Scholarlink

Background <p>Experimental studies consistently demonstrate that lithium modulates multiple intracellular signaling pathways involved in crucial neurobiological responses, highlighting its therapeutic potential in degenerative diseases. Lithium has demonstrated significant neuroprotective potential in preclinical models of Alzheimer’s disease (AD) and other neurodegenerative disorders.</p> Contents <p>This review examines the molecular mechanisms and biological effects of lithium at subtherapeutic concentrations, focusing on its ability to modulate key intracellular pathways, such as the inhibition of glycogen synthase kinase-3 beta (GSK-3β), reduction of Tau hyperphosphorylation, and enhancement of neurotrophic and anti-inflammatory responses. Evidence from animal and cellular studies underscores lithium’s ability to reduce amyloid plaques, maintain neuronal integrity, improve memory, and decrease neuroinflammation, even at doses much lower than those used clinically for mood stabilization.</p> Conclusion <p>Evidence from animal and cellular models indicates that subtherapeutic lithium doses may provide a safer and more practical approach to neuroprotection, particularly in AD. However, further research is necessary to optimize dosing strategies, assess long-term safety, and translate these findings into clinical applications.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Lithium and neuroprotection: a review of molecular targets and biological effects at subtherapeutic concentrations in preclinical models of Alzheimer’s disease

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年5月10日

查看全文
  • Vanessa de Jesus R. De-Paula,
  • Marcia Radanovic,
  • Orestes Vicente Forlenza

摘要

Background

Experimental studies consistently demonstrate that lithium modulates multiple intracellular signaling pathways involved in crucial neurobiological responses, highlighting its therapeutic potential in degenerative diseases. Lithium has demonstrated significant neuroprotective potential in preclinical models of Alzheimer’s disease (AD) and other neurodegenerative disorders.

Contents

This review examines the molecular mechanisms and biological effects of lithium at subtherapeutic concentrations, focusing on its ability to modulate key intracellular pathways, such as the inhibition of glycogen synthase kinase-3 beta (GSK-3β), reduction of Tau hyperphosphorylation, and enhancement of neurotrophic and anti-inflammatory responses. Evidence from animal and cellular studies underscores lithium’s ability to reduce amyloid plaques, maintain neuronal integrity, improve memory, and decrease neuroinflammation, even at doses much lower than those used clinically for mood stabilization.

Conclusion

Evidence from animal and cellular models indicates that subtherapeutic lithium doses may provide a safer and more practical approach to neuroprotection, particularly in AD. However, further research is necessary to optimize dosing strategies, assess long-term safety, and translate these findings into clinical applications.