The effects of additional pathology on the cognitive deficit in Alzheimer disease
The effects of additional pathology on the cognitive deficit in Alzheimer disease
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DOI：
10.1097/00005072-199702000-00007
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发表时间：
1997-02-01
影响因子：
3.2
通讯作者：
Smith, AD
中科院分区：
文献类型：
--
作者：
Nagy, Z;Esiri, MM;Smith, AD
根据目前的标准，阿尔茨海默病（AD）的诊断是一个结合临床和病理学的练习。当患者患有多种疾病时，AD与其他类型痴呆的临床区分可能会变得复杂。特别是伴随存在的其他神经系统疾病可能会显着影响认知缺陷的严重程度。在这项研究中，我们分析了血管和其他神经退行性病变对88名前瞻性评估的老年受试者的认知缺陷的影响程度。我们发现，对于任何给定水平的认知缺陷，无论是所有斑块或神经炎斑块单独在新皮层的密度显着低于AD与其他CNS病理混合的情况下，比AD与其他CNS病理的情况下。在AD合并脑血管病中，总斑块密度对认知功能障碍有显著影响，而神经纤维缠结（NFT）密度对认知功能障碍无显著影响。相比之下，在纯AD缠结密度是认知缺陷的主要决定因素。我们的研究结果提请注意共存的大脑病理学对AD患者痴呆临床表现的影响。这些发现表明AD的病理诊断标准应考虑到痴呆受试者的其他病理。它们还提高了对AD的淀粉样成分在促成临床痴呆中起决定性作用的情况的理解。
The diagnosis of Alzheimer disease (AD) according to current criteria is a combined clinical and pathological exercise. The clinical discrimination of AD from other types of dementia may be complicated when the patient suffers from more than one disease. Tn particular the concomitant presence of other neurological conditions may significantly influence the severity of cognitive deficit. In this study we analyze the extent of the influence of vascular and other neurodegenerative pathology on the cognitive deficit in a consecutive series of 88 prospectively assessed elderly subjects. We find that, for any given level of cognitive deficit, the densities of either all plaques or neuritic plaques alone in the neocortex are significantly lower in cases of AD mixed with other CNS pathology than in cases of AD with no other CNS pathology. In AD combined with cerebrovascular disease, the total plaque density makes a significant contribution to cognitive deficit, while neurofibrillary tangle (NFT) densities do not. In contrast, in pure AD tangle density is the major determinant of cognitive deficit. Our findings draw attention to the influence of coexisting brain pathologies on the clinical manifestation of dementia in subjects with AD. These findings indicate that pathological diagnostic criteria for AD should take into account such additional pathology in demented subjects. They also improve understanding of the circumstances in which the amyloid component of AD can play a decisive role in precipitating clinical dementia.