About
COVID-19 represents a traumatic experience characterized by its unpredictable nature and changes in lifestyle. Previous studies have reported distress in hospitalized patients infected with SARS-CoV-2, including anxiety, depression, and symptoms of post-traumatic stress (PTSS). Stressful experiences can also contribute to the development of rumination associated with symptoms of depression and anxiety. Hospitalization due to COVID-19, in turn, may contribute to the development of post-traumatic stress disorder (PTSD), anxiety, depression, and feelings of loneliness, which are associated with poor quality of life (QoL).
The inflammatory process contributing to COVID-19 disease can compromise cognitive functions, even in patients with C-reactive protein (CRP) levels indicating recovery. Chronic stress experiences have an inflammatory response similar to that observed in hospitalized patients with COVID-19. The hyperinflammatory response to SARS-CoV-2 can also contribute to the breakdown of the blood-brain barrier, which may impair cognitive function. SARS-CoV-2 can invade the central nervous system (CNS) using dopamine receptors (DRs) to enter and increase the virus's survival. COVID-19 can cause changes in dopamine and serotonin secretions, contributing to brain damage and lower QoL, consistent with the Stress and Cognitive Aging Model, which posits that rumination and PTSS events contribute to cognitive decline mediated by physiological dysregulation.
To date, no study on COVID-19 has addressed the impact of the inflammatory response and dopaminergic pathways on cognitive function and QoL. This project aims to understand the pathophysiological mechanism and determinants of cognitive decline, defining risk profiles in patients with COVID-19. Specifically, it aims to evaluate how rumination and PTSS may affect cognitive function and impact QoL in patients recently discharged from the hospital (within the last 6 months, 12 months, and 24 months).
Patients will be assessed for sociodemographic, clinical, and psychological variables (PTSS, morbidity, loneliness, life satisfaction, post-traumatic growth, cognitive function, QoL), and biochemical parameters (inflammatory markers and dopaminergic pathways). Given that one-third of severe COVID-19 patients may experience long-term complications and higher risk of premature death, the results of this study may identify new therapeutic targets (DRs) and related psychological comorbidities (profiles of cognitive decline risk) where dopaminergic circuits are affected to improve QoL, prevent cognitive decline, and reduce the high costs associated with SARS-CoV-2 infection.
