引起血管收缩和发炎的曲坦类药物可以阻止三叉神经中CGRP的释放。虽然CGRP的确促进了血管的扩张进程,但在偏头痛问题上,它对激活大脑神经所起的作用似乎才是最关键的。
In the mid-1980s, Peter Goadsby, a neurologist and headache specialist at the University of California San Francisco, and his colleagues found that CGRP is released in migraines and that triptans decreased CGRP action.
20世纪80年代中期,加州大学旧金山分校(University of California San Francisco)的神经病学家和头痛治疗专家彼得•戈德比(Peter Goadsby)和他的同事发现,CGRP在偏头痛发生时被释放出来,而曲坦类药物减少了CGRP的活动。
Several researchers and companies have been trying to develop drugs that bind to the CGRP receptors to prevent the chemical from activating the pain network. But because CGRP has a complex receptor - the slot where the molecule must bind in order to initiate actions in the body - it took chemists 15 years to figure out how to block the effects of CGRP, and even longer to develop a compound that could be taken orally, says Dr. Goadsby.
好几家研究机构和公司一直在努力研发可以作用于CGRP感应器官的药物,从而阻止这种化学物质激活疼痛网络。但是戈德比医生说,由于CGRP的感应器官非常复杂──药物分子必须作用于这种感应器官才能激发身体的行动──药物学家用了15年时间来研究如何阻止CGRP起效,而研制可以口服的药物还要更长时间。
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