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Synaptic Adhesion Molecule Pcdh-γC5 Mediates Synaptic Dysfunction in Alzheimer's Disease.

Yanfang Li1, Zhicai Chen2, Yue Gao2

  • 1Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, College of Medicine, Xiamen University, Xiamen 361005 Fujian, China, yfli@xmu.edu.cn huiz@bcm.edu.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
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PubMed
Summary

Protocadherin-γC5 (Pcdh-γC5) promotes inhibitory neuron function. In Alzheimer's disease (AD), aberrant Pcdh-γC5 expression may disrupt this balance, contributing to synaptic dysfunction and offering a therapeutic target.

Keywords:
Alzheimer's diseaseGABAPcdh-γC5micesynaptic transmission

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • Synaptic dysfunction and excitatory/inhibitory imbalance are key in Alzheimer's disease (AD) pathogenesis.
  • Mechanisms of inhibitory synaptic dysfunction in AD remain understudied.
  • Protocadherin-γC5 (Pcdh-γC5) promotes GABAergic synaptic transmission.

Purpose of the Study:

  • Investigate the role of Pcdh-γC5 in mediating inhibitory synaptic function in AD.
  • Determine how Pcdh-γC5 expression and function are affected by AD-related pathology.
  • Explore Pcdh-γC5 as a potential therapeutic target for AD.

Main Methods:

  • Immunohistochemistry to detect Pcdh-γC5 localization in synaptic puncta.
  • Analysis of Pcdh-γC5 and GABAergic protein levels in various models.
  • Genetic knock-down of Pcdh-γC5 to assess its functional impact on synaptic currents.
  • Treatment with beta-amyloid (Aβ) and use of APP/PS1 transgenic mice.

Main Results:

  • Pcdh-γC5 is enriched in GABAergic synaptic puncta.
  • Pcdh-γC5 expression increases with neuronal hyperexcitation, Aβ treatment, and in APP/PS1 mice.
  • Elevated Pcdh-γC5 correlates with increased GABAergic proteins and enhanced inhibition.
  • Pcdh-γC5 directly modulates synaptic currents and Aβ-induced synaptic alterations.

Conclusions:

  • Pcdh-γC5 acts as a sensor of neuronal hyperexcitation, augmenting GABAergic inhibition.
  • Dysregulation of Pcdh-γC5 in chronic excitation conditions like AD contributes to synaptic dysfunction.
  • Pcdh-γC5 represents a novel pathway and potential therapeutic target for AD-related synaptic dysfunction.