Transmission of Cerebral β-Amyloidosis Among Individuals

Transmission of Cerebral β-Amyloidosis Among Individuals
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DOI:
10.1007/s11064-022-03566-4
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发表时间:
2022-03-11
影响因子:
4.4
通讯作者:
Yamada, Masahito
Yamada, Masahito
中科院分区:
医学3区
文献类型:
--
作者:
Hamaguchi, Tsuyoshi;Ono, Kenjiro;Yamada, Masahito

文献摘要

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淀粉样β蛋白(Aβ)在大脑中的沉积(脑β淀粉样变性)是阿尔茨海默病(AD)的一个标志。到目前为止,越来越多的实验研究利用AD小鼠模型,认为大脑β-淀粉样变性可以通过类Pron机制在个体之间传播。此外,几项使用医源性CreutzFeldt-Jakob病(CJD)尸检患者的病理学研究表明,除了CJD的病理外,大脑β-淀粉样变性还可以通过医疗程序在人类之间传播,例如来自身体注射的人生长激素和身体硬脑膜移植。此外,尽管脑淀粉样脑血管病(CAA),即脑血管中的Aβ沉积,在年轻人中很少发生相关性脑出血,但已有一些55岁以下的CAA相关性脑出血患者的报告,他们在儿童早期曾接受或不接受硬脑膜移植的神经外科手术。这些患者可能表明,在人类脑β淀粉样变性的传播过程中,Aβ病理通常被认为是Aβ-CAA,而不是实质性的Aβ沉积,我们提出了一个新的概念,即获得性CAA。考虑到已有多名获得性CAA患者的神经外科潜伏期和CAA相关脑出血起病时间超过40年,未来病例数量可能会增加,需要进行详细的流行病学调查。有必要继续阐明获得性CAA的发病机制,迫切需要建立一种预防脑淀粉样变性在个体之间传播的方法。
Deposition of amyloid beta protein (A beta) in the brain (cerebral beta-amyloidosis) is a hallmark of Alzheimer's disease (AD). So far, there have been increasing number of experimental studies using AD mouse model that cerebral beta-amyloidosis could be transmitted among individuals as prion-like mechanism. Furthermore, several pathological studies using autopsied patients with iatrogenic Creutzfeldt-Jakob disease (CJD) showed that cerebral beta-amyloidosis in addition to the CJD pathology could be transmitted among humans via medical procedures, such as human growth hormone derived from cadaver injection and cadaveric dura mater graft. In addition, although cerebral amyloid angiopathy (CAA), which is A beta deposition in the cerebral vessels, related cerebral hemorrhage rarely develops in young people, several patients with CAA-related cerebral hemorrhage under the age of 55 with histories of neurosurgeries with and without dura mater graft in early childhood have been reported. These patients might show that A beta pathology is often recognized as A beta-CAA rather than parenchymal A beta deposition in the transmission of cerebral beta-amyloidosis in humans, and we proposed an emerging concept, "acquired CAA". Considering that there have been several patients with acquired CAA with an incubation period from neurosurgery and the onset of CAA related cerebral hemorrhage of longer than 40 years, the number of cases is likely to increase in the future, and detailed epidemiological investigation is required. It is necessary to continue to elucidate the pathomechanisms of acquired CAA and urgently establish a method for preventing the transmission of cerebral beta-amyloidosis among individuals.