Large epidemiological analyses showed that people who had COVID-19 were at an increased risk of cognitive deficits, such as memory problems.

Imaging studies done in people before and after their COVID-19 infections show shrinkage of brain volume and altered brain structure after infection.

A study of people with mild to moderate COVID-19 showed significant prolonged inflammation of the brain and changes that are commensurate with seven years of brain aging.

Severe COVID-19 that requires hospitalization or intensive care may result in cognitive deficits and other brain damage that are equivalent to 20 years of aging.

Laboratory experiments in human and mouse brain organoids designed to emulate changes in the human brain showed that SARS-CoV-2 infection triggers the fusion of brain cells. This effectively short-circuits brain electrical activity and compromises function.

Autopsy studies of people who had severe COVID-19 but died months later from other causes showed that the virus was still present in brain tissue. This provides evidence that contrary to its name, SARS-CoV-2 is not only a respiratory virus, but it can also enter the brain in some individuals. But whether the persistence of the virus in brain tissue is driving some of the brain problems seen in people who have had COVID-19 is not yet clear.

Studies show that even when the virus is mild and exclusively confined to the lungs, it can still provoke inflammation in the brain and impair brain cells’ ability to regenerate.

COVID-19 can also disrupt the blood brain barrier, the shield that protects the nervous system – which is the control and command center of our bodies – making it “leaky.” Studies using imaging to assess the brains of people hospitalized with COVID-19 showed disrupted or leaky blood brain barriers in those who experienced brain fog.

A large preliminary analysis pooling together data from 11 studies encompassing almost 1 million people with COVID-19 and more than 6 million uninfected individuals showed that COVID-19 increased the risk of development of new-onset dementia in people older than 60 years of age.