The viral hypothesis: how herpesviruses may contribute to Alzheimer's disease.

The viral hypothesis: how herpesviruses may contribute to Alzheimer's disease.
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DOI:
10.1038/s41380-021-01138-6
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发表时间:
2021-10
影响因子:
11
通讯作者:
Funk CC
Funk CC
中科院分区:
医学1区
文献类型:
--
作者:
Wainberg M;Luquez T;Koelle DM;Readhead B;Johnston C;Darvas M;Funk CC

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感染因子,特别是疱疹病毒,有助于阿尔茨海默病(AD)的发病机制的假设已经研究了几十年,但长期以来一直存在争议。在过去的3年中,在小鼠模型、人体组织模型和人群队列中的几项研究重新点燃了人们对这一假设的兴趣。总的来说,这些研究表明,AD的许多特征,如淀粉样蛋白β产生和神经炎症,可以作为对急性感染的保护性反应而出现,在慢性感染的情况下变得适应不良。我们把这项工作在其历史背景下,并探讨其病因学的影响。
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.
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