突触可塑性与Alzheimer's病OA
Synaptic plasticity and Alzheimer's disease
Alzheimer's 病(AD)是一种复杂的神经退行性疾病,以学习和记忆减退为特征.AD 的病理改变包括 β-淀粉样蛋白形成的老年斑沉积和异常过度磷酸化的 tau 蛋白形成的神经原纤维缠结(NFTs).AD的突触功能障碍发生在淀粉样斑块沉积和 NFTs 形成之前,并且与认知功能障碍呈正相关.本文将对突触可塑性在 AD 发病机制中的关键作用进行综述,阐明突触可塑性可能可以作为 AD 的治疗靶点,为 AD 的发病机制和干预方法研究提供新的思路.
Alzheimer's disease(AD)is a complex neurodegenerative disease characterized by impairments in learning and memory.The pathologic changes of AD include the deposition of senile plaques formed by amyloid-β protein and neurofibrillary tangles composed of excessive phosphorylation tau protein.Synaptic dysfunction in AD occurs prior to the formation of amyloid plaque deposition and neurofibrillary tangles and is positively correlated with cognitive impairment.This review will summarize the critical role of synaptic plasticity in the pathogenesis of AD,elucidating how synaptic plasticity may serve as a therapeutic target of AD,thereby providing new insights into the pathogenesis and interventions for AD.
俞希;朱晓蕾
210008 南京大学医学院附属鼓楼医院神经内科210008 南京大学医学院附属鼓楼医院神经内科
医药卫生
Alzheimer's病突触可塑性N-甲基-D-天冬氨酸受体α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体治疗靶点
Alzheimer's diseasesynaptic plasticityN-methyl-D-aspartic acid receptorα-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptorstherapeutic target
《临床神经病学杂志》 2026 (3)
227-233,7
江苏省自然科学基金面上项目(BK20231120)南京市卫生科技发展重点项目(ZKX22025)
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