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帕金森病和阿尔茨海默病中内嗅区和等皮质的阿尔茨海默病变

Alzheimer lesions in the entorhinal region and isocortex in Parkinson's and Alzheimer's diseases.

作者信息

Jellinger K, Braak H, Braak E, Fischer P

机构信息

L. Boltzmann Institute of Clinical Neurobiology, Lainz Hospital, Vienna, Austria.

出版信息

Ann N Y Acad Sci. 1991;640:203-9. doi: 10.1111/j.1749-6632.1991.tb00218.x.

DOI:10.1111/j.1749-6632.1991.tb00218.x
PMID:1776740
Abstract

Neuropathologic examination in elderly individuals and patients with Parkinson's disease with and without dementia reveals abundant isocortical amyloid deposits with no or only a few neuritic plaques, neuropil threads (NT), and neurofibrillary tangles (NFT), whereas NT and NFT may be present only in the entorhinal region of the parahippocampal cortex. In Down's syndrome, Alzheimer's disease, and Parkinson's disease, early neuronal degeneration with deposition of NT and NFT may selectively involve layer pre-alpha (II) of the entorhinal region (Brodmann 26 area) forming the origin of the glutamatergic perforant pathway. Its bilateral destruction isolates the hippocampus from isocortical influx. Comparative studies in a series of aged subjects and those with Parkinson's disease show that psychostatus correlates better with the number of NT and NFT in the entorhinal region than in hippocampal area CA-1 and isocortex. This pattern of neuronal degeneration may explain cognitive impairment in early stages of both Alzheimer's and Parkinson's diseases.

摘要

对患有和未患痴呆症的老年人及帕金森病患者进行神经病理学检查发现,在等皮质中有大量淀粉样沉积物,而神经炎性斑块、神经毡丝(NT)和神经原纤维缠结(NFT)不存在或仅有少量,而NT和NFT可能仅存在于海马旁皮质的内嗅区。在唐氏综合征、阿尔茨海默病和帕金森病中,早期神经元变性伴NT和NFT沉积可能选择性累及内嗅区(布罗德曼26区)的前α(II)层,该层形成谷氨酸能穿通通路的起源。其双侧破坏使海马与等皮质传入信号隔离。对一系列老年受试者和帕金森病患者的比较研究表明,精神状态与内嗅区NT和NFT数量的相关性比与海马CA-1区和等皮质的相关性更好。这种神经元变性模式可能解释了阿尔茨海默病和帕金森病早期的认知障碍。

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