PDF(Pubmed)
Abstract：
BACKGROUND: Traumatic brain injury (TBI) refers to damage to brain tissue by mechanical or blunt force via trauma. TBI is often associated with impaired cognitive abilities, like difficulties in memory, learning, attention, and other higher brain functions, that typically remain for years after the injury. Lithium is an elementary light metal that is only utilized in salt form due to its high intrinsic reactivity. This current review discusses the molecular mechanisms and therapeutic and neuroprotective effects of lithium in TBI.
METHODS: The \"Boolean logic\" was used to search for articles on the subject matter in PubMed and PubMed Central, as well as Google Scholar.
RESULTS: Lithium\'s therapeutic action is extremely complex, involving multiple effects on gene secretion, neurotransmitter or receptor-mediated signaling, signal transduction processes, circadian modulation, as well as ion transport. Lithium is able to normalize multiple short- as well as long-term modifications in neuronal circuits that ultimately result in disparity in cortical excitation and inhibition activated by TBI. Also, lithium levels are more distinct in the hippocampus, thalamus, neo-cortex, olfactory bulb, amygdala as well as the gray matter of the cerebellum following treatment of TBI.
CONCLUSIONS: Lithium attenuates neuroinflammation and neuronal toxicity as well as protects the brain from edema, hippocampal neurodegeneration, loss of hemispheric tissues, and enhanced memory as well as spatial learning after TBI.
METHODS: The \"Boolean logic\" was used to search for articles on the subject matter in PubMed and PubMed Central, as well as Google Scholar.
RESULTS: Lithium\'s therapeutic action is extremely complex, involving multiple effects on gene secretion, neurotransmitter or receptor-mediated signaling, signal transduction processes, circadian modulation, as well as ion transport. Lithium is able to normalize multiple short- as well as long-term modifications in neuronal circuits that ultimately result in disparity in cortical excitation and inhibition activated by TBI. Also, lithium levels are more distinct in the hippocampus, thalamus, neo-cortex, olfactory bulb, amygdala as well as the gray matter of the cerebellum following treatment of TBI.
CONCLUSIONS: Lithium attenuates neuroinflammation and neuronal toxicity as well as protects the brain from edema, hippocampal neurodegeneration, loss of hemispheric tissues, and enhanced memory as well as spatial learning after TBI.
摘要：
背景：创伤性脑损伤（TBI）是指机械或钝器通过外伤对脑组织的损伤。TBI通常与认知能力受损有关，比如记忆中的困难，学习,注意,和其他更高级的大脑功能，通常在受伤后保持数年。锂是一种元素轻金属，由于其高的固有反应性，只能以盐的形式使用。这篇综述讨论了锂在TBI中的分子机制以及治疗和神经保护作用。
方法：“布尔逻辑”用于在PubMed和PubMedCentral中搜索有关主题的文章，以及谷歌学者。
结果：锂的治疗作用极其复杂，涉及对基因分泌的多种影响，神经递质或受体介导的信号，信号转导过程，昼夜节律调制,以及离子传输。锂能够使神经元回路中的多种短期和长期修饰正常化，最终导致TBI激活的皮质兴奋和抑制的差异。此外，海马体内的锂含量更加明显,丘脑,新皮层,嗅觉灯泡,治疗TBI后的杏仁核和小脑灰质。
结论：锂可以减轻神经炎症和神经元毒性，并保护大脑免受水肿的影响，海马神经变性,半球组织的损失，增强记忆以及TBI后的空间学习。
方法：“布尔逻辑”用于在PubMed和PubMedCentral中搜索有关主题的文章，以及谷歌学者。
结果：锂的治疗作用极其复杂，涉及对基因分泌的多种影响，神经递质或受体介导的信号，信号转导过程，昼夜节律调制,以及离子传输。锂能够使神经元回路中的多种短期和长期修饰正常化，最终导致TBI激活的皮质兴奋和抑制的差异。此外，海马体内的锂含量更加明显,丘脑,新皮层,嗅觉灯泡,治疗TBI后的杏仁核和小脑灰质。
结论：锂可以减轻神经炎症和神经元毒性，并保护大脑免受水肿的影响，海马神经变性,半球组织的损失，增强记忆以及TBI后的空间学习。
