Evidence is mounting of a link between Covid-19 and the risk of Parkinson’s disease

A few years after the outbreak of the Spanish flu ended in 1918, doctors around the world began noticing an increase in cases of Parkinson’s disease. This link between viral infection and the risk of developing Parkinson’s disease continues to baffle scientists today. What is clear, however, is that contact is not only limited to the H1N1 influenza virus that caused the 1918 Spanish Flu pandemic. Various other viral infections have been linked to a risk of developing Parkinson’s disease. The researchers have now found new evidence that this association is also present in the case of SARS-CoV-2.

The relationship between viral infection and the risk of developing Parkinson’s disease

Already at the beginning of 2020, when the new coronavirus began to keep the world on guard, scientists warned of an increase in neurodegenerative diseases in the coming years. About five years after the 1918 pandemic, the diagnosis of Parkinson’s disease has nearly tripled. If you look at the characteristics of the SARS-CoV-2 virus, you can expect tens of millions of additional Parkinson’s diagnoses in the next 10 years.

In a new study, researchers at Thomas Jefferson University and New York University attempted to discover to what extent SARS-CoV-2 affects an individual’s risk of developing Parkinson’s disease. According to Richard Smein, the study’s first author, the current most likely hypothesis is that viral infection does not directly lead to neurodegenerative diseases, but rather makes the brain more susceptible to other risk factors that can lead to such diseases. “We’re considering the ‘multiple hit’ hypothesis of Parkinson’s disease – the virus itself doesn’t kill the neurons, but makes them more susceptible to a ‘second hit’, such as a toxin, bacteria or even an underlying genetic mutation.Sameen said.

Targeting SARS-CoV-2

In a previous study, Smeyne found that mice infected with H1N1 were more likely to develop symptoms when exposed to the molecule MPTP, which is used in animal models to induce Parkinson’s-like neurodegeneration.

In the new study, researchers examined a new mouse model in which the animals possess specific human receptors that allow them to be infected with SARS-CoV-2. The animals were exposed to a dose of virus roughly equivalent to a mild Covid-19 infection in humans. Then the animals had the opportunity to recover from the acute infection. A month later, mice were injected with a small dose of MPTP. This dose was so low that the healthy animals in the control group showed no neuronal degeneration.

However, in the group infected with SARS-CoV-2, this dose was sufficient to cause neuronal damage roughly consistent with degeneration in the case of Parkinson’s disease.

The connection is not clearly established

The the study shows a possible connection between SARS-CoV-2 infection, but could not explain how this connection occurred. In general, it is still debated whether the neurological symptoms associated with the novel coronavirus are a direct result of the virus’ action in brain cells.

Previous studies of H1N1 found that the virus does not directly affect neurons in the central nervous system, but does increase the risk of developing Parkinson’s disease. In the new study, researchers found increased levels of so-called microglia in the basal ganglia of mice infected with the coronavirus. These are immune cells in the brain that can cause damage when they are abnormally active.

So Smeyne and colleagues hypothesize that virus-induced brain cell responses make cells more vulnerable to future attacks, increasing the risk of developing Parkinson’s disease. However, researchers are still hesitant when it comes to transferring these findings to humans. “First of all, this is a preclinical work. It is too early to say whether we will see the same in humans, given that there appears to be a 5-10 year period between any changes in clinical manifestations of Parkinson’s disease in humans. If COVID-19 turns out to increase the risk of developing Parkinson’s disease, it will be a huge burden on our society and our health care system. But we can anticipate this challenge by enhancing our knowledge of potential “second outcomes” and mitigation strategiesSameen said.

via Thomas Jefferson University

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