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<p>Depression, a complicated psychiatric condition, is characterized by persistent low mood, disrupted emotional regulation, and cognitive impairment. Attenuated brain-derived neurotrophic factor (BDNF) and dysregulated glycogen synthase kinase-3 beta (GSK-3β) activity promote synaptic deterioration, oxidative imbalance, neuroinflammatory responses, and hippocampal dysfunction, hallmark features of depressive pathology. This review provides an overview of current preclinical and clinical findings explaining the independent and interactive roles of BDNF and GSK-3β in depression. It further illustrates emerging therapeutic approaches targeting this axis, such as metformin, famotidine, tideglusib, lithium, and ketamine. Collectively, the altered crosstalk between BDNF and GSK-3β contributes to the impaired neuroplasticity observed in depression, suggesting that this signaling axis is a promising therapeutic target.</p>

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BDNF and GSK-3β signaling in depression: molecular mechanisms underlying neural plasticity dysfunction

  • 期刊论文

  • 发表日期：

    2026年7月8日

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  • Hayder M. Al-kuraishy,
  • Shimaa A Abass,
  • Hitham Alaa Mohammed Mahana,
  • Osama Ashraf Elbanna,
  • Ibrahiym Yasser Shahin,
  • Abdelrahman Ali Radwan,
  • Omar El-sayed MohamedMohamed,
  • AbdAlRhman Mohamad Lotfy Baktoot,
  • Gaber El-Saber Batiha

摘要

Depression, a complicated psychiatric condition, is characterized by persistent low mood, disrupted emotional regulation, and cognitive impairment. Attenuated brain-derived neurotrophic factor (BDNF) and dysregulated glycogen synthase kinase-3 beta (GSK-3β) activity promote synaptic deterioration, oxidative imbalance, neuroinflammatory responses, and hippocampal dysfunction, hallmark features of depressive pathology. This review provides an overview of current preclinical and clinical findings explaining the independent and interactive roles of BDNF and GSK-3β in depression. It further illustrates emerging therapeutic approaches targeting this axis, such as metformin, famotidine, tideglusib, lithium, and ketamine. Collectively, the altered crosstalk between BDNF and GSK-3β contributes to the impaired neuroplasticity observed in depression, suggesting that this signaling axis is a promising therapeutic target.