Like a “fire in the brain”: COVID can cause brain inflammation that mimics the symptoms of Parkinson’s disease

Like a “fire in the brain”: COVID can cause brain inflammation that mimics the symptoms of Parkinson’s disease

Like a “fire in the brain”: COVID can cause brain inflammation that mimics the symptoms of Parkinson’s disease

SARS-CoV-2, the pathogen that causes COVID, is usually thought of as a respiratory virus. This makes sense given that it is airborne and usually infects people through the nose and lungs and causes respiratory symptoms As cough and sore throat. But perhaps we should also start thinking of SARS-CoV-2 as a brain virus.

After all, we have solid evidence for that SARS-2 can infect the brain, causing long-term or even permanent damage. This can result in life-threatening strokes and encephalitis, inflammation of the brain or as it is colloquially called “brain fog.”

Even anosmia, loss of taste and smell – which is still considered the main symptom of this disease that is changing – is neurological disorder, a category of conditions affecting the brain and central nervous system. This includes kicks, epilepsy, Alzheimer’s, Parkinson’s disease and meningitis. Incredibly, it appears that SARS-CoV-2 may play a role in all these neurological dysfunctions and more.

SARS-CoV-2 even appears to activate the same mechanisms in the brain that can cause Parkinson’s disease, a brain disorder characterized by involuntary movements, tremors and balance difficulties.

Fortunately, developing these neurological conditions from COVID seems to be rare. A person’s tendency to exhibit such symptoms also depends on how severe the infection is or has been, with vaccinated individuals generally experiencing milder or temporary symptoms. Medical history can also play a role in how likely you are to develop neurological disorders. However, age does not seem to be a major factor, as children may be affectedalso.

We also do not know how much repeated infections might play a role in this pathology or whether certain viral variants are more prone to neurological damage than others. with “variant of soupApparently poised to ravage North America and Europe this winter, experts still have a lot of questions about COVID and the brain, but what we’re learning isn’t reassuring.

What we do know is that SARS-CoV-2 appears to activate the same mechanisms in the brain that can cause Parkinson’s disease, a brain disorder characterized by involuntary movements, tremors, and balance difficulties. New study in journal Molecular psychiatry shows for the first time that SARS-2 can trigger the same inflammatory processes seen in patients with Alzheimer’s or Parkinson’s disease.


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The good news is that these researchers are identifying a way to stop this process with a drug, which means that in the future there could be a pill to prevent brain damage from COVID. To find out how, an international team of researchers led by Professor Trent Woodruff from the University of Queensland carried out several different experiments, including mice, African green monkey kidney cells and human immune cells called microglia, which act like white blood cells but specifically protect neurons.

In each of these experiments, scientists sought NLRP3, a type of protein called an inflammasome, which defends the brain against invaders by releasing a slew of inflammatory markers. NLRP3 has been widely studied, with some research incriminating this protein for the underlying causes of Parkinson’s disease.

dr. Albornoz Balmaceda described this cascade of inflammation as a “fire” in the brain, which permeates, killing neurons.

In each of these experiments, whether in Petri dishes or animal models, NLRP3 was found to be activated. This means that SARS-2 infection in the brain also appears to activate NLRP3, which could put people at greater risk of developing Parkinson’s disease or related neurological conditions.

“We studied the effect of the virus on the brain’s immune cells, ‘microglia’, which are key cells involved in the progression of brain diseases such as Parkinson’s and Alzheimer’s,” said Prof. Woodruff u statement. When his team grew human microglia in the lab and infected those cells with SARS-2, they showed signs of the intense inflammation familiar to neuroscientists studying Parkinson’s disease. “We found that the cells actually became ‘angry,’ activating the same pathway that Parkinson’s and Alzheimer’s proteins can activate in the disease, the inflammasome,” Woodruff said.

dr. Albornoz Balmaceda, another of the authors of the study, described this cascade of inflammation as a “fire” in the brain, which permeates, killing neurons. “It’s kind of a silent killer, because you don’t see any outward symptoms for years,” Balmaceda said in the same statement.

An angry fire in the brain sounds bad, but this inflammation actually has a purpose; it’s not evolution’s fault. When a pathogen like a virus crosses the blood-brain barrier, the shield around the brain to filter out unwanted substances, it can begin to cause damage, infecting neurons and forcing them to shrivel.

This can trigger the release of NLRP3, which then spreads more inflammatory proteins called caspases. They start telling the damaged cells to die to stop the spread of the invaders, clean up the damaged cells and start repairing themselves. This process is called pyroptosis, from the Latin “pyro” for fire and the Greek “ptosis” for falling off, like leaves from a tree. This type of inflammation causes a chain reaction that can kill many neurons like a firecracker going off.

A small part of this inflammation is natural and can be protective, like a controlled burn. But too much pyroptosis and you go from a confined fire to a whole forest aflame. The more neurons die, the brain begins to deteriorate.

To further confirm this theory, the researchers repeated the experiments using a drug that blocked this pathway. Obliquely called MCC950, this drug stops NLRP3 signaling and has been used in similar studies associated with this inflammatory pathway. MCC950 binds to NLRP3, preventing inflammation and stopping the brain from essentially firing angrily.

The MCC950 actually is under development as a way to treat Parkinson’s disease, although some research in mice suggests that MCC950 may have side effects, such as kidney damage. But other, similar drugs that stop NLRP3 from doing its job could be in the works, so hypothetically, a drug like this could also stop some of the harmful effects of SARS-CoV-2. We now know at least one of the ways SARS-CoV-2 can wreak havoc on the brain, but we’re also one step closer to finding treatments for it and other neurological conditions like Parkinson’s.

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