Common cellular and molecular mechanisms and interactions between microglial activation and aberrant neuroplasticity

Xiaoyun Guo1, Yanxia Rao2, Ruizhi Mao1

  • 1Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.

Neuropharmacology
|September 27, 2020
PubMed

Insights

Neuroinflammation involving microglia, the brain's immune cells, is linked to depression. Understanding neuron-microglia communication is key to exploring depression's causes and developing new treatments.

Area of Science:

  • Neuroscience
  • Immunology
  • Psychiatry

Background:

  • Inflammation is implicated in the pathophysiology of depression.
  • Microglia, the central nervous system's (CNS) resident macrophages, are crucial in neuroinflammation.
  • Microglia can adopt pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes.

Purpose of the Study:

  • To review cellular and molecular mechanisms of microglial activation in depression.
  • To examine the role of aberrant neuroplasticity in depression.
  • To discuss the interplay between microglia and neurons in depression pathogenesis.

Main Methods:

  • Literature review of cellular and molecular mechanisms.
  • Analysis of neuroinflammation and neuroplasticity in depression.
  • Exploration of neuron-microglia communication pathways.

Main Results:

  • Microglial activation and altered neuroplasticity are common in depression.
  • Neuron-microglia communication influences microglial phenotypes and neuronal activity.
  • Complex signaling pathways mediate these interactions.

Conclusions:

  • Microglial activation and neuroplasticity are integral to depression pathogenesis.
  • Understanding neuron-microglia communication offers novel therapeutic targets for depression.
  • Further research into these mechanisms is essential for advancing depression treatment.

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