The SARS-CoV-2 virus could increase the probability of the brain degeneration found in Parkinson’ disease, in keeping with a study in mice. COVID-19 patients commonly report symptoms such
as brain fog, headaches, and insomnia, complications which 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 influenza pandemic,they said.
The SARS-CoV-2 virus may increase the brain’s vulnerability to a toxin that triggers nerve cell death in Parkinson’s disease, according to a study published in the journal Movement Disorders.
“Although Parkinson’s disease is an uncommon disease that affects 2 per cent of the population over the age of 55, the increased risk isn’t necessarily cause for concern,” said research first author Richard Smeyne of Thomas Jefferson University in the United States.
“But understanding how coronavirus impacts the brain can help us prepare for the long-term consequences of this pandemic,”Richard J Smeyne said.
The study expands on prior findings from the Smeyne lab indicating that viruses can increase the susceptibility of brain cells or neurons to damage or death.
Researchers discovered that mice exposed to the H1N1 influenza strain that caused the 2009 flu pandemic were more susceptible to MPTP in that investigation.
MPTP is a toxin that has been linked to several of the hallmark symptoms of Parkinson’s disease, including the loss of dopamine-expressing neurons and increased inflammation in the basal ganglia, a brain region important for movement.
The current study used mice that had been genetically modified to express the human ACE-2 receptor, which is used by the SARS-Cov-2 virus to get access to cells in our airways.
These mice were infected with SARS-Cov-2 and then allowed to recover, the researchers said.
According to the researchers, the dosage applied in this research corresponds to a mild COVID-19 infection in humans, with roughly 80 per cent of infected mice surviving.
After the surviving mice had healed for 38 days, one group was given a low dose of MPTP that would not normally cause neuron loss.
The control group was given saline. The animals were sacrificed and their brains were examined two weeks later.
COVID-19 infection had no effect on dopaminergic neurons in the basal ganglia, according to the researchers.
After recovering from infection, mice given a low dose of MPTP showed the characteristic pattern of neuron loss seen in Parkinson’s disease.
This enhanced sensitivity following COVID-19 infection was equivalent to that shown in the influenza study, suggesting that both viruses may raise the risk of Parkinson’s disease in the same way.
“We think about a ‘multi-hit’ hypothesis for Parkinson’s – the virus itself does not 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,” Smeyne explained.
Both influenza and SARS-CoV2 have been found to cause a “cytokine storm” or an overproduction of pro-inflammatory chemicals.
These chemicals can pass through the blood-brain barrier and activate microglia, the brain’s immune cells.
The researchers discovered more activated microglia in the basal ganglia of mice who had recovered from SARS-CoV2 and had been given MPTP.
They suspect that more microglia inflame the basal ganglia and produce cellular stress, though the mechanism is unknown. This decreases the threshold of the neurons, allowing them to endure future stress.
“We were concerned about the long-term consequences of viral infection.” said Peter Schmidt, a neuroscientist from New York University in the US, who co-led the study.
The researchers want to see if vaccinations can help reduce the experimental increase in Parkinson’s disease pathology connected to prior SARS-COV-2 infection.
They’re also testing different virus types, as well as levels that correspond to milder human instances.