Acute TNFα levels predict cognitive impairment 6–9 months after COVID-19 infection

Nuber-Champier, Anthony; Cionca, Alexandre; Bréville, Gautier; Voruz, Philippe; Alcântara, Isabele Jacot de; Allali, Gilles; Lalive, Patrice H.; Benzakour, Lamyae; Lövblad, Karl‐Olof; Braillard, Olivia; Nehme, Mayssam; Coen, Matteo; Serratrice, Jacques; Reny, Jean‐Luc; Pugin, Jérôme; Guessous, Idris; Landis, Basile Nicolas; Griffa, Alessandra; Ville, Dimitri Van De; Assal, Frédéric; Péron, Julie Anne

doi:10.1016/j.psyneuen.2023.106104

Cited by 11 publications

(7 citation statements)

References 49 publications

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“…This variable should therefore be regarded as one risk factor among others (e.g. behavioral, immunological, and/or genetic) [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

“…The fact that so many patients with neuropsychological deficits at 6–9 months did not return may have influenced our results for cumulative deficits in the mild subgroup. Fourth, many potentially important variables, such as levels of vitamin D [ 50 ] and immunological markers [ 16 , 18 ] were not collected, even though they may play a role in the progression of neuropsychological symptoms following SARS-CoV-2 infection. Fifth, this study was carried out in a high-income country, so the question of cognitive long-term effects in low- and middle-income countries with socio-economic and cultural specificities remains unanswered [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

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Persistence and emergence of new neuropsychological deficits following SARS-CoV-2 infection: A follow-up assessment of the Geneva COVID-COG cohort

Voruz,

de Alcântara,

Nuber-Champier

et al. 2024

J Glob Health

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Background Despite numerous observations of neuropsychological deficits immediately following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, little is known about what happens to these deficits over time and whether they are affected by changes in fatigue and any psychiatric symptoms. We aimed to assess the prevalence of neuropsychological deficits at 6–9 months and again at 12–15 months after coronavirus disease 2019 (COVID-19) and to explore whether it was associated with changes in fatigue and psychiatric symptoms. Methods We administered a series of neuropsychological tests and psychiatric questionnaires to 95 patients (mean age = 57.12 years, standard deviation (SD) = 10.68; 35.79% women) 222 (time point 1 (T1)) and 441 (time point 2 (T2)) days on average after infection. Patients were categorised according to the severity of their respiratory COVID-19 symptoms in the acute phase: mild (no hospitalisation), moderate (conventional hospitalisation), and severe (hospitalisation in intensive care unit (ICU) plus mechanical ventilation). We ran Monte-Carlo simulation methods at each time point to generate a simulated population and then compared the cumulative percentages of cognitive disorders displayed by the three patient subgroups with the estimated normative data. We calculated generalised estimating equations for the whole sample to assess the longitudinal associations between cumulative neuropsychological deficits, fatigue, and psychiatric data (anxiety, depressive symptoms, posttraumatic stress disorder, and apathy). Results Most participants (>50%) exhibited a decrease in their neuropsychological impairments, while approximately 25% showed an escalation in these cognitive deficits. At T2, patients in the mild subgroup remained free of accumulated neuropsychological impairments. Patients with moderate severity of symptoms displayed a decrease in the magnitude of cumulative deficits in perceptual and attentional functions, a persistence of executive, memory and logical reasoning deficits, and the emergence of language deficits. In patients with severe symptoms, perceptual deficits emerged and executive deficits increased, while attentional and memory deficits remained unchanged. Changes in executive functions were significantly associated with changes in depressive symptoms, but the generalised estimating equations failed to reveal any other significant effect. Conclusion While most cumulative neuropsychological deficits observed at T1 persisted and even worsened over time in the subgroups of patients with moderate and severe symptoms, a significant proportion of patients, mainly in the mild subgroup, exhibited improved performances. However, we identified heterogeneous neuropsychological profiles both cross-sectionally and over time, suggesting that there may be distinct patient phenotypes. Predictors of these detrimental dynamics have yet to be identified.

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“…This variable should therefore be regarded as one risk factor among others (e.g. behavioral, immunological, and/or genetic) [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Persistence and emergence of new neuropsychological deficits following SARS-CoV-2 infection: A follow-up assessment of the Geneva COVID-COG cohort

Voruz,

de Alcântara,

Nuber-Champier

et al. 2024

J Glob Health

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“…We next sought to clarify whether these biochemical markers related to neuropsychological test results in PACS patients, as previous studies have inconsistent results regarding the association of inflammatory marker levels and neuropsychological tests. Results have ranged from no association 72 to an association between cytokine levels and fatigue or executive functions (Stroop Color Word test) 73 , or TNF-α levels and memory 74 . In our research, we discovered a surprising positive correlation between higher GFAP levels and enhanced Stroop Word test performance.…”

Section: Discussionmentioning

confidence: 99%

Cognitive profile, neuroimaging and fluid biomarkers in post-acute COVID-19 syndrome

Guillén,

Pérez-Millan,

Falgàs

et al. 2024

Sci Rep

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We aimed to characterize the cognitive profile of post-acute COVID-19 syndrome (PACS) patients with cognitive complaints, exploring the influence of biological and psychological factors. Participants with confirmed SARS-CoV-2 infection and cognitive complaints ≥ 8 weeks post-acute phase were included. A comprehensive neuropsychological battery (NPS) and health questionnaires were administered at inclusion and at 1, 3 and 6 months. Blood samples were collected at each visit, MRI scan at baseline and at 6 months, and, optionally, cerebrospinal fluid. Cognitive features were analyzed in relation to clinical, neuroimaging, and biochemical markers at inclusion and follow-up. Forty-nine participants, with a mean time from symptom onset of 10.4 months, showed attention-executive function (69%) and verbal memory (39%) impairment. Apathy (64%), moderate-severe anxiety (57%), and severe fatigue (35%) were prevalent. Visual memory (8%) correlated with total gray matter (GM) and subcortical GM volume. Neuronal damage and inflammation markers were within normal limits. Over time, cognitive test scores, depression, apathy, anxiety scores, MRI indexes, and fluid biomarkers remained stable, although fewer participants (50% vs. 75.5%; p = 0.012) exhibited abnormal cognitive evaluations at follow-up. Altered attention/executive and verbal memory, common in PACS, persisted in most subjects without association with structural abnormalities, elevated cytokines, or neuronal damage markers.

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“…[84] A longitudinal study by Lindbergh et al showed that TNF-α was associated with gray matter loss, accelerated brain atrophy, and global cognitive decline in older adults. [85] Elevated plasma TNF-α levels may be a long-term risk factor for COVID-19associated CI. [85] A senescence-associated secretory phenotype (SASP) similar to that of senescent cells, accompanied by proinflammatory cytokine and chemokine secretion, was observed in patients with COVID-19, indicating that SARS-CoV-2 infection can induce a senescence phenotype, especially in patients with lower respiratory tract infections.…”

Section: Inflammatory Cytokinesmentioning

confidence: 99%

COVID‐19 and cognitive impairment: From evidence to SARS‐CoV‐2 mechanism

Pan,

Niu,

Feng

et al. 2024

Brain-X

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Caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), coronavirus disease 2019 (COVID‐19) primarily manifests as respiratory dysfunction. However, emerging evidence suggests SARS‐CoV‐2 can invade the brain, leading to cognitive impairment (CI). It may spread to other brain regions through transsynaptic neurons, including the olfactory, optic, and vagus nerves. Moreover, it may invade the central nervous system through blood transmission or the lymphatic system. This review summarizes the neuroimaging evidence from clinical and imaging studies of COVID‐19‐associated CIs, including magnetic resonance imaging and 18F‐fluorodeoxyglucose positron emission tomography‐computed tomography. The mechanisms underlying COVID‐19‐associated CIs are currently being actively investigated. They include nonimmune effects, such as viral proteins, tissue hypoxia, hypercoagulability, and pathological changes in neuronal cells, and immune effects, such as microglia and astrocyte activation, peripheral immune cell infiltration, blood‐brain barrier impairment, cytokine network dysregulation, and intestinal microbiota. Inflammation is the central feature. Both central and systemic inflammation may cause acute and persistent neurological changes, and existing evidence indicates that inflammation underlies the elevated risk of Alzheimer's disease. Finally, potential therapeutic options for COVID‐19‐associated CIs are discussed. In‐depth research into the pathological mechanisms is still needed to help develop new therapies.

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Acute TNFα levels predict cognitive impairment 6–9 months after COVID-19 infection

Cited by 11 publications

References 49 publications

Persistence and emergence of new neuropsychological deficits following SARS-CoV-2 infection: A follow-up assessment of the Geneva COVID-COG cohort

Persistence and emergence of new neuropsychological deficits following SARS-CoV-2 infection: A follow-up assessment of the Geneva COVID-COG cohort

Cognitive profile, neuroimaging and fluid biomarkers in post-acute COVID-19 syndrome

COVID‐19 and cognitive impairment: From evidence to SARS‐CoV‐2 mechanism

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