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A recent study from scientists at the University of Colorado Boulder reveals that proteins remaining in the body after COVID-19 infection can significantly impact cortisol levels in the brain, triggering inflammation in the nervous system and heightening immune cell reactions to future stressors. Published in the journal Brain Behavior and Immunity, the research provides valuable insights into the neurological symptoms associated with Long COVID, a complex syndrome affecting an estimated 35% of individuals who have contracted the virus.
This findings come at a time when COVID-19 cases are resurging globally, with reports of increased infections in 84 countries and notable cases among athletes participating in the Paris Olympics.
Lead researcher Matthew Frank, PhD, a senior research associate in the Department of Psychology and Neuroscience at CU Boulder, noted, “Our study suggests that reduced cortisol could be a critical factor influencing the various physiological changes experienced by those suffering from Long COVID.”
Prior investigations have established that SARS-CoV-2 antigens — protein byproducts released by the virus — can persist in the bloodstream of Long COVID patients for up to a year post-infection, and these proteins have also been identified in the brains of deceased COVID patients.
To delve into the effects of these antigens on the central nervous system, the research team administered an antigen known as S1, a component of the virus’s spike protein, into the spinal fluid of rats. They then conducted comparisons with a control group.
Notably, after a period of seven days, rats injected with S1 exhibited a 31% drop in levels of corticosterone — a hormone similar to cortisol — within the hippocampus, a vital brain region linked to memory and cognitive function. By day nine, this reduction increased to 37%.
“For rats, nine days is a significant duration,” Frank pointed out, considering their average lifespan of two to three years.
Cortisol plays an essential role in regulating inflammation, energy metabolism, blood pressure, and the sleep-wake cycle, while also mitigating the immune response against infections. Previous studies have indicated that individuals suffering from Long COVID, as well as those with chronic fatigue syndrome, often display lower cortisol levels.
Frank remarked, “The diminished presence of cortisol could lead to a cascade of detrimental effects due to its numerous protective roles.”
In a subsequent experiment, the researchers subjected various groups of rats to an immune stressor, specifically a weakened bacterial strain, monitoring their physiological responses including heart rate, temperature, behavior, and the activity of glial cells in the brain.
The results demonstrated that rats previously exposed to the S1 antigen exhibited heightened reactions to the stressor, evident in more substantial alterations in eating, drinking, behavior, as well as elevated core body temperatures and heart rates, alongside increased neuroinflammation and glial cell activation.
“This is the first time we have shown that antigens left behind by COVID can modify the immune response in the brain to the extent that it becomes overly sensitive to later stressors or infections,” Frank explained.
While the study was conducted on animal subjects, Frank emphasizes the need for further research to elucidate the potential implications of low cortisol levels on Long COVID symptoms in humans.
He hypothesizes a potential sequence of events: COVID-19 antigens may lower cortisol levels, disrupting the brain’s ability to manage inflammatory responses effectively. When faced with subsequent stressors — be they minor infections, work-related stress, or physical exertion — the immune response may become severely exaggerated, reintroducing intense symptoms such as fatigue, depression, cognitive impairment, and sleep disturbances.
Frank expressed skepticism regarding the use of cortisol treatments alone as a solution for Long COVID, noting that such approaches may not address the underlying issues and could lead to adverse side effects. He advocates for strategies aimed at identifying and minimizing various stressors as a means to alleviate symptoms.
Additionally, Frank suggests that investigating the origins of persisting antigens, including potential viral reservoirs within the body, could warrant further exploration as a viable avenue for treatment.
The research received funding from the PolyBio Research Foundation, and ongoing studies are expected to advance understanding in this area.
“Many individuals continue to suffer from this challenging condition. Our findings bring us closer to deciphering the neurobiological mechanisms at play and highlight cortisol’s potential involvement,” Frank concluded.
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