血管性痴呆是临床发病率排在第二位的认知障碍性疾病,以白质损伤引起的认知功能障碍和胶质细胞的激活为主要病理表现。目前临床上药物治疗疗效有限,且不能有效逆转损伤、减缓疾病的进程,因此,对新药物的研发存在迫切的需求。肌肽(β-丙氨酰-L-组氨酸)是由β-丙氨酸和L-组氨酸两种氨基酸组成的天然二肽,能够由外周进入神经中枢系统,转变成组氨酸后成为组胺,是体内组胺的天然储存库,对急性脑缺血损伤发挥保护作用。近年研究发现肌肽对血管性痴呆的保护作用不是通过肌肽-组氨酸-组胺的途径,而是通过抑制兴奋性氨基酸毒性、氧自由基的产生、胶质细胞的激活以及髓鞘的退化发挥保护作用,由此证明肌肽对于血管性痴呆有着潜在的临床治疗作用。本文针对肌肽对血管性痴呆治疗的研究进展进行综述。
Vascular dementia (VaD),which is recognized as the second most prevalent type of dementia is often observed in patients with hypertension or atherosclerosis.Its characteristic damage involves progressive demyelination,cognitive impairment and white matter rarefaction.However,pathogenetic mechanisms are far from understood,with currently no effective agents to prevent or reverse its progression.Therefore,it's necessary to develop new agents for treatment or prevention ofVaD.Carnosine (β3-alanyl-L-histidine) is a natural dipeptide that is highly expressed in the central nervous system,and can easily enter the brain from the periphery.Carnosine can converse to histidine and then histamine.Carnosine had a protective effect in VaD,which did not involve the carnosine-histidine-histamine metabolic pathway,but may be due to an inhibition of excitatory amino acid,reactive oxygen specie generation,glia activation and myelin degeneration.These data suggest that carnosine may have potential value for the therapeutic treatment in VaD.This review focuses on the role of carnosine in vascular dementia.