Gene usage in the brains of those who suffered severe COVID-19 infections was similar to that observed in the aging brain. Researchers say COVID-19 is associated with molecular signatures of brain aging.
People with PTSD had a 9% increased risk of hospitalization and an 8% increased risk of death following contracting COVID-19 than people without the disorder. Those with psychosis had a 58% increased risk of death associated with COVID-19, and those with bipolar disorder had a 29% increased risk of dying from coronavirus.
People who contracted COVID-19 are significantly more likely to develop epilepsy or experience a seizure within 6 months of infection than those who contracted influenza.
Recent stressful experiences, such as the loss of a loved one or economic insecurity are strong predictors as to whether a person hospitalized for COVID-19 will experience symptoms of long COVID a year later.
Those with pre-existing anxiety, depression, chronic stress, and distress caused by loneliness are at 50% increased risk of developing Long-COVID following coronavirus infection.
COVID-19 infection causes microglia to excessively engulf synaptic structures and the upregulation of factors involved in phagocytosis.
Patterns of cognitive impairments suffered by those infected with COVID-19 were similar to those of healthy people who are sleep deprived. Additionally, worse symptoms of cognitive impairment in coronavirus patients were directly correlated with more severe infection.
Smaller life expectancy deficits associated with the COVID-19 pandemic were found in countries with more fully vaccinated people, researchers report.
During the COVID-19 pandemic, the number of patients admitted to hospitals for clinical depression care dropped significantly. However, the number of people seeking out-patient care for depression increased.
Brain cells exposed to blood taken from COVID-19 patients with delirium showed a decrease in neurogenesis and an increase in cell death. The findings also indicate a key role for cytokines produced in the immune system during infection and shed light on the molecular mechanisms of COVID-19 related delirium.
SARS_CoV_2, the virus responsible for COVID-19 infects and replicates in astrocytes, reducing neural viability.