The Cold Truth: Common Colds Linked to Alzheimer’s Risk

Summary: Suffering from frequent colds and flus can impact brain aging, accelerate cognitive decline and increase the risk of developing Alzheimer’s disease. In mice, intermittent experiences of moderate inflammation, such as those caused by the flu or the common cold, caused impaired cognition and disrupted neural communication.

Source: tulane university

Getting sick often can impact how quickly the brain ages and increase the risk of dementia or other forms of cognitive decline.

These are the results of a Tulane University study conducted in partnership with West Virginia University and the National Institutes of Occupational Safety and Health and published in the journal Brain, behavior and immunity.

The study looked at aging male mice and found that repeated and intermittent experiences of mild inflammation, such as those caused by the flu or a seasonal head cold, caused impaired cognition and disrupted communication between neurons. in these mice.

“We were interested in asking whether differences in infection experience could explain, at least in part, the differences in dementia rates we observe in the population,” said lead author Elizabeth Engler-Chiurazzi, PhD, behavioral neuroscientist at the Tulane Department. of Neurosurgery.

“The mice we were studying were adults in their late fifties who had intact faculties, yet when exposed to intermittent inflammation, they remembered less and their neurons functioned worse.”

This study is the first to model repeated and intermittent infections in mice and examine the long-term consequences for brain function and health.

Humans often suffer from infections and inflammation at significantly higher rates than laboratory mice. But given that impairments were seen in mice after just five intermittent inflammatory treatments, the cognitive change in humans might be more robust.

“Our mice only experienced intermittent disease-like inflammation a handful of times, so the fact that we observed impairments was surprising,” Engler-Chiurazzi said.

“The effects were subtle, but that’s why I find these results significant: in a human, cognitive impairment from a similar number of inflammatory experiences might not be noticeable in their daily lives, but might have cumulative effects that have a negative impact on the aging brain.”

The results may have important implications for the standard of care regarding how infections are treated in the elderly and those at risk of dementia. And they are perhaps more relevant in light 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 impact the brain and how to mitigate those effects. In addition, she hopes that follow-up studies will determine whether more vulnerable populations affected by health disparities face a higher burden of neurological effects.

“The biggest benefit of this research, in our view, is the importance of staying as healthy and infection-free as possible,” she said.

About this Alzheimer’s disease research news

Author: Andrew Yawn
Source: tulane university
Contact: Andrew Yawn – Tulane University
Picture: Image is in public domain

Original research: Free access.
“Intermittent systemic exposure to lipopolysaccharide-induced inflammation disrupts long-term hippocampal potentiation and impairs cognition in aging male mice” by Elizabeth Engler-Chiurazzi et al. Brain, behavior and immunity

Abstract

Intermittent systemic exposure to lipopolysaccharide-induced inflammation disrupts long-term hippocampal potentiation and impairs cognition in aging male mice

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.

While the complexity of the mechanisms underlying cognitive aging is still being elucidated, microbial exposure and 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, such as that modeled by lipopolysaccharide (LPS) treatment, are well documented. Yet the brain aging impacts of repeated and intermittent inflammatory challenges are less well studied.

To extend the emerging literature assessing the impact of infection load on cognitive function in normally aging mice, here we repeatedly exposed adult mice to intermittent LPS challenges during the aging period. Ten-month-old male C57BL6 mice were given increasing doses of LPS systemically once every two weeks for 2.5 months.

We assessed cognitive consequences using the non-spatial inhibitory avoidance task and the spatial working and reference memory versions of the Morris water maze. We also probed several potential mechanisms, including cortical and hippocampal cytokine/chemokine gene expression, as well as hippocampal neuronal function via extracellular field potential recordings.

Although there is limited evidence of an ongoing inflammatory state 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 associated with subtle but significantly impaired cognition in normally aging mice.

The broader impact of these findings may have important implications for the standard of care involving infections in aging individuals or populations at risk of dementia.