The new study, published in the journal Movement Disorders, discovered that the novel Covid can make the mouse brain more susceptible to a toxin that causes the nerve-cell loss seen in Parkinson’s disease.
“Parkinson’s is a rare disease that affects 2% of the population over the age of 55, so the increase in risk is not necessarily cause for concern,” said Richard Smeyne, Director of Thomas Jefferson University in the United States.
“However, understanding how Coronavirus affects the brain can help us prepare for the long-term effects of this pandemic,” he added.
The new findings build on prior research that shows viruses can make brain cells or neurons more vulnerable to damage or death.
In a previous study, the researchers discovered that mice infected with the H1N1 strain of influenza responsible for the 2009 flu pandemic were more susceptible to MPTP – a toxin known to induce some of the hallmarks of Parkinson’s disease, including the loss of neurons expressing the chemical dopamine and increased inflammation in the basal ganglia, a brain region critical for movement.
Later human studies revealed that influenza nearly doubled the risk of developing Parkinson’s disease within 10 years of infection.
The researchers used mice that had been genetically modified to express the human ACE-2 receptor, which the SARS-CoV-2 virus uses to gain access to the cells in our airways. These mice were infected with SARS-CoV-2 and then given time to recover.
A month after the surviving animals had recovered, one group was given a low dose of MPTP that would not normally cause neuron loss. Saline was given to the control group. The brains of the animals were examined two weeks later.
The researchers discovered that Covid-19 infection had no effect on dopaminergic neurons in the basal ganglia on its own. Mice given a low dose of MPTP after recovering from infection, on the other hand, displayed the classic pattern of neuron loss seen in Parkinson’s disease.
This increased sensitivity following Covid-19 infection was similar to what was observed in the influenza study, implying that both viruses could cause an equivalent increase in risk of developing Parkinson’s.
“We consider a’multi-hit’ hypothesis for Parkinson’s disease – the virus does not kill the neurons, but it does make them more vulnerable to a’second hit,’ such as a toxin or bacteria, or even an underlying genetic mutation,” Smeyne explained.
“It is too early to say whether we would see the same thing in humans,” he cautioned.
