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Related Experiment Video

Updated: May 9, 2025

Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders
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Synaptic Function and Sensory Processing in ZDHHC9-Associated Neurodevelopmental Disorder: A Mechanistic Account.

Rebeca Ianov Vitanov1, Jascha Achterberg1, Danyal Akarca1

  • 1MRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK.

The European Journal of Neuroscience
|May 1, 2025
PubMed
Summary

Loss-of-function ZDHHC9 variants impair brain function, potentially by reducing neural inhibition. This study used MEG and computational modeling to reveal how ZDHHC9 impacts cortical activity and cognition.

Keywords:
MEGZDHHC9epilepsyintellectual disabilitylanguagerecurrent neural networks

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Area of Science:

  • Neuroscience
  • Computational Biology
  • Genetics

Background:

  • Loss-of-function variants in ZDHHC9 gene are linked to X-linked intellectual disability (XLID), rolandic epilepsy (RE), and developmental language disorders.
  • Understanding the neural mechanisms underlying ZDHHC9-associated neurodevelopmental conditions is crucial for targeted interventions.

Purpose of the Study:

  • To investigate the neural mechanisms underlying ZDHHC9-associated differences in cortical function and cognition.
  • To integrate human neurophysiological data with computational modeling to explain ZDHHC9's impact.

Main Methods:

  • Magnetoencephalography (MEG) was used to record auditory-evoked fields (AEFs) and magnetic mismatch negativity (mMMN) in individuals with ZDHHC9 variants and controls.
  • A recurrent neural network (RNN) model was developed to simulate auditory-evoked responses and test the effects of synaptic dysfunction.

Main Results:

  • Individuals with ZDHHC9 variants exhibited larger amplitude and later peak latency in AEFs, along with increased mMMN amplitude, indicating altered neural processing.
  • RNN model simulations demonstrated that reducing inhibitory synaptic weights recapitulated the observed group differences in evoked responses.
  • Strengthening excitatory connections did not yield similar results, supporting the role of reduced inhibition.

Conclusions:

  • Reduced neural inhibition is a likely mechanism explaining ZDHHC9 loss-of-function effects on cortical dynamics during sensory processing.
  • These findings provide a potential neural basis for ZDHHC9-associated neurodevelopmental conditions.