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jobaeid Hasan
Aug 02, 2022
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Although the diagnosis rate of Omicron is mostly mild, the neurological sequelae of the brain caused by infection may still cause serious consequences. Relevant studies have pointed out that infection with COVID-19 (severe special infectious pneumonia, new coronary pneumonia, Wuhan pneumonia) can cause brain inflammation and chronic hypoxia, and it does not occur in severe cases, even mild patients may have severe symptoms. suffer from it. Research published in the recent issue of Nature Communications shows that even "minor brain hypoxia" is enough to cause localized central nervous system hypoxia and energy decline. Chronic brain hypoxia caused by COVID-19? Asymptomatic infection also? unnamed Photo Credit: Tide Science A research team from Tulane Special Database University in the United States constructed a model of primates infected with COVID-19 to explore the effect of the virus on neural tissue. It was found that there are about five symptoms similar to those of humans infected with the virus: marked inflammation of the brain, neuronal damage and apoptosis, minor cerebral hemorrhage and chronic cerebral hypoxia. The above phenomenon happelieves that most of the subjects had no obvious respiratory symptoms, so it is difficult to directly associate hypoxia in the brain. However, from the results of animal experiments, it is known that chronic hypoxia or nerve inflammation in the brain, as well as the reduction of cerebral blood flow caused by acute minor cerebral hemorrhage, may be the main causes of damage to the human central nervous system. Fischer said that the brain is an organ that needs to be "highly metabolized", and glucose is involved in the metabolic process to produce "adenosine triphosphate" (ATP), which is used to store and transmit brain chemicals. However, infection with COVID-19 may lead to this impairment, resulting in hypoxia and failure of the central nervous system.
Nature Communications study: Even asymptomatic, COVID-19 may cause 'chronic brain damage'  content media
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