ArticleAmerican journal of neurodegenerative disease2023
Cognitive impairment and changes of red blood cell components and serum levels of IL-6, IL-18, and L-tryptophan in methamphetamine abusers.
Article in American journal of neurodegenerative disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Differential alterations in peripheral tryptophan pathways in methamphetamine versus MDMA users are linked to their contrasting psychiatric symptoms.Translational psychiatry · 2026Article
- Measurement of Impulsivity and Its Role in Drug Use Behaviours and Related Health, Harm and Treatment Outcomes Among People Who Use Illicit Drugs-A Scoping Review.International journal of mental health and addiction · 2026Article
- The impact of endurance training on reducing inflammatory markers in the cardiac tissue of methamphetamine-exposed rats.PloS one · 2026Article
- Methamphetamine produces behavioral flexibility deficits that are attenuated by COX-2 inhibition in both male and female rats.Addiction neuroscience · 2025Article
- The Role and Mechanism of TRIM13 Regulation of TRAF6 Ubiquitination in the Synergy of Inflammatory Responses and Neurotoxicity Induced by METH and HIV- 1 Tat Protein in Astrocytes.Neurotoxicity research · 2025Article
- Characterization of serum and brain cytokine levels following prolonged binge-like methamphetamine self-administration and cued methamphetamine seeking.Journal of neuroimmunology · 2025Article
- Impact of Substance Use Disorder on Tryptophan Metabolism Through the Kynurenine Pathway: A Narrative Review.Metabolites · 2024Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
objectivesThis retrospective study aimed to determine blood-inflammatory markers, tryptophan metabolite-related molecules, and cognitive function in MA abusers compared to healthy control (HC) participants.
methodsThe 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.
resultsMA 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.
conclusionThese 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.
Indexed as
Identifiers
36937109PMC10018000W4327900143What OpenQuestion holds
Registered trials
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