People who die of severe COVID-19 have brain abnormalities that resemble changes seen in Alzheimer’s disease – accumulation of a protein called tau inside brain cells, and abnormal amounts of the protein beta-amyloid that accumulates into amyloid plaques – small studies have found.
At Columbia University, Dr. Andrew Marks and colleagues studied the brains of 10 COVID-19 patients and found defects in proteins called ryanodine receptors that control the passage of calcium into cells. In Alzheimer’s disease, defective ryanodine receptors are linked to accumulation of tau into so-called neurofibrillary tangles.
These tangles were present in high levels in the COVID-19 patients’ brains, the Columbia team reported on Thursday in Alzheimer’s & Dementia. Other research teams have looked for – and found – abnormal amyloid levels in brains of COVID-19 patients, according to reports posted online ahead of peer review on bioRxiv and on The Lancet’s preprint server.
In all the studies, patients had experienced the most severe forms of COVID-19. If similar changes are occurring in the brains of patients with milder illness, that might help explain the “brain fog” associated with long COVID, Marks said.
Patients with severe COVID-19 might be at higher risk for dementia later in life, but it is too soon to know, he added. His advice: Get a booster vaccine and avoid the virus. “If you get COVID-19, you probably won’t die, but we still don’t know a lot about the long-term effects.”