People who die from COVID-19 have brain damage similar to the changes seen in Alzheimer's disease.
At autopsies, pathologists have detected an accumulation of a protein called tau inside brain cells and abnormal amounts of beta-amyloid protein that congregates in amyloid plaques, a small study found.
These findings may help explain the memory problems reported by those with "long COVID-19,” although researchers warn that the study is small, with data from only 10 patients, and should be replicated.
Dr. Andrew Marx, an expert in cellular physiology and biophysics at Columbia University, and his colleagues studied the brains of 10 COVID-19 patients and found defects in proteins called Ryanodine receptors that control the transfer of calcium to cells in Alzheimer's disease. Defective Ryanodine receptors are linked to the accumulation of tau proteins into so-called neurofibrillary tangles. These tangles were present at high levels in the brains of COVID-19 patients, the research team reported in Alzheimer's & Dementia: The Journal of the Alzheimer's Association.
Other research teams found abnormal amyloid levels in the brains of COVID-19 patients, according to reports posted online prior to peer review in the preprint bioRxiv and on the site of The Lancet.
In all studies, patients experienced the most severe forms of COVID-19. If similar changes occur in the brains of patients with milder disease, it may help explain the cerebral fog associated with long COVID, Marx said. Patients with severe COVID-19 may be at higher risk for dementia later in life but it’s too early to know, he added. His advice: get a booster vaccine and avoid the virus.
He made it clear that much more research needs to be conducted before definite conclusions can be published.