Institute for Systems Biology, Seattle, WA, USA.
Department of Medicine, University of Washington, Seattle, WA, USA.
Mol Psychiatry. 2021 Oct;26(10):5476-5480. doi: 10.1038/s41380-021-01138-6. Epub 2021 May 10.
The hypothesis that infectious agents, particularly herpesviruses, contribute to Alzheimer's disease (AD) pathogenesis has been investigated for decades but has long engendered controversy. In the past 3 years, several studies in mouse models, human tissue models, and population cohorts have reignited interest in this hypothesis. Collectively, these studies suggest that many of the hallmarks of AD, like amyloid beta production and neuroinflammation, can arise as a protective response to acute infection that becomes maladaptive in the case of chronic infection. We place this work in its historical context and explore its etiological implications.
几十年来，人们一直在研究感染因子，特别是疱疹病毒，是否会导致阿尔茨海默病（AD）的发病机制，但这一假说一直存在争议。在过去的 3 年中，一些在小鼠模型、人类组织模型和人群队列中的研究重新激发了人们对这一假说的兴趣。这些研究表明，AD 的许多特征，如淀粉样β的产生和神经炎症，可以作为对急性感染的一种保护反应出现，但在慢性感染的情况下会变得适应不良。我们将这项工作置于其历史背景下，并探讨其病因学意义。
