Can Maternal Autoantibodies Play an Etiological Role in ASD Development?

0531281 - FGÚ 2021 RIV NZ eng J - Článek v odborném periodiku
Dudová, I. - Horáčková, K. - Hrdlička, M. - Balaštík, Martin
Can Maternal Autoantibodies Play an Etiological Role in ASD Development?
Neuropsychiatric Disease and Treatment. Roč. 16, Jun (2020), s. 1391-1398. E-ISSN 1178-2021
Grant CEP: GA MZd(CZ) NV18-04-00085
Institucionální podpora: RVO:67985823
Klíčová slova: maternal autoantibodies * autism spectrum disorder * animal models * CRMP2 * therapy
Obor OECD: Clinical neurology
Impakt faktor: 2.570, rok: 2020
Způsob publikování: Open access
https://www.dovepress.com/can-maternal-autoantibodies-play-an-etiological-role-in-asd-developmen-peer-reviewed-article-NDT

Autism spectrum disorder (ASD) is a heterogeneous condition with multiple etiologies and risk factors - both genetic and environmental. Recent data demonstrate that the immune system plays an important role in prenatal brain development. Deregulation of the immune system during embryonic development can lead to neurodevelopmental changes resulting in ASD. One of the potential etiologic factors in the development of ASD has been identified as the presence of maternal autoantibodies targeting fetal brain proteins. The type of ASD associated with the presence of maternal autoantibodies has been referred to as maternal antibodies related to ASD (MAR ASD). The link between maternal autoantibodies and ASD has been demonstrated in both clinical studies and animal models, but the exact mechanism of their action in the pathogenesis of ASD has not been clarified yet. Several protein targets of ASD-related maternal autoantibodies have been identified. Here, we discuss the role of microtubule-associated proteins of the collapsin response mediator protein (CRMP) family in neurodevelopment and ASD. CRMPs have been shown to integrate multiple signaling cascades regulating neuron growth, guidance or migration. Their targeting by maternal autoantibodies could change CRMP levels or distribution in the developing nervous system, leading to defects in axon growth/guidance, cortical migration, or dendritic projection, which could play an etiological role in ASD development. In addition, we discuss the future possibilities of MAR ASD treatment.
Trvalý link: http://hdl.handle.net/11104/0309969