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Microglia-Mediated Synaptic Dysfunction Contributes to Chemotherapy-Related Cognitive Impairment.

Jingxiong Wang1, Hua Zhang1, Marc Augenreich2

  • 1Department of Medicine, University of Missouri-Columbia School of Medicine, Columbia, Missouri, USA.

Journal of Neurochemistry
|February 28, 2025
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Chemotherapy impairs cognition by affecting microglia and synaptic plasticity. Minocycline treatment reversed these effects, suggesting microglial dysfunction drives chemotherapy-related cognitive impairment (CRCI).

Keywords:
chemotherapycognitive deficitslong‐term potentiationmicrogliasynaptic transmission

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Area of Science:

  • Neuroscience
  • Oncology
  • Pharmacology

Background:

  • Chemotherapy-related cognitive impairment (CRCI) is a significant challenge for cancer survivors.
  • The underlying mechanisms of CRCI remain unclear, limiting effective treatment development.
  • Microglia and synaptic plasticity are potential key players in CRCI pathogenesis.

Purpose of the Study:

  • To investigate if microglia-mediated deficits in synaptic plasticity contribute to CRCI.
  • To determine the effects of 5-fluorouracil and leucovorin (5-Fu/LV) on cognitive function, microglial activity, and synaptic plasticity in mice.
  • To assess the therapeutic potential of minocycline in mitigating 5-Fu/LV-induced cognitive deficits.

Main Methods:

  • Adult male mice received 5-Fu/LV chemotherapy or vehicle treatment.
  • Cognitive function was evaluated using the novel object recognition (NOR) test.
  • Microglial morphology and activity were assessed via Iba1 and CD68 staining.
  • Hippocampal long-term potentiation (LTP) and N-methyl-D-aspartic acid receptor-excitatory postsynaptic currents (NMDAR-EPSCs) were measured.
  • Mice were co-treated with the microglial inhibitor minocycline.

Main Results:

  • 5-Fu/LV treatment induced cognitive deficits in the NOR test.
  • Chemotherapy altered microglial morphology, increasing CD68-positive microglia and reducing phagocytosis.
  • 5-Fu/LV reduced hippocampal LTP and NMDAR-EPSCs.
  • Minocycline treatment restored cognitive function, normalized microglial changes, and reversed synaptic plasticity deficits.

Conclusions:

  • Microglial dysfunction, characterized by altered morphology and reduced phagocytosis, is implicated in chemotherapy-induced cognitive impairment.
  • Synaptic plasticity deficits, specifically reduced LTP and NMDAR-EPSCs, contribute to CRCI.
  • Targeting microglial activity with agents like minocycline may offer a therapeutic strategy for CRCI.