Leissring M A, Sugarman M C, LaFerla F M
Department of Psychobiology, University of California, Irvine, USA.
Drugs Aging. 1998 Sep;13(3):193-8. doi: 10.2165/00002512-199813030-00002.
Interest in the possible role of herpes simplex virus type 1 (HSV1) as a cofactor in the pathogenesis of Alzheimer's disease (AD) has re-emerged following the detection of viral DNA sequences in the central nervous system (CNS). Evidence from 2 independent laboratories indicates that HSV1 may interact with a host-specific factor, the apolipoprotein E epsilon 4 allele, to further augment the risk for AD. In this review, we consider the arguments implicating HSV1 in the pathogenesis of AD. Although further studies are required to confirm a role for HSV1 in AD and to elucidate its underlying molecular basis, implicating a virus in the pathogenesis of this insidious disease clearly offers novel potential treatments.
在中枢神经系统(CNS)中检测到病毒DNA序列后,对1型单纯疱疹病毒(HSV1)作为阿尔茨海默病(AD)发病机制中的辅助因子的潜在作用的关注再度兴起。来自两个独立实验室的证据表明,HSV1可能与一种宿主特异性因子——载脂蛋白Eε4等位基因相互作用,从而进一步增加患AD的风险。在这篇综述中,我们考虑了将HSV1与AD发病机制相关联的论据。尽管需要进一步研究来证实HSV1在AD中的作用并阐明其潜在的分子基础,但将一种病毒与这种隐匿性疾病的发病机制联系起来显然提供了新的潜在治疗方法。