People who die of Covid-19 have brain damage similar to the changes seen in Alzheimer’s disease, according to a small study published by the Alzheimer’s Association, after several autopsies in which pathologists detected the accumulation of a protein called ‘tau’ inside of brain cells and abnormal amounts of beta-amyloid protein that collects in amyloid plaques.
The findings may help explain the memory problems reported by many patients with ‘Long Covid’ symptoms, while noting that the fact that the study was small – it was conducted with data from just 10 patients – necessitates more extensive replication.
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Andrew Marx, a specialist in cell physiology and biophysics at Columbia University in the United States, and his colleagues studied the brains of 10 patients with Covid-19 and found defects in proteins called ryanodine receptors, which control the transfer of calcium to the cells. cells in Alzheimer’s disease. Defective ryanodine receptors are linked to the accumulation of tau proteins in so-called neurofibrillary tangles. These tangles were present at high levels in the brains of Covid-19 patients, the team of experts reported.
Other studies conducted have concluded that abnormal levels of amyloid were found in the brains of Covid-19 patients, according to reports published online prior to peer review in preprint bioRxiv and on The Lancet website.
In all studies, patients experienced the most severe forms of Covid-19. If such changes occur in the brains of patients with milder illnesses, it could help explain the brain fog associated with ‘Long Covid’, Marx explained. Infected patients may be at increased risk of dementia later in life, but it’s too early to make that conclusion, he said.
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