Summary: Frequent colds and flus can affect brain aging, accelerate cognitive decline and increase the risk of Alzheimer’s disease. In mice, intermittent exposure to moderate inflammation, such as that caused by the flu or the common cold, impaired cognition and disrupted neural communication.
Source: Tulane University
Being sick often can affect how quickly the brain ages and increase the risk of dementia or other forms of cognitive decline.
The results of a Tulane University study conducted in partnership with West Virginia University and the National Institute of Occupational Safety and Health and published in the journal Brain, behavior and immunity.
The study examined aging male mice and found that repeated, intermittent experiences with moderate inflammation, such as those caused by the flu or seasonal head colds, led to impaired cognition and communication between neurons in those mice.
“We were interested in asking whether differences in the experience of infection could account, at least in part, for differences in dementia rates between populations,” said lead author Elizabeth Engler-Chiurazzi, PhD, a behavioral neuroscientist in the Tulane Department. Neurosurgery
“The mice we were studying reached middle age with intact faculties, and yet, when exposed to occasional inflammation, they remembered less and their neurons functioned more poorly.”
This study examines a model of repeated, intermittent infection in mice and the long-term consequences for brain function and health.
Humans often experience significantly higher rates of infection and inflammation than laboratory mice. But while impairments were observed in mice after only five intermittent inflammatory treatments, cognitive changes in humans may be even stronger.
“Our mice only experienced intermittent illness-like inflammation a few times, so the impairments we observed were surprising,” Engler-Chiurazzi said.
“The effects were subtle, but that’s why I think these results are meaningful: In a human, cognitive impairments from a similar number of inflammatory experiences may not be noticeable in their daily life but may have cumulative effects that negatively affect the aging brain.”
The findings may have important implications for standards of care around how infections are managed in adults and people at risk of dementia. And they are perhaps even more relevant in light of ongoing research around the effects of the COVID-19 pandemic and long-COVID syndrome.
Going forward, Engler-Chiurazzi said, more work is needed to understand why infections affect the brain and how to minimize those effects. In addition, he hopes that follow-up studies will investigate whether more vulnerable populations affected by health disparities face a higher burden of neurological effects.
“In our opinion, the biggest takeaway from this study is the importance of staying as healthy and infection-free as possible,” he said.
Alzheimer’s disease research news
Author: Andrew Yan
Source: Tulane University
Contact: Andrew Yan – Tulane University
Image: Image is in public domain
Original Research: Access to all.
“Intermittent systemic exposure to lipopolysaccharide-induced inflammation impairs hippocampal long-term potentiation and impairs cognition in aging male rats.” by Elizabeth Engler-Chiurazzi et al. Brain, behavior and immunity
abstract
Intermittent systemic exposure to lipopolysaccharide-induced inflammation impairs hippocampal long-term potentiation and impairs cognition in aging male rats.
Age-related cognitive decline, a common component of the brain aging process, is associated with significant impairment in daily functioning and quality of life in geriatric adults.
Although the complexities of the mechanisms underlying cognitive aging are still being elucidated, multifactorial inflammatory cascades associated with microbial exposure and systemic infections are emerging as potential drivers of neurological senescence.
The negative cognitive and neurobiological consequences of experiencing a single pathogen-associated inflammation, as modeled by treatment with lipopolysaccharide (LPS), are well documented. Yet, the brain aging effects of repeated, intermittent inflammatory challenges are less well studied.
To extend the emerging literature assessing the effects of infection burden on cognitive function in normally aged mice, here, we exposed adult mice to repeated intermittent LPS challenges during the aging period. Male 10-month-old C57BL6 mice were systemically administered increasing doses of LPS once every two weeks for 2.5 months.
We assessed cognitive outcomes using both the spatial task and reference memory versions of the non-spatial step-through inhibitory avoidance task and the Morris water maze. We also investigated several potential mechanisms, including cortical and hippocampal cytokine/chemokine gene expression, as well as hippocampal neuronal function through extracellular field potential recordings.
Although there was limited evidence for ongoing inflammatory conditions in the cortex and hippocampus, we observed impaired learning and memory and disruption of hippocampal long-term potentiation. These data suggest that a history of intermittent exposure to LPS-induced inflammation is generally associated with subtle but significantly impaired cognition in aged mice.
These findings may have important implications for broader standards of care involving transmission in aging individuals or populations at risk for dementia.
