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从神经原纤维缠结和老年斑的纤维性病变中厘清阿尔茨海默病。

Untangling Alzheimer's disease from fibrous lesions of neurofibrillary tangles and senile plaques.

作者信息

Mori H

机构信息

Department of Neuroscience, Osaka City University Medical School, Osaka, Japan.

出版信息

Neuropathology. 2000 Sep;20 Suppl:S55-60. doi: 10.1046/j.1440-1789.2000.00317.x.

Abstract

Neuropathological evidence suggests that the two fibril lesions of neurofibrillary tangles (NFT) and senile plaques are the major findings in brain tissue of Alzheimer's disease (AD) and that their occurrence is strongly associated with the symptoms of dementia. Genetic findings have indicated that the pathological molecules from the lesions function as causal agents. There is little evidence, however, to directly indicate that fibril lesions themselves kill neuronal cells in vivo. In spite of such limitations it is important to consider the molecular events involved in AD etiology. In this review of the contribution of Japanese neuropathologists to studies of AD, I will introduce briefly their work and highlight some current topics for consideration on the etiology of AD, and the basis of cell death, and will offer my perspective on outstanding conflicting issues.

摘要

神经病理学证据表明,神经原纤维缠结(NFT)和老年斑这两种纤维状病变是阿尔茨海默病(AD)脑组织中的主要发现,且它们的出现与痴呆症状密切相关。遗传学研究结果表明,这些病变中的病理分子起着致病作用。然而,几乎没有证据直接表明纤维状病变本身在体内会杀死神经元细胞。尽管存在这些局限性,但考虑AD病因中涉及的分子事件仍然很重要。在这篇关于日本神经病理学家对AD研究贡献的综述中,我将简要介绍他们的工作,重点阐述一些当前关于AD病因、细胞死亡基础的研究课题,并就一些突出的争议问题发表我的看法。

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