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Abstract
COVID-19 has been associated with a wide range of systemic and neurological complications, known as long COVID or postacute sequelae of COVID-19 (PASC). Such sequelae can be observed among all infected individuals, even among those with a mild disease course. Dysbiosis, a common condition associated with low-grade inflammation, has been proposed as a potential mechanism of PASC by altering levels of circulating lipopolysaccharide (LPS) and the tryptophan pathway metabolites kynurenine and quinolinic acid, known to affect neurocognitive function. The authors evaluated the evolution of neurological, neurocognitive, and neuropsychiatric COVID-19 sequelae and their relationship with circulating LPS and kynurenine and quinolinic acid levels. A prospective, longitudinal, and analytical study was conducted. Neurological, neurocognitive, and neuropsychiatric assessments of participants who had recovered from COVID-19 and did not require hospitalization during the acute stages of the infection were performed. Peripheral levels of LPS and tryptophan metabolites were measured 1, 3, 6, and 12 months after infection. Of 95 participants recruited, 67 COVID-19-convalescent individuals and 20 COVID-19-free individuals were included. Significantly higher occurrences of asthenia, olfaction and taste alterations, headache, memory dysfunction, and systemic symptoms such as dyspnea, cough, and periodontal diseases were found among participants in the COVID-19-convalescent group compared with participants in the comparison group. A significant decrease in kynurenine levels, which correlated with cognitive impairment, was observed among PASC convalescents. Significant neurocognitive and neuropsychiatric impairments were observed among COVID-19-convalescent individuals, along with decreased kynurenine levels, which recovered during a 12-month follow-up period.
Published Version
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