G蛋白介导的信号传递在阿尔采末病中的功能变化

阿尔采末病 (AD)是一种神经退行性疾病 ,病理特点主要有 β 淀粉样蛋白的沉积和神经纤维缠结的形成。一直以为AD脑中神经元功能受损与突触后受体变化无关 ,但近来越来越多的证据表明中枢神经递质受体 /G蛋白介导的腺苷酸环化酶和磷酯酰肌醇水解信号转导途径在AD病程中均受到不同程度的损害 ,这亦解释了神经递质替代疗法在治疗AD中疗效有限的原因 ,同时为进一步研究和开发防治AD新药提供新思路

Attenuation of G-protein modulation signal transduction in Alzheimers disease

Alzheimers disease is a progressive neurodegeneration disorder that is characterised by the accumulation of β amyloid deposits and neurofibrillary tangles. It has been long assumed that the disrupted interneuronal communication that occurs in AD brain does not involve widespread changes in postsynaptic receptor function. However, recent evidence suggests that both the neurotransmitter receptor/G protein modulated adenyl cyclase and the phosphatidylinositol hydrolysis signal transduction cascades are disrupted in AD. Such disruption in AD may provide a reason for the relative lack of success of neurotransmitter replacement therapies for the disorder. Moreover it can direct drug research and development for AD treatment.