Cognitive impairment and changes of red blood cell components and serum levels of IL-6, IL-18, and L-tryptophan in methamphetamine abusers.

UNLABELLED

The deficit in cognitive function is more concerning in methamphetamine (MA) users. The cognitive deficit was suspected to be the consequence of neuroinflammation-induced neurological dysregulation. In addition, activating the key enzyme in the tryptophan metabolic pathway by pro-inflammatory cytokines results in metabolite toxicity, further generating cognitive impairments. However, the evidence for the role of neuroinflammation and tryptophan metabolites involved in MA-induced cognitive deficit needs more conclusive study.

OBJECTIVES

This retrospective study aimed to determine blood-inflammatory markers, tryptophan metabolite-related molecules, and cognitive function in MA abusers compared to healthy control (HC) participants.

METHODS

The cognitive functions were evaluated using Stroop, Go/No-Go, One Back Task (OBT), and Wisconsin Card Sorting Test-64 (WCST-64). Blood samples were analyzed for complete blood count (CBC) analysis, serum inflammatory cytokines interleukin (IL)-6 and IL-18 and tryptophan metabolites.

RESULTS

MA group exhibited poor cognitive performance in selective attention, inhibition, working memory, cognitive flexibility, concept formation and processing speed compared to HC. Reduction in red blood cell (RBC) components but induction in white blood cells (WBCs) and IL-6 were observed in MA abusers, which might indicate anemia of (systemic chronic low-grade) inflammation. In addition, the depletion of precursor in the tryptophan metabolic pathway, L-tryptophan was also observed in MA users, which might represent induction in tryptophan metabolites.

CONCLUSION

These findings emphasize that blood biomarkers might be a surrogate marker to predict the role of neuroinflammation and abnormal tryptophan metabolite in MA-induced cognitive impairments.