No objective evidence of neuropsychological deficits in people with subjective cognitive changes following COVID-19 infection

Abstract/SummaryO_ST_ABSBackgroundC_ST_ABSAmong those who develop Long COVID, many experience persistent cognitive "brain fog." The degree to which these subjective complaints reflect measurable neuropsychological deficits remains unclear. Prior work suggests that subjective cognitive impairment may be more closely associated with affective symptoms than objective performance. This study examines the relationship between subjective and objective cognitive function in adults with post-COVID cognitive complaints, and assesses the association between self-reported deficits and biological markers of dementia risk and inflammation. MethodsEighty-six adults with prior COVID-19 infection (mean age 41.5 years) completed neuropsychological testing (MATRICS; CVLT-III) and self-report measures of depression and anxiety (Beck Inventories). Participants were classified as Cases (n=47) if they endorsed worsening memory or concentration since infection or Controls (n=38) if they did not. Objective cognitive impairment was defined as performance <1 SD below normative means on at least one test. APOE-{varepsilon}4 status and soluble CD14 (sCD14) levels were assessed. ResultsCases reported higher depression and anxiety symptoms than Controls (both p<0.001), but groups did not differ on objective cognitive performance (p=0.39). Cases were more likely to be APOE-{varepsilon}4 carriers (p=0.01) and had higher sCD14 levels (p=0.01). Neither marker was associated with objective performance. ConclusionsSubjective cognitive complaints following COVID-19 were not accompanied by measurable neuropsychological deficits but were linked to elevated affective symptoms and biological risk markers. Findings highlight a dissociation between perceived and objective cognition and suggest that inflammatory, genetic, and affective factors may shape self-perceived decline. Longitudinal studies are needed to determine whether these markers confer vulnerability to cognitive decline.