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A study from the University of Twente (The Netherlands) has shown that, at least in the test tube, the protein N of the SARS-CoV-2 interacts with a neuronal protein called α-synuclein and accelerates the formation of amyloid fibrils, bundles of pathological proteins that are implicated in the disease of Parkinson.
In addition to respiratory symptoms, SARS-CoV-2 can cause neurological problems, such as loss of smell, headaches, and “brain fog.” However, it remains controversial whether these symptoms are caused by the virus entering the brain or, on the contrary, are caused by chemical signals released in the brain by the immune system in response to the virus.
In Parkinson’s disease, a protein called a-sinucleina forms abnormal amyloid fibrils, leading to the death of dopamine-producing neurons in the brain.
Interestingly, the loss of smell it is a common premotor symptom in Parkinson’s disease.
This fact, as well as the Parkinson’s cases in patients with Covid-19, made scientists Christian Blum, Mireille Claessens and their colleagues wonder if the protein components of SARS-CoV-2 could trigger the aggregation of α-synuclein in amyloid. .
They decided to study the two most abundant proteins in the virus: the spike protein (S-), which helps SARS-CoV-2 enter cells, and the nucleocapsid protein (N-), which encapsulates the genome of RNA within the virus.
In experiments in test tubes, published in the journal ACS Chemical Neuroscience, the researchers used a fluorescent probe that binds to amyloid fibrils to show that, in the absence of coronavirus proteins, α-synuclein needed more than 240 hours to aggregate into fibrils. The addition of protein S had no effect, but protein N reduced aggregation time to less than 24 hours.
In other experiments, the team showed that the N and α-synuclein proteins interact directly, in part through their opposing electrostatic charges, with at least 3-4 copies of α-synuclein attached to each N protein.
The researchers then injected protein N and fluorescently labeled α-synuclein into a cellular model of Parkinson’s disease, using a concentration of protein N similar to that expected within a SARS-CoV-infected cell. two.
Compared to control cells injected with α-synuclein only, approximately twice as many cells died when injecting both proteins. Furthermore, the distribution of α-synuclein was altered in cells coinjected with both proteins, and elongated structures were observed, although the researchers could not confirm that they were amyloid.
It is unknown if these interactions also occur within neurons in the human brain, but if so, they could help explain the possible link between Covid-19 infection and Parkinson’s disease.
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