阿尔茨海默病理条件下突触系统病变的研究进展

Changes in synaptic system under the pathology of Alzheimer's disease

阿尔茨海默病(Alzheimer’s disease,AD)是一种起病隐匿的进行性发展的神经系统退行性疾病,主要病理特征表现为淀粉样蛋白沉积形成的老年斑、tau蛋白过度磷酸化导致的神经纤维缠结以及神经元丢失和突触损伤。其中,淀粉样蛋白沉积和tau蛋白过度磷酸化均可导致突触和神经棘缺失,严重影响神经递质系统功能,最终造成大脑学习记忆和认知能力损伤。从突触损伤角度出发,总结AD病理条件下,突触和神经递质及其受体的变化,为后期开展生物活性物质对AD病理中神经细胞信号通路的研究提供思路和理论基础。

Alzheimer＇s disease is a common central nervous system degenerative disease which is characterized by accumulation of β-amyloid in senile plagues, hyperphosphorylated tau in neurofibrillary tangles and synaptic loss. Hyperphosphorylated tau and β-amyloid accumulation not only lead to synaptic loss but cause dysfunction of neurotransmitter system. From the perspective of synaptic damage, this review summarized the changes on synaptic junction, neurotransmitter, and its receptors under physiological and pathological conditions, which might be helpful for the further study on the effect ofbioactive substances based on neuronal signal pathway.