It has been observed that some of the patients with COVID-19 develop prolonged neurological-like symptoms including memory problems, related to the inflammation caused by the infection. A study by researchers at Columbia University Vagelos College of Physicians and Surgeons may help explain their occurrence in people with “long COVID”. Published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, it reports that the brains of deceased COVID patients show the same brain abnormalities than those observed in the brain of Alzheimer’s patients.
What are they ? an accumulation of a protein called tau in brain cells. In Alzheimer’s disease, the tau protein aggregates in neurons and these aggregates spread throughout the brain. Reports from COVID survivors of “brain fog” have prompted researchers to study how certain molecules calleds ryanodine receptors were affected upon infection. “What we found is truly unexpected: not only did we find defective ryanodine receptors in the hearts and lungs of deceased COVID patients, but we also found them in the brain. “, explains Professor Andrew Marks.
The tau protein, the link between COVID and Alzheimer’s
The team studied the brains of 10 patients deceased from COVID-19 and found defects in these proteins called ryanodine receptors that control the passage of calcium into cells. Inside neurons, defective ryanodine receptors have previously been associated with an increase inhas phosphorylated tau protein, this known hallmark of Alzheimer’s disease. In this study, researchers found elevated levels of phosphorylated tau in the brains of COVID patients in addition to defective ryanodine receptors. Phosphorylated tau protein has been found in areas where it is usually localized in patients with Alzheimer’s disease.
But not only: this phosphorylated tau protein has also been found in areas where it is not localized in Alzheimer’s patients. The researchers therefore suggest that “in COVID patients, this could be a sign of early-stage Alzheimer’s and also contribute to other neurological symptoms observed in these patients. Among the most cited symptoms: headaches or anxiety-depressive symptoms. Based on this constant, they believe that a rise in levels of phosphorylated tau in the brain is linked to memory problems. in Alzheimer’s disease, and could cause similar problems in people with long COVID.
The track of a treatment already mentioned
This phenomenon could be explained by the fact that the characteristic immune response severe COVID-19 causes inflammation in the brain, which in turn leads to dysfunctional ryanodine receptors, and increased phosphorylated tau protein. In contrast, no change in the pathways that lead to the formation of beta-amyloid – another hallmark of Alzheimer’s disease – was found. “One interpretation of these results is that long COVID could be an atypical form of Alzheimer’s and/or patients with severe COVID could be predisposed to developing Alzheimer’s disease later in life. concludes Professor Andrew Marks.
However, other studies must be carried out on a larger sample of patients before this finding can be confirmed. However, the scientific team is already working on the development of a treatment if neurological problems in connection with this long COVID are well attributed to defective ryanodine receptors. The drug in question is already in early clinical trials as part of a treatment for a muscle disease caused by an inherited defect of the ryanodine receptor. The latter could therefore correct this defect of defective ryanodine receptors insofar as it targets the brain tissue of patients with severe COVID-19.