Covid infection may increase risk of Parkinson’s, mice study suggests – Jammu Kashmir Latest News | Tourism

WASHINGTON, June 20: SARS-CoV-2 virus may increase the risk of brain degeneration in Parkinson’s disease, according to a study in mice.
COVID-19 patients often report symptoms such as brain fog, headaches and insomnia, complications that are not new after a viral infection, the researchers said.
It took nearly a decade for patients to develop the neurological disease known as “post-encephalic parkinsonism” after the 1918 flu pandemic, they said.
The study, published in the journal Movement Disorders, found that the SARS-CoV-2 virus can increase the brain’s sensitivity to a toxin that causes the death of nerve cells seen in Parkinson’s disease.
“Parkinson’s is a rare disease that affects 2 percent of the population over the age of 55, so the increase in risk is not necessarily a cause for alarm,” said lead researcher Richard Smeyne of Thomas Jefferson University in the US.
“But understanding how the coronavirus affects the brain can help us prepare for the long-term consequences of this pandemic,” Smeyne said.
The study builds on previous findings from the Smeyne lab, indicating that viruses can increase the susceptibility of brain cells or neurons to damage or death.
In that study, the researchers found that mice exposed to the H1N1 influenza strain that caused the 2009 flu pandemic were more vulnerable to MPTP.
MPTP is a toxin known to cause some of the characteristic symptoms of Parkinson’s disease, most notably the loss of neurons that express the chemical dopamine and increased inflammation in the basal ganglia, a brain region crucial for movement. .
The latest study used mice that had been genetically altered to express the human ACE-2 receptor, which the SARS-CoV-2 virus uses to access the cells in our airways.
These mice were infected with SARS-CoV-2 and were allowed to recover afterward, the researchers said.
The dosage used in this study is equivalent to a mild COVID-19 infection in humans, with about 80 percent of infected mice surviving, they said.
Thirty-eight days after the surviving mice recovered, one group received a modest dose of MPTP that would not normally cause neuron loss.
The control group received saline. The animals were sacrificed and their brains examined two weeks later.
The researchers found that COVID-19 infection alone did not affect dopaminergic neurons in the basal ganglia.
However, mice given a modest dose of MPTP after recovery from infection showed the classic pattern of neuron loss found in Parkinson’s disease.
This increased susceptibility after COVID-19 infection was similar to what was reported in the flu study, suggesting that both viruses could cause an equal increase in the risk of developing Parkinson’s.
“We’re thinking of a ‘multi-hit’ hypothesis for Parkinson’s — the virus itself doesn’t kill the neurons, but it does make them more susceptible to a ‘second hit,’ such as a toxin or bacteria or even an underlying genetic mutation,” explains Smith.
Both influenza and SARS-CoV2 have been shown to trigger a “cytokine storm,” or an overproduction of pro-inflammatory chemicals. These chemicals can cross the blood-brain barrier and activate the brain’s immune cells – microglia.
The researchers found increased numbers of activated microglia in the basal ganglia of mice that recovered from SARS-CoV2 and received MPTP.
Although the mechanism is not fully understood, they believe that the increased microglia inflame the basal ganglia and cause cellular stress. This then lowers the neurons’ threshold to withstand subsequent stress.
“We were concerned about the long-term consequences of viral infection,” said Peter Schmidt, a neuroscientist at New York University in the US who led the study.
The researchers plan to determine whether vaccines can reduce the experimental increase in Parkinson’s disease associated with previous SARS-CoV-2 infection.
They are also testing other variants of the virus, as well as doses corresponding to milder cases in humans. (PTI)

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