Risk factors contributing to dementia are multifactorial. Accumulating evidence suggests a role for pathogens as risk factors, but data is largely correlative with few causal relationships. Here, we demonstrate that intermittent murine cytomegalovirus (MCMV) infection of mice, alters blood brain barrier (BBB) permeability and metabolic pathways. Increased basal mitochondrial function is observed in brain microvessels cells (BMV) exposed to intermittent MCMV infection and is accompanied by elevated levels of superoxide. Further, mice score lower in cognitive assays compared to age-matched controls who were never administered MCMV. Our data show that repeated systemic infection with MCMV, increases markers of neuroinflammation, alters mitochondrial function, increases markers of oxidative stress and impacts cognition. Together, this suggests that viral burden may be a risk factor for dementia. These observations provide possible mechanistic insights through which pathogens may contribute to the progression or exacerbation of dementia.

导致痴呆症的危险因素是多因素的。越来越多的证据表明病原体作为危险因素的作用，但数据在很大程度上与因果关系相关。在这里，我们证明小鼠的间歇性鼠巨细胞病毒（MCMV）感染会改变血脑屏障（BBB）的通透性和代谢途径。在暴露于间歇性 MCMV 感染的脑微血管细胞 (BMV) 中观察到基础线粒体功能增加，并伴有超氧化物水平升高。此外，与从未接受过 MCMV 的年龄匹配的对照组相比，小鼠在认知测试中的得分较低。我们的数据表明，MCMV 的反复全身感染会增加神经炎症标志物、改变线粒体功能、增加氧化应激标志物并影响认知。总之，这表明病毒负荷可能是痴呆症的危险因素。这些观察结果提供了可能的机制见解，病原体可能通过这些机制促进痴呆症的进展或恶化。