Systemic cytokines related to memory function 6-9 months and 12-15 months after SARS-CoV-2 infection

Area of Science:

• Neuroscience
• Immunology
• Infectious Diseases

Background:

• Cognitive impairment, particularly affecting episodic memory, is a persistent sequela of COVID-19, lasting up to two years post-infection.
• The link between acute-phase cytokine levels and chronic cognitive deficits following SARS-CoV-2 infection remains largely unidentified in human studies.
• Understanding this relationship is crucial for predicting and potentially mitigating long-term neurological consequences of COVID-19.

Purpose of the Study:

• To investigate the association between acute-phase cytokine levels (IL-1β, IL-6, TNFα) and episodic memory performance in COVID-19 patients.
• To determine if these cytokine levels predict verbal and visuospatial episodic memory function at 6-9 and 12-15 months post-infection.

Main Methods:

• Analysis of plasma cytokine concentrations (IL-1β, IL-6, TNFα) from 33 hospitalized COVID-19 patients during the acute phase.
• Assessment of verbal and visuospatial episodic memory performance at 6-9 months and 12-15 months post-infection.
• Statistical analysis using Spearman correlations and generalized linear mixed models to evaluate associations and predictive values.

Main Results:

• Elevated interleukin-1 beta (IL-1β) levels in the acute phase were associated with reduced verbal episodic memory recall at 6-9 months post-infection.
• Interleukin-6 (IL-6) levels during acute infection predicted verbal episodic memory scores at 12-15 months post-infection.
• Tumor necrosis factor alpha (TNFα) levels did not show significant associations with episodic memory performance in the studied timeframes.

Conclusions:

• The inflammatory response during the acute phase of SARS-CoV-2 infection, specifically IL-1β and IL-6 levels, can predict long-term verbal episodic memory deficits.
• These findings underscore the potential role of early-stage inflammation in the pathogenesis of chronic cognitive impairment following COVID-19.
• Further research is warranted to explore therapeutic strategies targeting the inflammatory cascade to improve long-term cognitive outcomes in COVID-19 survivors.