Washington, May 23 (PTI) The SARS-CoV-2 virus, which causes COVID-19, could increase the risk of brain degeneration seen in Parkinson’s disease, according to a study performed in mice.
The study, published in the journal Movement Disorders, used mice that were genetically engineered to express the human ACE-2 receptor, which the SARS-CoV-2 virus uses to gain access to the cells in our airway.
These mice were infected with SARS-CoV-2 and allowed to recover.
The dose chosen in the study corresponds to moderate COVID-19 infection in humans, with around 80 per cent of the infected mice surviving.
Thirty-eight days after the surviving animals recovered, one group was injected with a low dose of MPTP — a chemical which causes permanent symptoms of Parkinson’s disease — that would not normally cause any loss of neurons. The control group was given saline.
Two weeks later, the animals were sacrificed and their brains examined.
The researchers found that COVID-19 infection alone had no effect on the neurons in the basal ganglia, a region in the brains of vertebrates.
However, mice that were given the low dose of MPTP after recovering from infection exhibited the classic pattern of neuron loss seen in Parkinson’s disease, the researchers found.
This increased sensitivity after COVID-19 infection was similar to what was seen in the influenza study, suggesting that both viruses could induce an equivalent increase in risk for developing Parkinson’s. “We think about a ‘multi-hit’ hypothesis for Parkinson’s — the virus itself does not kill the neurons, but it does makes them more susceptible to a ‘second hit’, such as a toxin or bacteria or even an underlying genetic mutation,” said Richard Smeyne, from the Thomas Jefferson University, US, and first author of the study.
Both influenza and SARS-CoV-2 have been found to cause a “cytokine storm” or an overproduction of pro-inflammatory chemicals, which 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.
While the mechanism is not fully understood, the researchers believe the increased microglia inflame the basal ganglia and cause cellular stress.
This then lowers the neurons’ threshold to withstand subsequent stress, they said.
“We were concerned about the long-term consequences of viral infection,” said Peter Schmidt, a neuroscientist from New York University, US, who co-led the study.
The researchers are planning to determine whether vaccines can mitigate the experimental increase in Parkinson’s pathology linked to prior SARS-CoV-2 infection.
They are also testing other variants of the virus, as well as doses that correspond to milder cases in humans.
“Parkinson’s is a rare disease that affects 2 per cent of the population above 55 years, so the increase in risk is not necessarily a cause for panic,” said Smeyne.
“But understanding how coronavirus impacts the brain can help us prepare for the long-term consequences of this pandemic,” he added. PTI SAR SAR
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