In a recent study conducted by the scientists at Thomas Jefferson University and New York University, they have tried to understand how SARS-CoV-2 could increase a person’s risk of Parkinson’s disease. According to reports, a few years after the 1918 Spanish Flu pandemic doctors around the world began to notice an increase in new Parkinson’s disease cases. Researchers claim that a variety of other viral infections have been linked to increased Parkinson’s risk, from Japanese encephalitis to HIV.
When the ongoing coronavirus pandemic began in 2020, several scientists had warned of a potential spike in neurodegenerative disease in the coming years. Around five years after the 1918 pandemic new Parkinson’s diagnoses had almost tripled, and considering how pervasive COVID-19 infections have been even just a mild increase in Parkinson’s cases could lead to tens of millions of extra diagnoses over the coming decade.
Richard Smeyne, first author of the study, said that the most common explanation is called the “multi-hit hypothesis.” According to Smeyne, a viral infection doesn’t directly cause neurodegenerative disease, but instead, it makes the brain more susceptible to other risk factors that can trigger the disease. The findings of the new study was published in the journal Movement Disorders.
“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,” said Smeyne.
In this new research, the scientists engineered a novel mouse model, with certain human receptors to allow it to be infected with SARS-CoV-2. Later, the animals were exposed to a dose of the virus that corresponded with a mild COVID-19 infection in humans.
“The animals were allowed to recover from the acute viral infection, and then about one month later were injected with a small dose of MPTP. The dose of MPTP was so low that healthy control mice not exposed to SARS-CoV-2 did not display any neuron damage. However, in the animals exposed to the coronavirus, the MPTP was enough to trigger a pattern of neuron damage in the basal ganglia similar to what is seen in Parkinson’s disease. The animals exposed to SARS-CoV-2 were as sensitive to MPTP damage as those animals in the prior H1N1 study,” the scientists stated.
Moreover, some scientists have found traces of SARS-CoV-2 in human brains but it’s unclear whether this is what could be causing issues such as the brain fog or cognitive decline associated with COVID-19. The scientists discovered an increased volume of microglia in the basal ganglia of the coronavirus-infected mice. Microglia are a type of brain immune cell than can cause damage when they are abnormally activated.
“First of all, this is preclinical work. It is too soon to say whether we would see the same thing in humans, given that there seems to a 5-10 year lag between any changes in clinical manifestation of Parkinson’s in humans. If it does turn out that COVID-19 increases the risk of Parkinson’s, it will be a major burden on our society and healthcare system. But we can anticipate that challenge by advancing our knowledge of potential ‘second hits’ and mitigating strategies,” Smeyne noted.