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. 2016 Feb 1;7:9. doi: 10.3389/fneur.2016.00009

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Copyright © 2016 Edmonson, Ziats and Rennert.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic representation of hypothesized non-immune microglial contributions to ASD, as described in the text. It is proposed that inherited defects in the microglial genome/epigenome in autistic patients (center) result in abnormal or exaggerated execution of normal developmental microglial functions, such as (A) abnormal secretion of trophic factors necessary for normal neuronal growth, (B) incorrect synaptic pruning, (C) failure of appropriate apoptosis of neurons, and (D) exaggerated activation and cytokine secretion.