Some viral infections can potentially trigger neurodegenerative diseases, according to researchers from the German Center for Neurodegenerative Diseases.

In a paper published in the journal Nature Communications, the researchers have revealed that molecules within certain viruses can spread protein aggregates between cells, which can trigger diseases such as Alzheimer’s.

The research provides fresh insights into how chronic viral infections can cause Neurodegeneration.

Misfolded protein aggregates occur in diseases such as Creutzfeldt-Jakob disease, which are called prion diseases. These diseases can transfer between cells and corrupt the proteins in healthy cells. This helps the disease to rapidly spread within the brain, in a similar phenomenon exhibited by both Parkinson’s and Alzheimer’s diseases.

The researchers say the protein aggregates could transmit between individual cells or when they are released “naked” into extracellular space, or through vesicles, the communication bubbles used by cells.

“The precise mechanisms of transmission are unknown”, said Ina Vorberg, co-author of the paper, and a professor at the University of Bonn, in the press release. “However, it is an obvious guess, that aggregate exchange by both direct cell contact and via vesicles depends on ligand-receptor interactions. This is because, in both scenarios, membranes need to make contact and fuse. This is facilitated when ligands are present that bind to receptors on the cell surface and then cause the two membranes to fuse.”

The researchers mimicked the results of a viral infection by inducing cells to produce protein usually released during a viral infection that targets cell binding and membrane fusion. The spike protein from the SARS-CoV-2 virus and the glycoprotein VSV-G from the vesicular stomatitis virus was chosen for the experiment.

The researchers found that the presence of these viral proteins increased the spread of protein aggregates between cells through cellular membranes and extracellular vesicles.

Although the researcher’s model does not replicate all the different aspects of the brain and its specialized cells, the experiment did produce the protein aggregates that clearly increased the spread of misfolded proteins into other, healthy cells.

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