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 in Alzheimer's & Dementia https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.12558.
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 https://www.biorxiv.org/content/10.1101/2022.01.31.478476v2 and on The Lancet's preprint server https://papers.ssrn.com/sol3/papers.cfm?abstract_id=4003213.
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."
SOURCES:
https://bit.ly/3Gv7wex Alzheimer's & Dementia, online February 3, 2022.
https://bit.ly/3HyYe2r bioRxiv, online February 1, 2022.
https://bit.ly/34ubDdv Preprints with The Lancet, online January 14, 2022.
By Reuters Staff
Posted on
site created by:
© 2024 Medicom Medical Publishers. All rights reserved. Terms and Conditions | Privacy Policy
HEAD OFFICE
Laarderhoogtweg 25
1101 EB Amsterdam
The Netherlands
T: +31 85 4012 560
E: publishers@medicom-publishers.com