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Dynamic Clamp Methods to Investigate Impaired Neuronal Excitability Associated with Autism
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Published on: October 17, 2025

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Developmental microglial priming in postmortem autism spectrum disorder temporal cortex.

Andrew S Lee1, Efrain C Azmitia2, Patricia M Whitaker-Azmitia3

  • 1Department of Psychology, Stony Brook University, Stony Brook, NY 11794, USA; Department of Biology, New York University, New York, NY 10003, USA; Max Planck Institute for Biological Cybernetics, 72076 Tuebingen, Germany.

Brain, Behavior, and Immunity
|February 5, 2017
PubMed
Summary
This summary is machine-generated.

In autism spectrum disorder (ASD), microglial phenotypes shift, with fewer ramified and more primed microglia observed. This suggests potential impaired synaptic plasticity and heightened immune responses in the brain.

Keywords:
Autism spectrum disorderDevelopmental primingMicrogliaNeuroinflammationPostmortem human brainTemporal cortex

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Area of Science:

  • Neuroscience
  • Immunology
  • Neurodevelopmental Disorders

Background:

  • Microglia, the immune cells of the central nervous system (CNS), exhibit diverse morphologies linked to CNS function and pathology.
  • Previous studies indicated increased microglial density in autism spectrum disorder (ASD), suggesting neuroinflammation, but specific phenotype contributions remain unclear.

Purpose of the Study:

  • To quantify distinct microglia phenotypes in the temporal cortex of individuals with and without ASD.
  • To investigate the relationship between microglial phenotypes and ASD pathophysiology.

Main Methods:

  • Employed an unbiased stereological approach to analyze postmortem human temporal cortex samples.
  • Immuno-stained tissue with Iba1 to identify and quantify six distinct microglia phenotypes.

Main Results:

  • No significant difference in total microglia density was found between ASD and typically developing individuals.
  • A significant decrease in ramified microglia and a significant increase in primed microglia were observed in the gray matter of ASD donors.
  • Primed microglia density positively correlated with donor age in ASD individuals.

Conclusions:

  • Findings suggest a shift in microglial phenotypes in ASD, characterized by reduced ramified and increased primed forms.
  • This shift may indicate impaired synaptic plasticity and a predisposition to exaggerated immune responses in ASD.
  • Microglia phenotype alterations, rather than density changes, may be more critical in ASD pathophysiology.