Understanding how to prevent the build-up of toxic tau in cell models

Research project: Cellular control of seeded protein aggregation by interferon-stimulated genes.

Lead Investigator: Dr Will McEwan 

  • Institution: University of Cambridge
  • Grant type: PhD Studentship
  • Duration: 36 months
  • Amount: ÂŁ85,000

Why did we fund this research?

Comments from our Research Network volunteers:

Great to see work on 'stopping' tau leading from the study of the role of interferon and viruses and with a clear long term possibility of identifying targets for future drug treatment.

Project summary

In Alzheimer’s disease there is a build-up of two proteins that researchers believe play a role in the the death of nerve cells in the brain – amyloid and tau.

When a cell is attacked by a virus it releases a substance called interferon. Interestingly this research team found that interferon prevents the build-up of tau and during this project want to understand more about how and why this takes place and if this might be the key to a new treatment for Alzheimer's disease.

The background 

The human body is made up of 30 trillion cells who must communicate with each other in order grow, survive and respond to new situations. 

When a virus tries to infect a cell, that cell will respond by producing a substance called interferon, which it uses to communicate to its neighbouring cells that a threat has been detected. This interferon signal allows neighbouring cells to act to prevent further virus replication. 

In Alzheimer’s disease there is a build-up of two toxic proteins, amyloid and tau. This research team have discovered that this interferon signal causes cells to enter a state where the build-up of tau is inhibited.

What does this project involve?

In this project Dr McEwan will aim to understand exactly how and why interferon stops and protects against the build-up of tau. 

The team will collaborate with virologists at the University of Glasgow to investigate around 1,200 genes which could contribute to this protection against tau in cell models. Once they have identified the genes that appear to be protective they will study these genes in greater details to understand exactly how they prevent the build-up of tau and how relevant this might be to dementia.

How will this project help people with dementia?

This project will give the research team a comprehensive understanding of the role interferon in preventing the build-up of toxic tau in Alzheimer’s disease.

This knowledge could pave the way for this research team and others in the field to identify new drug targets for treatments in the future. 

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