A recent study published in the journal Cell (16/10/23) found that post-acute COVID-19 syndrome (PASC) is associated with reduced blood levels of the neurotransmitter serotonin. Viral infection and inflammation-induced interferons lower serotonin through multiple mechanisms including decreased intestinal absorption of the serotonin precursor tryptophan, reduced platelet serotonin storage due to thrombocytopenia, and increased degradation by monoamine oxidases.
Mouse models showed viral persistence drives sustained interferon responses, intestinal expression changes that reduce tryptophan uptake, and platelet activation – all contributing to serotonin deficiency. Tryptophan or serotonin precursor supplementation restored serotonin levels and improved cognition impaired by inflammation.
In humans, the degree of serotonin reduction correlated with PASC symptom severity. The study proposes peripheral serotonin deficiency dampens vagus nerve signaling to the brain, impairing cognitive function. Supporting this, stimulating vagal neurons restored hippocampal activation and memory deficits in inflammation-treated mice.
The findings suggest strategies like SSRIs, precursor supplementation, or agents blocking serotonin degradation may hold promise for alleviating neurological symptoms in PASC. The role of vagus nerve activity in relaying peripheral inflammation to the brain merits further exploration.
Overall, the study reveals interconnected mechanisms linking viral persistence to serotonin loss and cognitive dysfunction, providing biological insights and potential therapeutic avenues to explore for PASC neurological manifestations. Limitations include differences between human PASC and mouse models. More research is warranted investigating proposed pathways.
You can read the whole study here.