Jun 19, 2022 22:00:00

Infection with the new corona may increase the risk of developing Parkinson's syndrome

The new coronavirus infection (COVID-19) is known to affect the human brain, and it has been reported that

concentration and cognitive function may decline even after recovery, and severe COVID- Studies have shown that 19 has a cognitive effect comparable to 20 years of aging. Research teams from Thomas Jefferson University and East Carolina University in the United States report that 'COVID-19 may increase the risk of developing Parkinsonism .'

COVID-19 Infection Enhances Susceptibility to Oxidative Stress–Induced Parkinsonism --Smeyne ---- Movement Disorders --Wiley Online Library
https://doi.org/10.1002/mds.29116

Study in mice suggests that COVID-19 increases risk of developing Parkinson's disease
https://medicalxpress.com/news/2022-05-mice-covid-parkinson-disease.html

Parkinson's disease is a neurodegenerative disease that causes a deficiency of dopamine due to a decrease in dopamine nerve cells, and is a neurodegenerative disease that shows movement disorders such as hand tremor and slow movement. In addition, cases of Parkinson-like symptoms after drug administration, mental illness, encephalitis, etc. have been confirmed, and those with some of these causes are called Parkinson's syndrome.

One of the factors that causes such Parkinson syndrome is 'infectious disease caused by a virus', and after the Spanish flu that prevailed in 1918, it has been reported that patients who develop Parkinson syndrome about 10 years after the infection. .. A study published in 2021 found that people infected with influenza had a 70% or greater risk of developing Parkinson's syndrome more than 10 years after infection compared to non-infected people. A 2009 study showed that mice infected with the influenza virus were more susceptible to the toxic substance MPTP that induces Parkinson's disease.

Therefore, a research team in the United States is using a protein used when SARS-CoV-2 invades cells to investigate whether infection with the

new coronavirus (SARS-CoV-2) increases the risk of Parkinson's syndrome. We conducted an experiment in which mice genetically modified to express a human ACE2 receptor were infected with SARS-COV-2. In this experiment, SARS-CoV-2 was administered in an amount that causes moderate COVID-19 when converted to humans, and 80% of infected mice survived.

Surviving mice were divided into two groups, 38 days after recovery, one receiving a low dose of MPTP, which normally does not cause Parkinson's syndrome, and the control group receiving saline. Two weeks after administration of MPTP or saline, the team dissected the mouse brain to see if there were any changes in the neurons that synthesize dopamine.

As a result, although COVID-19 alone did not affect neurons, the neuronal loss pattern seen in Parkinson's syndrome was confirmed in mice treated with MPTP after recovery. This pattern is similar to that previously identified with influenza, suggesting that COVID-19 may increase the risk of developing Parkinson's syndrome as well as influenza.

Dr. Richard Smeyne of Thomas Jefferson University, the lead author of the paper, points out that the virus itself may not kill neurons, but may make them more susceptible to things like toxins and bacteria. Influenza and COVID-19 can cause cytokine release syndrome (cytokine storms) , which release large amounts of inflammation-inducing chemicals, which may make neurons vulnerable to subsequent stress. Insisted.

Smeyne emphasizes that Parkinson's syndrome is a rare disease and should not be panicked in the results of this study, and it is unclear whether the phenomenon that occurs in mice will occur in humans as well. On top of that, understanding the effects of SARS-CoV-2 on the brain is important in preparing for the long-term effects of a pandemic. The research team said they would like to study the effects of lower doses of SARS-CoV-2 on the risk of Parkinson's syndrome and whether the vaccine helps reduce the risk of developing Parkinson's syndrome.