(ORDO NEWS) — A small study, the authors of which studied the brains of patients who died from coronavirus infection, showed that they have some of the molecular changes characteristic of Alzheimer’s disease, a chronic neurodegenerative disease.
Scientists from the Clyde and Helen Wu Center for Molecular Cardiology at Columbia University (USA) found in patients who died due to a severe form of coronavirus disease, brain abnormalities that are similar to changes observed in Alzheimer’s disease – in particular, the accumulation of tau protein inside cells organ. The study is published in Alzheimer’s & Dementia .
People infected with coronavirus not only experience stress on the respiratory and cardiovascular systems, about a third develop neurological symptoms: headache, impaired consciousness (“brain fog”), numbness of the limbs, and so on. In addition, there are cases of cerebral edema, stroke, neuronal degeneration and encephalitis. Do not forget about such common signs of Covid-19 as hyposmia and hypogeusia – loss of smell and taste.
The fact that coronavirus causes a real systemic failure in the body is associated with angiotensin-converting enzyme 2, a membrane protein that is expressed in the process cells of the loose connective tissue of the heart, epithelial cells of the respiratory tract, kidneys, intestines and blood vessels, as well as in the brain.
It is ACE2 that acts as the target of SARS-CoV-2, thanks to which the virus enters the cells, and thereby makes all of the above tissues more vulnerable to viral invasion. But according to scientists, it remained unclear whether the coronavirus actually affects the neurons of the brain.
The team of Professor Andrew Marks, Head of the Department of Physiology and Cellular Biophysics, studied brain lysates of ten patients from 38 to 84 years old who died from Covid-19 and had various pathologies, for example, acute hypoxic-ischemic damage to the hippocampus, encephalopathy, dementia, and others.
Six of them were men. The control group consisted of people of the same age and gender, but they did not have neurological disorders, cardiovascular disease or lung disease.
According to scientists, those who died from coronavirus experienced severe oxidative stress with a 3.8- and 3.2-fold increase in the ratio of glutathione disulfide to glutathione in the cortex and cerebellum. They also showed high levels of phosphorylated tau in addition to defective ryanodine-sensitive channels .
Tau protein is predominantly found in brain neurons; among its numerous functions in healthy cells, stabilization of internal microtubules, structures of the cellular cytoskeleton, is distinguished. This protein also forms insoluble filaments that accumulate in the form of neurofibrillary tangles in chronic neurodegenerative Alzheimer’s disease.
In patients who died from a severe form of coronavirus infection, phosphorylated tau protein was found, including in areas where it is usually localized in those suffering from Alzheimer’s disease.
Therefore, it may be a sign of an early stage of the disease, leading to a decrease in intelligence, memory impairment and personality changes, as well as contribute to the appearance of other neurological symptoms.
According to the researchers, the immune response characteristic of severe coronavirus disease provokes inflammation in the brain, which in turn is responsible for the dysfunction of ryanodine receptors, and then to increase levels of phosphorylated tau protein.
Although researchers at Columbia University did not find changes in the signaling pathways leading to the accumulation of the beta-amyloid protein – a key molecule in the pathogenesis of Alzheimer’s disease – the authors of another work just found its focal deposits in the brains of patients with Covid-19.
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