![]() On top of that, these cytokines also lead to clotting of blood platelets - which store serotonin - further reducing the amount of serotonin in circulation. "If there's less tryptophan, there's less serotonin production ," says Thaiss. Except, this inflammatory response in the gut actually impaired the absorption of tryptophan. The amino acid tryptophan is critical to this task - it's a precursor to serotonin and gets absorbed in the gastrointestinal tract from the food we eat. The gut produces 90% of serotonin in the body. This led to further experiments focused on a cytokine, called type 1 interferon, revealing that this signaling protein was driving inflammation and interfering with serotonin levels in the bloodstream in several ways. ![]() Those experiments revealed that a chronic viral infection (they used lymphocytic choriomeningitis virus as a stand-in for SARS-CoV-2) also led to reductions in serotonin and that the body's own immune response seemed to be the culprit. "In about 30% of patients, we could find viral RNA in their gastrointestinal tract, so we took this and tried to model it in mice," says Levy, an assistant professor of microbiology at the University of Pennsylvania. Maayan Levy, a senior author, says they looked for evidence of viral persistence by checking the stool of their long COVID subjects for genetic material from the virus. Multiple studies show that well after the initial illness passes, some long COVID patients may have a lingering infection in certain parts of the body, sometimes called a "viral reservoir," which could be driving some of their symptoms. Their hunch was that "viral persistence" - a major suspect in long COVID - could underlie the depletion of serotonin. With serotonin on their minds, the researchers tried to start from the very beginning of the disease process, primarily using experiments on mice to trace its course. So what exactly did they find? Tracing the cause of brain fog "Everyone who's engaged in this research should now be thinking about this serotonin pathway," says Iwasaki. Given that much of the work was done on mice, the implications for long COVID patients still need to be fully explored in future studies, but the results tell a "very nice linear story," says Akiko Iwasaki, an immunologist at Yale University. "I think they did a beautiful job showing the causality of these changes. Michelle Monje, a professor of neurology at Stanford University. The study weaves together several prominent lines of evidence on the potential drivers of the condition - the ongoing presence of viral material, blood clotting and chronic inflammation - and offers up possible targets for clinical trials that can test treatments in humans. ![]() The work has made an impression on those studying long COVID, a condition that still has no validated treatment or widely accepted biomarker that doctors can use to diagnose the condition. "Basically, we can explain some of the neurocognitive manifestations of long COVID through this pathway that leads to serotonin reduction," says Christoph Thaiss, a senior author on the study and an assistant professor of microbiology at the University of Pennsylvania. Their findings, published in the journal Cell, point to an intriguing hypothesis that winds its way from the gut up through the vagus nerve and ultimately into the brain.
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