“One interpretation of these findings is that long COVID could be an atypical form of Alzheimer’s and/or that patients who had severe COVID could be predisposed to developing Alzheimer’s later in life,” says Marks, “but much more research needs to be done before we can make more definitive conclusions.”

If the memory and neurological problems of long COVID can be traced to defective ryanodine receptors, a drug under development by Marks may help. The drug is now in early clinical trials to treat a muscle disease caused by an inherited defect in the ryanodine receptor. The drug was able to fix the ryanodine defect when applied to the COVID patients’ brain tissue.

“My greatest hope is that other laboratories will look into our findings, and if they are validated, generate interest in a clinical trial for long COVID,” says Marks.


More information

The research appears in a paper titled, “Alzheimer’s-like signaling in brains of COVID-19 patients(link is external and opens in a new window).”

Andrew Marks is professor and chair of the Department of Physiology & Cellular Biophysics and the Clyde’56 and Helen Wu Professor of Molecular Cardiology (in Medicine) at the Vagelos College of Physicians and Surgeons and professor of biomedical engineering at Columbia University’s Fu Foundation School of Engineering and Applied Science.

All authors: Steve Reiken, Leah Sittenfeld, Haikel Dridi, Xiaoping Liu, and Andrew R. Marks (all from Columbia).

The research was supported by the NIH (grant R01NS114570).

Columbia University and Andrew Marks own stock in ARMGO Pharma Inc., a company developing compounds targeting the ryanodine receptor, and have patents on the compounds. Steven Reiken has consulted for ARMGO Pharma in the past 36 months.