Stanford University study found that the brains of patients who died from COVID-19 had inflammation
Visit: Alibaba Cloud 6.18 Main Venue: Explosive products will be sold for a limited time at 10 o’clock every day
Stanford University neuroscientist Tony Wyss-Coray’s most famous work may be transplanting plasma from young mice into older mice and discovering that it can reverse age-related cognition decline. Now, he is still studying the mechanism that can explain the discovery of mice, and there is no evidence that young blood has the same beneficial effects on humans. One hypothesis is that the inflammatory response in the brain can be triggered by factors in the blood outside the brain.
With the outbreak of the COVID-19 pandemic last year, Wyss-Coray noticed that patients often reported neurological symptoms after infection. Many patients still report neurological symptoms a few months after recovering from the acute illness. Therefore, this new study raises two questions: Can SARS-CoV-2 really cross the blood-brain barrier to infect the human brain? What unusual molecular markers can be detected in the brains of patients who have died from COVID-19?
The research team systematically analyzed 30 brain tissue samples from 8 COVID-19 patients and 14 healthy controls. It is reported that the brain tissue comes from the frontal cortex and choroidal plexus.
Researchers measured the gene expression levels of more than 65,000 individual cells through single-cell RNA sequencing, and found that a large number of genes related to the inflammatory process in the brain tissue of COVID-19 patients were activated. The level of T cells in the brains of COVID-19 patients is also more abundant than that of healthy controls.
“Viral infection seems to trigger a systemic inflammatory response, which may cause inflammatory signals to cross the blood-brain barrier and trigger neuroinflammation in the brain,” Wyss-Coray said. “Many COVID-19 patients are particularly Those patients who reported or showed neurological problems or were hospitalized are likely to have neuroinflammation markers that we have seen in people who died of this disease.”
Wyss-Coray said the study The inflammatory molecular markers detected in Alzheimer’s disease and Parkinson’s disease have the same obvious features as those observed in neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease.
It is worth noting that none of these patients showed any signs of nerve damage before death. To better understand the potential long-term effects, further work is necessary to find signs of neuroinflammation in the cerebrospinal fluid of surviving COVID-19 patients.
This study indeed pointed out a precedent for acute viral infections leading to long-term neuroinflammation. Therefore, although the relationship between COVID-19 and neuroinflammation is reasonable, it is of course still too early to judge what kind of chronic diseases this may cause. Wyss-Coray hypothesized that this underlying inflammatory mechanism could explain the symptoms of long-term anger dry virus infections-including fatigue, brain fog, and depression.
An even more controversial finding in this new study is that the researchers could not find any traces of SARS-CoV-2 in the brain tissue of the deceased. Scientists are still debating whether this new type of coronavirus can actually cross the blood-brain barrier and directly infect brain tissue.
A study conducted by Yale University researchers earlier this year found that this virus can infect brain cells, but it is not clear whether this will happen in real-world infections. . Wyss-Coray said his team could not detect any viruses in the brain tissue samples they studied.
However, this new study puts forward a reasonable hypothesis that the neurological symptoms associated with COVID-19 and the long-term new coronavirus are caused by the way the virus induces peripheral inflammation in the brain, rather than the virus directly Infect the brain.
The conclusion of this study is that it is very important to clarify these molecular processes, because the long-term effects of COVID-19 will not be known in the next few years. Other researchers have warned that excessive neuroinflammation caused by COVID-19 may increase a person’s risk of developing neurodegenerative diseases such as Parkinson’s disease, so understanding how this virus affects the brain will help us in the emergence of infections. Keep track of the neurological consequences.