People who experience symptoms such as brain fog, fatigue or memory loss after overcoming coronavirus infection, a condition known as long or long COVID, may have low levels of serotonin, a neurotransmitter involved in the control of emotions. and it is related to the state of mind, and perhaps that is why it has been called the happiness hormone.
That is the conclusion reached by a new study led by researchers at the Perelman School of Medicine at the University of Pennsylvania that has been published in the journal Cell and that could help understand how persistent inflammation after contracting the SARS-CoV-2 virus CoV-2 can cause long-term neurological symptoms.
Most patients with persistent COVID report general fatigue and neurological problems such as brain fog, difficulties concentrating, memory failures and headaches. The causes of long COVID have not been studied in depth and effective treatments to combat it are also lacking.
“Our findings provide biomarkers that can help doctors diagnose patients with long COVID and measure their response to individual treatments”
“Many aspects of the basic biology underlying long COVID have long remained unclear. As a result, we lack effective tools for diagnosing and treating the disease,” said Maayan Levy, assistant professor of Microbiology at Penn Medicine and lead author of the work. “Our findings may not only help unravel some of the mechanisms that contribute to long COVID, but also provide us with biomarkers that can help doctors diagnose patients and objectively measure their response to individual treatments.”
From acute coronavirus infection to long COVID
The researchers evaluated the effects of long COVID in blood and stool samples from various clinical studies and in small animal models, and determined that a subset of patients with long COVID had traces of the SARS-CoV-2 virus in their stool samples for up to months. after acute coronavirus infection, suggesting that virus components remain in the intestine of some patients long after infection.
They discovered that this residual virus, called the viral reservoir, triggers an immune response in which the immune system releases proteins known as interferons to fight the virus. These interferons cause inflammation that reduces the absorption of the amino acid tryptophan in the gastrointestinal tract.
Tryptophan is a fundamental element of several neurotransmitters, including serotonin, which is produced mainly in the gastrointestinal tract and is responsible for the transmission of messages between nerve cells in the brain and the rest of the body. It plays a key role in regulating memory, sleep, digestion, wound healing, and other functions that maintain homeostasis within the body.
Serotonin is also an important regulator of the vagus nerve, a system of neurons that mediates communication between the body and the brain. The researchers found that when tryptophan absorption decreases as a result of persistent viral inflammation, serotonin is depleted, leading to a disruption in vagus nerve signaling, which, in turn, can cause several of the symptoms associated with Persistent COVID, such as memory loss.
Possible targets for persistent COVID treatments
The authors studied whether replenishing tryptophan or serotonin in patients who were deficient could alleviate the symptoms of long COVID. In small animal models they demonstrated that it was possible to restore serotonin levels and reverse memory impairment through treatment with serotonin precursors or selective serotonin reuptake inhibitors (SSRIs).
“There has been some evidence to suggest that SSRIs could be effective in preventing long COVID, and our research now presents an opportunity for future studies to select specific patients for a trial based on serotonin depletion, and to be able to measure the response.” to treatment,” explained another of the authors, Dr. Benjamin Abramoff, director of the Post-COVID Evaluation and Recovery Clinic, and assistant professor of Clinical Physical Medicine.
“COVID varies from patient to patient, and we don’t fully understand what causes the differences in symptoms,” said another author, Christoph Thaiss, assistant professor of Microbiology. “Our study offers a unique opportunity to continue research to determine how many individuals with long COVID are affected by the pathway linking viral persistence, serotonin deficiency, and vagus nerve dysfunction, and discover additional targets for treatments in the different symptoms that patients experience.
