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作 者:李腾飞 郭志全 王晔[1] Li Tengfei;Guo Zhiquan;Wang Ye(Department of Neurology,the First Affiliated Hospital of Harbin Medical University,Harbin 150001,China)
机构地区:[1]哈尔滨医科大学附属第一医院神经内科,150001
出 处:《神经疾病与精神卫生》2022年第12期904-908,共5页Journal of Neuroscience and Mental Health
摘 要:阿尔茨海默病(AD)临床常见进行性认知功能下降,行为异常,最终出现痴呆。神经病理可见tau蛋白神经纤维缠结、β-淀粉样蛋白(Aβ)蓄积形成老年斑,以及小胶质细胞增生和神经元、白质、突触的大量缺失。由于淀粉样蛋白病理可能早于tau蛋白病理,早于AD脑萎缩及临床症状的出现,现阐述Aβ代谢异常与AD的相关性。Alzheimer disease(AD) is characterized by clinical progressive decline in cognitive function and behavioral abnormalities, and eventually dementia. Its neuropathological features include tau protein neurofibrillary tangles, senile plaques formed by the accumulation of β-amyloid(Aβ). Other changes include reactive microglia proliferation and widespread loss of neurons, white matter, and synapses. Since amyloid pathology may precede tau protein pathology and the appearance of AD brain atrophy and clinical symptoms, the correlation between Aβ metabolic abnormalities and AD is elaborated in this paper.
关 键 词:阿尔茨海默病 淀粉样蛋白 代谢异常 淀粉样前体蛋白 综述
分 类 号:R749.16[医药卫生—神经病学与精神病学]
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