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NCOA3 as a Key Regulator in Diabetic Cognitive Dysfunction.

Yanfang Su1, Lijing Zhang1, Hengzhen Cui1

  • 1Department of Neurobiology, School of Basic Medical Sciences, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Molecular Neurobiology
|January 20, 2026
PubMed
Summary
This summary is machine-generated.

Nuclear receptor coactivator 3 (NCOA3) plays a crucial role in preventing diabetes-related cognitive dysfunction (DCD). Lowering NCOA3 levels worsens cognitive deficits, while increasing NCOA3 levels improves them.

Keywords:
Behavioral testCognitive dysfunctionDiabetesGene knockoutNCOA3Neuron

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Endocrinology

Background:

  • Diabetes-related cognitive dysfunction (DCD) is a serious complication of diabetes mellitus.
  • The molecular mechanisms underlying DCD are not fully understood.

Purpose of the Study:

  • To investigate the role of nuclear receptor coactivator 3 (NCOA3) in the pathogenesis of DCD.
  • To explore the molecular mechanisms involving NCOA3 in cognitive impairment.

Main Methods:

  • Utilized conditional knockout (cKO) and lentivirus-mediated overexpression mouse models of NCOA3.
  • Induced diabetes using a high-fat diet and streptozotocin (STZ).
  • Conducted behavioral tests (NORT, Y-maze, CFC) and molecular analyses (NCOA3, AGO2, SYP, PSD-95, miR-138-5p).

Main Results:

  • Diabetic mice showed reduced NCOA3 expression in the cortex and hippocampus.
  • NCOA3 ablation exacerbated cognitive deficits, while NCOA3 overexpression ameliorated them.
  • NCOA3 deficiency correlated with reduced AGO2, SYP, and PSD-95, and altered miR-138-5p levels.

Conclusions:

  • NCOA3 is a key regulator in preventing DCD.
  • NCOA3 may influence synaptic plasticity through the AGO2/miR-138-5p signaling pathway.
  • Findings offer insights into the molecular basis of DCD and potential therapeutic targets.