TY - JOUR
T1 - Cognitive impairment in long-COVID and its association with persistent dysregulation in inflammatory markers
AU - Damiano, Rodolfo Furlan
AU - Rocca, Cristiana Castanho de Almeida
AU - Serafim, Antonio de Pádua
AU - Loftis, Jennifer M.
AU - Talib, Leda Leme
AU - Pan, Pedro Mário
AU - Cunha-Neto, Edecio
AU - Kalil, Jorge
AU - de Castro, Gabriela Salim
AU - Seelaender, Marilia
AU - Guedes, Bruno F.
AU - Nagahashi Marie, Suely K.
AU - de Souza, Heraldo Possolo
AU - Nitrini, Ricardo
AU - Miguel, Euripedes Constantino
AU - Busatto, Geraldo
AU - Forlenza, Orestes V.
N1 - Publisher Copyright:
Copyright © 2023 Damiano, Rocca, Serafim, Loftis, Talib, Pan, Cunha-Neto, Kalil, de Castro, Seelaender, Guedes, Nagahashi Marie, de Souza, Nitrini, Miguel, Busatto, Forlenza and HCFMUSP COVID-19 Study Group.
PY - 2023
Y1 - 2023
N2 - Objective: To analyze the potential impact of sociodemographic, clinical and biological factors on the long-term cognitive outcome of patients who survived moderate and severe forms of COVID-19. Methods: We assessed 710 adult participants (Mean age = 55 ± 14; 48.3% were female) 6 to 11 months after hospital discharge with a complete cognitive battery, as well as a psychiatric, clinical and laboratory evaluation. A large set of inferential statistical methods was used to predict potential variables associated with any long-term cognitive impairment, with a focus on a panel of 28 cytokines and other blood inflammatory and disease severity markers. Results: Concerning the subjective assessment of cognitive performance, 36.1% reported a slightly poorer overall cognitive performance, and 14.6% reported being severely impacted, compared to their pre-COVID-19 status. Multivariate analysis found sex, age, ethnicity, education, comorbidity, frailty and physical activity associated with general cognition. A bivariate analysis found that G-CSF, IFN-alfa2, IL13, IL15, IL1.RA, EL1.alfa, IL45, IL5, IL6, IL7, TNF-Beta, VEGF, Follow-up C-Reactive Protein, and Follow-up D-Dimer were significantly (p<.05) associated with general cognition. However, a LASSO regression that included all follow-up variables, inflammatory markers and cytokines did not support these findings. Conclusion: Though we identified several sociodemographic characteristics that might protect against cognitive impairment following SARS-CoV-2 infection, our data do not support a prominent role for clinical status (both during acute and long-stage of COVID-19) or inflammatory background (also during acute and long-stage of COVID-19) to explain the cognitive deficits that can follow COVID-19 infection.
AB - Objective: To analyze the potential impact of sociodemographic, clinical and biological factors on the long-term cognitive outcome of patients who survived moderate and severe forms of COVID-19. Methods: We assessed 710 adult participants (Mean age = 55 ± 14; 48.3% were female) 6 to 11 months after hospital discharge with a complete cognitive battery, as well as a psychiatric, clinical and laboratory evaluation. A large set of inferential statistical methods was used to predict potential variables associated with any long-term cognitive impairment, with a focus on a panel of 28 cytokines and other blood inflammatory and disease severity markers. Results: Concerning the subjective assessment of cognitive performance, 36.1% reported a slightly poorer overall cognitive performance, and 14.6% reported being severely impacted, compared to their pre-COVID-19 status. Multivariate analysis found sex, age, ethnicity, education, comorbidity, frailty and physical activity associated with general cognition. A bivariate analysis found that G-CSF, IFN-alfa2, IL13, IL15, IL1.RA, EL1.alfa, IL45, IL5, IL6, IL7, TNF-Beta, VEGF, Follow-up C-Reactive Protein, and Follow-up D-Dimer were significantly (p<.05) associated with general cognition. However, a LASSO regression that included all follow-up variables, inflammatory markers and cytokines did not support these findings. Conclusion: Though we identified several sociodemographic characteristics that might protect against cognitive impairment following SARS-CoV-2 infection, our data do not support a prominent role for clinical status (both during acute and long-stage of COVID-19) or inflammatory background (also during acute and long-stage of COVID-19) to explain the cognitive deficits that can follow COVID-19 infection.
KW - COVID-19
KW - SARS- CoV-2
KW - cognition
KW - cohort study (or longitudinal study)
KW - inflammation
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U2 - 10.3389/fimmu.2023.1174020
DO - 10.3389/fimmu.2023.1174020
M3 - Article
C2 - 37287969
AN - SCOPUS:85161008624
SN - 1664-3224
VL - 14
JO - Frontiers in immunology
JF - Frontiers in immunology
M1 - 1174020
ER -