Search for a transmissible agent in Alzheimer's disease: studies of human buffy coat.
Search for a transmissible agent in Alzheimer's disease: studies of human buffy coat.
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寻找阿尔茨海默病的传播因子：人类血沉棕黄层的研究。
DOI：
10.1007/978-3-642-76540-7_16
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发表时间：
1991
影响因子：
--
通讯作者：
Manuelidis,L
中科院分区：
文献类型：
--
作者：
Manuelidis,EE;Manuelidis,L
阿尔茨海默病（AD）的病因是完全未知的，尽管近年来在一些实验室的积极努力，以解决这个谜。在描述AD的一种或多种潜在病因方面缺乏成功可能是由于没有直接源自该疾病的动物模型。此外，几乎所有AD的调查研究都集中在疾病的终末期，其中完全发展的病变是明显的。在寻找AD的潜在病因时，这些完全发展的病例可能代表疾病谱的错误一端，并且相对于原始激发事件而言信息不多（EE EQUELIDIS 1985）。在AD患者的尸检大脑中，有明确的证据表明存在神经元墓地，在选定的大脑区域存在神经元破坏和神经胶质增生。缠结和更广泛的斑块和淀粉样沉积物是与终末期神经元变性相关的剩余骨架和灌木丛。我们推测，这些非常重要的主要病变是AD的最终结果，而不是起源原因。虽然这些后遗症及其相关的生化过程可能在AD的进展中发挥作用，但最初的诱发事件尚不清楚。在不低估我们的同事对这些病变的生物化学和组织学产生的数据的价值的情况下，我们集中精力，正确或错误地，在疾病的早期阶段，一个传染性因子可能是AD的基础。在这样的早期阶段，人类可能会有轻微或无法识别的神经系统症状。如果我们证明成功地证明了一种传染性因子，我们的发现不一定与我们的同事的结果相冲突，他们有不同的工作假设。在考虑传播因子作为AD病因之一的可能性时，我们对克雅氏病（CJD）的研究极大地影响了我们，CJD是一种罕见的病毒性痴呆（EE Escherelidis et al. 1976; 1978 a; EE Escherelidis and L. L.C. Elidis 1989; L. Escherichielidis和EE Escherichielidis 1986，1989）。尽管感染因子的性质存在争议，但CJD的感染性与核酸共同纯化，并显示出与病毒结构最一致的物理性质（AKOWITZ等，1990; MURDOCH等，1990; SKLAVIADIS等，1989，1990）。我们认为，事件发生的过程中，
The etiology of Alzheimer's disease (AD) is totally unknown, despite the vigorous efforts in several laboratories during recent years to solve this mystery. The lack of success in delineating one or more underlying etiologies for AD may be due to the fact that there are no animal models directly derived from this disease. Further, almost all investigative studies of AD concentrate on end stages of disease where fully developed lesions are apparent. In searching for potential etiologies of AD, such fully developed cases might represent the wrong end of the disease spectrum and be relatively uninformative with respect to original inciting events (EE MANUELIDIS 1985). In autopsy brains of individuals with AD, there is clear evidence of a neuronal cemetery, with neuronal devastation and gliosis in selected brain regions. Tangles and more widespread plaques and amyloid deposits are the remaining skeletons and bushes associated with end stage neuronal degeneration. We have postulated that these very important cardinal lesions are the end result rather than the originating causes of AD. Although these sequelae and their associated biochemical processes may playa role in the progression of AD, the initial inciting events are not known. Without underestimating the value of the data generated by our colleagues on the biochemistry and histology of these lesions, we concentrate, rightly or wrongly, on the concept that a transmissible agent may underlie AD during very early stages of disease. At such early stages, humans may have mild or unrecognized neurological symptoms. Should we prove successful in demonstrating a transmissible agent, our findings would not necessarily be in conflict with the results of our colleagues who have different working hypotheses. In considering of the possibility of a transmissible agent as one etiology of AD, we were greatly influenced by our investigations with Creutzfeldt-Jakob Disease (CJD), a rare dementia of viral etiology (EE MANUELIDIS et al. 1976; 1978a; EE MANUELID1S and L. MANUELIDIS 1989; L. MANUELIDIS and EE MANUELIDIS 1986, 1989). Although the nature of the infectious agent is controversial, infectivity in CJD copurifies with nucleic acid and displays physical properties that are most consistent with a viral structure (AKOWITZ et al. 1990; MURDOCH et al. 1990; SKLAVIADIS et al. 1989, 1990). We felt that events set in motion during the