Summary: Suffering from frequent colds and flu can affect brain aging, accelerate cognitive decline, and may increase the risk of developing Alzheimer’s disease. In mice, intermittent experiences of mild inflammation, such as that caused by the flu or the common cold, caused cognitive impairment and disruption of neural communication.
Source: Tulane University
Frequent illness can affect how quickly the brain ages and increase the risk of dementia or other forms of cognitive decline.
These are the findings of a Tulane University study conducted in collaboration with West Virginia University and the National Institutes 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 mild inflammation, such as those caused by the flu or seasonal head colds, caused impaired aging. understanding and disruption of communication between neurons in mice.
“We were interested in asking whether differences in infection experience could account, at least in part, for the differences in dementia rates we see in the population,” said lead author Elizabeth Engler- Chiurazzi, PhD, a behavioral neuroscientist in the Tulane Department of Neurosurgery.
“The mice we studied were adults approaching middle age with intact abilities, but when exposed to intermittent inflammation, they remembered less and their neurons functioned more weaker.”
This study is the first to model repeated, intermittent infections in mice and examine the long-term consequences for brain function and health.
Humans often experience infections and inflammation at a higher rate than laboratory rats. But because impairments were observed in mice after only five repeated inflammatory treatments, cognitive change in humans may be more robust.
![It shows an old woman taking her temperature](https://neurosciencenews.com/files/2023/04/cold-dementia-neurosicnes-public.jpg)
“Our mice only experienced repeated inflammation-like pain a few times, so the fact that we observed impairments was surprising,” says Engler-Chiurazzi.
“The effects are subtle, but that’s why I find these results significant: In one person, cognitive impairments from a similar number of traumatic experiences may not be noticeable in their daily lives but may have cumulative effects that negatively affect the aging brain.”
The findings may have important implications for the standard of care in how infections are managed in the elderly and those at risk for dementia. And they are perhaps even more relevant because of the COVID-19 pandemic and ongoing research into the effects of long-COVID syndrome.
Going forward, Engler-Chiurazzi said more work needs to be done to understand why infections affect the brain and how to mitigate 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.
“The biggest takeaway from this research, in our opinion, is the importance of staying as healthy and infection-free as possible,” he said.
About this Alzheimer’s disease research news
Author: Andrew Yawn
Source: Tulane University
Contact: Andrew Yawn – Tulane University
Image: The image is in the public domain
Original Research: Open access.
“Repeated systemic exposure to lipopolysaccharide-induced inflammation disrupts hippocampal long-term potentiation and impairs cognition in aging male rats.” by Elizabeth Engler-Chiurazzi et al. Brain, Behavior, and Immunity
Abstract
Repeated systemic exposure to lipopolysaccharide-induced inflammation disrupts hippocampal long-term potentiation and impairs cognition in aging male rats
Age-related cognitive decline, a common part of the brain aging process, is associated with significant impairment in daily functioning and quality of life in geriatric adults.
While the complexity of the mechanisms underlying cognitive aging is still being elucidated, microbial exposure and the multifactorial inflammatory cascades associated with systemic infections are emerging as potential drivers of neurological senescence.
The negative cognitive and neurobiological consequences of a single pathogen-associated inflammatory experience, as modeled by treatment with lipopolysaccharide (LPS), are well documented. However, the effects on brain aging of repeated, intermittent inflammatory challenges are less studied.
To extend the emerging literature assessing the impact of infection burden on cognitive function in normal aging mice, here, we repeatedly exposed adult mice to intermittent that is challenged by LPS during aging. Male 10-month-old C57BL6 mice were systemically administered escalating doses of LPS once every two weeks for 2.5 months.
We examined cognitive consequences using a non-spatial step-through avoidance task, and both spatial working and reference memory versions of the Morris water maze. We also examined several potential mechanisms, including cortical and hippocampal cytokine/chemokine gene expression, as well as hippocampal neuronal function through extracellular field potential recordings.
Although there is limited evidence for a persistent inflammatory state in the cortex and hippocampus, we observed impaired learning and memory and a disruption of hippocampal long-term potentiation. These data suggest that a history of intermittent exposure to LPS-induced inflammation is associated with mild but significant cognitive impairment in normal aging mice.
The broader implications of these findings may have important implications for standards of care involving infections in aging individuals or populations at risk for dementia.