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  Developmental Microglial Priming in Postmortem Autism Spectrum Disorder Temporal Cortex

Lee, A., Azmitia, E., & Whitaker-Azmitia, P. (2017). Developmental Microglial Priming in Postmortem Autism Spectrum Disorder Temporal Cortex. Brain, Behavior, and Immunity, 62, 193-202. doi:10.1016/j.bbi.2017.01.019.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0000-C305-E Version Permalink: http://hdl.handle.net/21.11116/0000-0000-C306-D
Genre: Journal Article

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Lee, AS1, 2, Author              
Azmitia, EC, Author
Whitaker-Azmitia, PM, Author
Affiliations:
1Max Planck Institute for Biological Cybernetics, Max Planck Society, ou_1497794              
2Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society, ou_1497798              

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 Abstract: Microglia can shift into different complex morphologies depending on the microenvironment of the central nervous system (CNS). The distinct morphologies correlate with specific functions and can indicate the pathophysiological state of the CNS. Previous postmortem studies of autism spectrum disorder (ASD) showed neuroinflammation in ASD indicated by increased microglial density. These changes in the microglia density can be accompanied by changes in microglia phenotype but the individual contribution of different microglia phenotypes to the pathophysiology of ASD remains unclear. Here, we used an unbiased stereological approach to quantify six structurally and functionally distinct microglia phenotypes in postmortem human temporal cortex, which were immuno-stained with Iba1. The total density of all microglia phenotypes did not differ between ASD donors and typically developing individual donors. However, there was a significant decrease in ramified microglia in both gray matter and white matter of ASD, and a significant increase in primed microglia in gray matter of ASD compared to typically developing individuals. This increase in primed microglia showed a positive correlation with donor age in both gray matter and white of ASD, but not in typically developing individuals. Our results provide evidence of a shift in microglial phenotype that may indicate impaired synaptic plasticity and a chronic vulnerability to exaggerated immune responses.

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 Dates: 2017-05
 Publication Status: Published in print
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 Identifiers: DOI: 10.1016/j.bbi.2017.01.019
BibTex Citekey: LeeAW2017
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Title: Brain, Behavior, and Immunity
Source Genre: Journal
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Pages: - Volume / Issue: 62 Sequence Number: - Start / End Page: 193 - 202 Identifier: -