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机构地区:[1]New York State Institute for Basic Research in Developmental Disabilities,Staten Island,New York 10314,USA [2]华中科技大学同济医学院病理生理学系
出 处:《医学分子生物学杂志》2006年第3期163-169,共7页Journal of Medical Molecular Biology
摘 要:对老年性痴呆症发病的分子机理的研究在近20余年取得了很大进展,其中一个里程碑式的发现就是阐明了高度磷酸化的微管相关蛋白tau为组成病理性双螺旋细丝的主要蛋白成分。进一步研究显示tau的过度磷酸化在以tau异常沉积于神经元中为特征的神经原纤维退行性病变中起关键作用。由于神经原纤维退行性病变与老年性痴呆症的痴呆症状直接相关,文章综述并讨论了tau蛋白、tau过度异常磷酸化及其形成机理,并在此基础上提出了老年性痴呆症神经原纤维退行性病变的分子机理。Significant progress in research on the molecular pathogenesis of Alzheimer disease (AD) has been made in the last two decades. One of the milestone discoveries is the demonstration of hyperphosphorylated microtubule-associated protein tau to be the major protein component of paired helical filaments in AD brain. Further studies have indicated that abnormal hyperphosphorylation of tau plays a key role in Alzheimer neurofibrillary degeneration, which is characterized by the fibrillar deposition of the abnormal tau protein. Because neurofibrillary degeneration is directly related to the severity of dementia symptoms of AD patients, here we have reviewed and discussed tau protein, abnormal hyperphosphorylation of tau and its mechanisms. On the basis of the critical review, we propose a modified molecular mechanism of neurofibrillary degeneration of AD.
关 键 词:老年性痴呆症 TAU蛋白 异常过度磷酸化 神经原纤维退行性变
分 类 号:R749.16[医药卫生—神经病学与精神病学]
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