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expert reaction to study looking at how glycoproteins on the surface of viruses may aid spread of protein aggregates associated with neurodegenerative diseases

A study published in Nature Communications suggests that glycoproteins on the surface of viruses, which aid their entry into target cells, may facilitate the spread of protein aggregates associated with neurodegenerative diseases.


Dr Richard Oakley, Head of Research at Alzheimer’s Society said:

“This research highlights a potential interaction between a component of viruses and some of the abnormal proteins involved in the diseases causing dementia. This is really interesting research, but more work is needed before any conclusions can be made and any implications can be drawn.

“Previous research in the lab has suggested these proteins may spread between cells – this study suggests parts of viruses that help them infect cells might also make it easier for abnormal proteins to enter. This work has only been observed in cells in the lab, so we can’t currently say if this interaction happens in the human brain.

“What this research doesn’t tell us is whether having a viral infection impacts the development or progression of the diseases that cause dementia. More research will be needed to better understand the diseases underlying dementia and how viral infection might alter them.”


Dr Stephanie Fowler, Senior Research Fellow at the UK Dementia Research Institute, UCL, said:

“This is an exciting new study adding further evidence that viral infections may enhance the spread of toxic proteins in several neurodegenerative conditions, including Alzheimer’s disease. It also highlights the need to better understand which extracellular vesicle surface proteins are involved in controlling the cell-to-cell transfer of their pathogenic cargoes. If we can find ways to specifically target and disrupt these processes, new treatments could be developed to slow the progression of disease.”


Dr Susan Kohlhaas, Director of Research at Alzheimer’s Research UK, said:

“Diseases like Alzheimer’s are caused by a build-up of certain proteins in the brain, triggering a cascade of events that leads to damage to nerve cells and a subsequent decline in a person’s memory and thinking abilities.

“Previous research suggests that proteins associated with Alzheimer’s can spread through a person’s brain in a similar way to the prion protein responsible for Creutzfeldt-Jakob disease (CJD). Preventing these proteins from spreading through the brain could potentially stop a disease like Alzheimer’s in its tracks, so it is important that we understand the factors involved in their passing between cells.

“In this study, scientists showed that two virus related proteins, including the spike protein that allows the coronavirus to enter cells, aided the transmission of proteins between human brain cells. This study was done in experiments in a dish.

“While past research has suggested possible links between viruses and the diseases that cause dementia, this research suggests that viruses may open the door for Alzheimer’s-related proteins and allow them to enter cells.

“While this research is intriguing and carried out in several well-conducted experiments, we need to be careful how we interpret results of lab-based experiments. Further research is required to determine whether this could happen in the real-world context.

“Importantly this research is into transmission of proteins within the brain and not between people, and this study doesn’t show that COVID-19 causes diseases like Alzheimer’s.

“Early in the COVID-19 pandemic, people with dementia emerged as a group at particular risk of severe infection. While there are likely to be several reasons for this, this study raises the possibility that the virus could play a role in the progression of diseases like Alzheimer’s.

“Studying the long-term effects of COVID-19, including studying people who have long-COVID, will be essential in understanding the relationship between COVID-19 and dementia.

“Fundamental research like this is an important first step to understanding the development of diseases like Alzheimer’s and more research will be key to developing treatments against it.”


Dr Richard Stanton, Reader, Division of Infection & Immunity, School of Medicine, Cardiff University, said:

“The paper by Liu et al investigates novel ways by which extracellular vesicles carrying protein aggregates that are associated with neurodegenerative disease might spread within a person. They show that the presence of viral entry proteins in cells can result in those aggregate-containing vesicles spreading more easily between cells. This is an interesting phenomenon, however a large amount of additional work is required before it’s clear whether this mechanism is relevant in vivo. In particular, they only use cells expressing a single virus protein. In reality, cells would be infected with an entire virus, expressing many more viral proteins. This will significantly change how the cell generates and secretes extracellular vesicles. Furthermore, to be relevant in vivo, the virus would need to infect the exact cells where those aggregates were forming, so that it could cause them to be released, and lead to further spread of disease – we don’t currently know how likely that is. These lines of investigation will need to be followed up before we can understand whether this phenomenon might contribute to neurodegenerative disease in vivo.



‘Highly efficient intercellular spreading of protein misfolding mediated by viral ligand-receptor interactions’ by Shu Liu et al. was published in Nature Communications at 16:00 UK time on Tuesday 19 October.




Declared interests

Dr Stephanie Fowler:  “No conflicts of interest.”

Dr Susan Kohlhaas: “No conflicts.”

None others received.

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