Neurodegeneration through viral infections? Healing practice

Does viral infection accelerate brain degeneration?

According to a recent study, viral infections appear to lead to brain regression, a process known in medicine as neurodegeneration. The results of the study provide evidence that acute or chronic viral diseases are involved in the development of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s.

Results of the current study by researchers at the German Center for Neurodegenerative Diseases eV (DZNE) indicate that some viral diseases contribute to neurodegeneration. In laboratory experiments, the team showed that viral particles contribute to the diffusion of small protein particles, so-called protein clusters, into the space between cells. These aggregates are typical markers of neurodegenerative diseases. The results of the research were recently published in the famous specialized journal “Nature Connections” Foot.

When proteins become pathogens

The working group explains that so-called prion diseases such as Creutzfeldt-Jakob disease are also caused by clumps of faulty proteins. Small molecules of defective proteins have the ability to move from one cell to another and there pass their abnormal shape to proteins of the same type. This is how the disease spreads in the brain.

A similar effect is hypothesized for neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s, as these diseases also lead to the accumulation of abnormal proteins. “The exact mechanisms by which it spreads are unknown,” confirms professor and research group leader Ina Vorberg. However, it is clearly hypothesized that the transport of aggregates is via mechanisms similar to those in prion diseases.

How are protein aggregates spread?

Researchers believe that the exchange of aggregates occurs either through direct cellular contact, through the release of aggregates into the spaces between cells, or through the passage of so-called vesicles. Vesicles are small vesicles surrounded by a fatty shell that are released for intercellular communication.

According to the team, the most obvious assumption is that “transportation of cumulus occurs with both direct cellular contact and via vesicles.” The reason for the assumption is the so-called ligand-receptor interactions. Bonding is a molecule that activates or deactivates a receptor by binding.

“In both scenarios, the membranes have to touch and fuse with each other. This is easier if there are ligands that bind to the receptors on the cell surface and then cause the two membranes to fuse,” explains the scientist.

What does this process have to do with viruses?

The working group conducted a wide series of experiments with different cell cultures in order to better understand the distribution of the aggregates. To do this, the researchers examined the intracellular transport of prions or pools of tau proteins, which are typical of Alzheimer’s disease. It turns out that some viral proteins, including the SARS-CoV-2 barbed S protein, promote the proliferation of protein clumps.

We have been able to show that viral proteins are embedded in the cell membrane as well as in extracellular vesicles. Their presence significantly increased the spread of protein clumps between cells, both through direct cellular contact and through extracellular vesicles, Furberg summarizes the results.

Viruses act as smugglers for dangerous goods

The viral proteins ensured “effective transduction” or “effective delivery of the assemblies to recipient cells,” according to the study leader. As a result, the harmful aggregate was transferred to the new cell. Viral links acted “like switches that open recipient cells and thus escape dangerous goods.”

The limits of the study

“Our cellular models certainly do not depict many aspects of the brain with highly specialized cell types,” the professor notes. However, the study shows that viral ligands can contribute to the increased spread of denatured proteins between cells, regardless of cell type. “Overall, our data suggest that viral ligand-receptor interactions can in principle influence the transmission of pathogenic proteins,” summarizes Voorberg.

Do viruses increase the risk of developing neurodegenerative diseases?

“With neurodegenerative diseases, sometimes certain viruses can be found in the patient’s brain,” the expert explains. So far it has been assumed that these viruses cause inflammatory or toxic reactions and thus accelerate neurodegenerative changes.

The current study opens up another possible view of the processes: “Viral proteins can increase the intracellular spread of protein clusters, which is already underway in neurodegenerative diseases such as Alzheimer’s,” suspects Voorberg. The researchers now want to examine the processes more closely with viruses that attack the nervous system. (FP)