Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) triggered the pandemic
Coronavirus Disease 19 (COVID-19), causing millions of deaths. The elderly and those already living with comorbidity are likely to die after
SARS-CoV-2 infection. People suffering from
Alzheimer's disease (AD) have a higher risk of becoming infected, because they cannot easily follow health roles. Additionally, those suffering from
dementia have a 40% higher risk of dying from
COVID-19. Herein, we collected from Gene Expression Omnibus repository the brain samples of AD patients who died of
COVID-19 (AD+COVID-19), AD without
COVID-19 (AD),
COVID-19 without AD (COVID-19) and control individuals. We inspected the transcriptomic and interactomic profiles by comparing the
COVID-19 cohort against the control cohort and the AD cohort against the AD+COVID-19 cohort. SARS-CoV-2 in patients without AD mainly activated processes related to immune response and cell cycle. Conversely, 21 key nodes in the interactome are deregulated in AD. Interestingly, some of them are linked to
beta-amyloid production and clearance. Thus, we inspected their role, along with their interactors, using the gene ontologies of the biological process that reveals their contribution in brain organization, immune response, oxidative stress and viral replication. We conclude that SARS-CoV-2 worsens the AD condition by increasing neurotoxicity, due to higher levels of
beta-amyloid,
inflammation and oxidative stress.