Shin Samuel S, Dixon C Edward
1 Brain Trauma Research Center, University of Pittsburgh , Pittsburgh, Pennsylvania.
2 Department of Neurological Surgery, University of Pittsburgh , Pittsburgh, Pennsylvania.
J Neurotrauma. 2015 Oct 1;32(19):1429-40. doi: 10.1089/neu.2014.3445. Epub 2015 Jun 29.
Traumatic brain injury (TBI) results in varying degrees of disability in a significant number of persons annually. The mechanisms of cognitive dysfunction after TBI have been explored in both animal models and human clinical studies for decades. Dopaminergic, serotonergic, and noradrenergic dysfunction has been described in many previous reports. In addition, cholinergic dysfunction has also been a familiar topic among TBI researchers for many years. Although pharmacological agents that modulate cholinergic neurotransmission have been used with varying degrees of success in previous studies, improving their function and maximizing cognitive recovery is an ongoing process. In this article, we review the previous findings on the biological mechanism of cholinergic dysfunction after TBI. In addition, we describe studies that use both older agents and newly developed agents as candidates for targeting cholinergic neurotransmission in future studies.
创伤性脑损伤(TBI)每年都会导致大量人员出现不同程度的残疾。数十年来,在动物模型和人类临床研究中都对TBI后认知功能障碍的机制进行了探索。先前许多报告中都描述了多巴胺能、5-羟色胺能和去甲肾上腺素能功能障碍。此外,胆碱能功能障碍多年来一直是TBI研究人员熟悉的话题。尽管在先前的研究中,调节胆碱能神经传递的药物已取得不同程度的成功,但改善其功能并最大限度地促进认知恢复仍是一个持续的过程。在本文中,我们回顾了先前关于TBI后胆碱能功能障碍生物学机制的研究结果。此外,我们还描述了在未来研究中使用旧药物和新开发药物作为靶向胆碱能神经传递候选药物的研究。