The SARS-CoV-2 It is a very recent virus and, despite all the effort that has been put into its research in the last year, we still do not know a lot about it. For example, your wide range of symptoms or the different forms in which it affects different people are enigmas that continue to intrigue scientists.

What is certain is that since the first months of the pandemic there have been researchers who have searched possible neurological effects, and several studies have pointed in this direction.

Now, a study carried out by the universities of Stanford (USA) and Saarland (Germany) and published in the journal Nature has come to a curious conclusion. The researchers analyzed brain tissue samples from eight patients who died of Covid-19 and found that they had inflammation and a impairment of neural circuits similar to that caused by some neurodegenerative diseases such as Alzheimer’s or Parkinson’s. However, what they failed to find was the presence of the virus in those brain tissues.

The complex relationship between Covid-19 and the human brain

The interest of scientists in the effects that SARS-CoV-2 can have on the human brain is easy to explain: since the beginning of the pandemic, it has been observed that hospitalized patients frequently present neurological symptoms, such as headaches, dizziness, myalgia and anosmias.

Incidence data as of June 28.

In fact, a study published in the journal Brain and carried out by scientists from University College London and the NHS already found in July of last year Acute demyelinating encephalomyelitis in 40 patients of covid-19.

This type of damage could explain the most important neurological symptoms that occur in patients who suffer from Covid-19 more seriously, but also the sequelae, of greater or lesser severity, suffered by many mild patients for a time after their infection.

For example, it is known that it is not uncommon for the symptom of anosmia (loss of smell) it lasts for a time in some mild patients, as does “brain fog” (a colloquial name to describe a grouping of symptoms including memory, concentration, confusion, and headache problems) even months after infection.

However, the recent investigation, as happened with other previous ones, although it documented and detailed some of the neuropathological features present in the brain of the deceased Covid-19 patients, they failed to find viral RNA or proteins in brain tissue.

Still, the fact that the virus does not penetrate brain tissue it is still under discussion by the scientific community.

Thus, there are works, such as the one published in The Lancet and directed by the Institute of Neuropathology at the University of Hamburg in October 2020, which they do claim to have found virus debris in brain tissues of a significant number of deceased patients. On the other hand, others, such as the one published in Brain in April 2021 by researchers at the Irving Medical Center of Columbia University, argue that this previous detection could be due to contamination, since the virus could be stored in the blood vessels of the brain.

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Damage the brain without infecting it

To explain this absence of traces of the virus in brain tissues, the Stanford team led by Tony Wyss-Coray draws on his previous work on the barrier between the blood and the brain.

This barrier, which is nothing more than part of the cells of the blood vessels that separates the blood from the brain cells, is very selective in letting any cell pass or molecule from outside the brain to the brain.

In those investigations, the Stanford team found, as published in Nature, that certain factors can induce inflammatory responses in the brain through this barrier, which could explain these changes in the brain, similar to the degeneration that occurs with age and as a consequence of diseases such as Alzheimer’s or dementia.

The researchers also rely on the inflammatory responses that the virus provokes in other parts of the body, and which in their opinion could trigger the neuroinflammation observed in corpses.

Changes in the cerebral cortex

The researchers’ methodology was the cell RNA sequencing obtained from brain tissue samples.

This technique allowed us to observe the activation levels of hundreds of types of genes in all the main types of cells. In addition, these values ​​were compared with those obtained from a control group consisting of samples of deceased who did not suffer from Covid-19.

The result is that patients who had died from Covid-19 showed much higher activation levels in many of the genes, especially in certain classes related to neuroinflammatory processes.

In addition, it was found that in the cerebral cortex, those who died from the coronavirus presented molecular changes that indicated a suppressed activity in excitatory neurons and enhanced in inhibitory neurons. These imbalances, which occur in a part of the brain that plays a vital role in decision-making, mathematical reasoning and memory, also appear in numerous severe neurodegenerative diseases.

On the other hand, they found that, in all the cell types analyzed, the disturbances caused by Covid-19 they occurred in genetic variants associated with cognition, schizophrenia, and depression.

Neurological Covid-19

In summary, these findings could help explain the neurological symptoms that have been described in Covid-19 patients, both during and after infection, and could shed light on treatment routes for these pictures.

In addition, it advances the relationship between immune and inflammatory responses and various neurological and psychiatric conditions, such as depression, chronic fatigue and the most severe neurodegenerative disorders.

In any case, Wyss-Coray cautions that markers of inflammation may be found in a very high number of Covid-19 patients, even in mild patients or those who have not shown symptoms of a neurological nature; In other words, the virus could affect the brain of many people who contract it, even those who have not shown serious symptoms or pictures, which carries certain possibilities of later sequelae.

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