After the 1918 Spanish Flu pandemic, physicians started to see an increase in new cases of Parkinson's disease. Doctors encountered this phenomenon worldwide. Five years after the 1918 pandemic ended, new Parkinson's patients nearly tripled.
However, the relationship isn't limited to the virus behind the 1918 pandemic. Other viral infections have increased Parkinson's risk, from Japanese encephalitis to HIV. The link between viral infection and increased Parkinson's risk remains a puzzle for scientists.
Well-known phenomenon
Clinicians and scientists are familiar with the neurological consequences of a viral infection. For example:
…following the 1918 influenza pandemic, it took almost a decade for patients to present with the neurological syndrome called "post-encephalic parkinsonism." —Thomas Jefferson University, Philadelphia PA
What about COVID-19 and new cases of Parkinson's in the future? In 2020, scientists warned of a possible future spike in neurodegenerative disease. Given the way COVID-19 engulfed the world, it could lead to "tens of millions of extra diagnoses over the coming decade."
Parkinson's and the multi-hit hypothesis
A new study from researchers at Thomas Jefferson University and New York University attempts to uncover how COVID-19 could increase the risk of Parkinson's. Richard Smeyne, the lead author of the study, said the most common explanation is called the multi-hit hypothesis.
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," —Richard Smeyne, Thomas Jefferson University
In other words, a viral infection doesn't directly cause neurodegenerative disease; it makes the brain more open to other risk factors that can trigger the disease.
The new research used mice with human receptors, which allowed them to be infected with corona-virus disease, the equivalent of a mild COVID-19 infection in humans. After the mice fully recovered, they were injected with a tiny dose of a drug-like neurotoxin MPTP that causes Parkinson's.
The uninfected control mice not exposed to corona-virus disease didn't have any neuron damage. But the mice exposed to the coronavirus showed neuron damage similar to Parkinson's disease (increased amounts of microglia in the basal ganglia).
Early research leads to better planning
Dr. Smeyne says it's way too soon to say this will happen to humans.
First of all, this is preclinical work," Smeyne noted. "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.
Thanks to Dr. Smeyne and his colleagues, researchers can now better anticipate this potential challenge with more research to find solutions.
And for the rest of us, another reason to follow COVID-19 precautions and get vaccinated.
