contribute to BPD pathogenesis through an interaction with WNT5A. CONCLUSIONS: We suggest investigating the role of SNPs on different genes which are in relation with the Wnt pathway in BPD pathogenesis. We identified eight SNPs as risk factors for BPD in this study. In-silico functional maps show an interaction of the genes harboring these SNPs with the WNT pathway, supporting its role in BPD pathogenesis. TRIAL REGISTRATION: NCT03467828. IMPACT: It is known that genetic factors may contribute to the development of BPD in preterm infants. Further studies are required to identify specific genes that play a role in the BPD pathway to evaluate them as a target for therapeutic interventions. Our study shows an association of BPD predisposition with certain polymorphisms on MBL2, NFKBIA, CEP170, MAGI2, and VEGFA genes at allele level and polymorphisms on CHST9 and KLF12 genes at both allele and genotype level. In-silico functional mapping shows a functional relationship of these five genes with WNT5A, suggesting that Wnt pathway disruption may play a role in BPD pathogenesis