Investigating how to clear toxic amyloid protein from the brain in Alzheimer’s disease
Research project: Understanding the molecular basis of Amyloid beta peptide interaction by neprilysin in Alzheimer’s disease.
Lead Investigator: Professor K. Ravi Acharya
- Institution: University of Bath
- Grant type: PhD Studentship
- Duration: 36 months
- Amount: £84,900
Why did we fund this research?
Comment from one of our Research Network volunteers:
'Any research aiming to reduce the build-up of toxic amyloid plaques in the brain has to be given top priority.'
Alzheimer’s disease is characterised by build ups or plaques of a toxic protein called amyloid beta, which causes the brain cells to get sick and die.
This project will investigate a special protein or enzyme called neprilysin to understand how it breaks down amyloid beta protein in the healthy brain.
Understanding how to target parts of the brain cell that break down amyloid beta is one strategy researchers can use to develop new treatments for Alzheimer’s disease.
A hallmark of Alzheimer’s disease is the build-up of toxic proteins in the brain. One of these proteins, known as amyloid beta, clumps together to form plaques, causing brain cells to die.
In the healthy brain, the amyloid beta proteins are broken down by enzymes, stopping them from building up in the brain. This mechanism is thought to protect our brains and prevent a decline in cognitive function.
Previous research has studied mouse models with lower levels of these enzymes. These mice have higher levels of the amyloid beta proteins and an increased risk of developing Alzheimer’s disease.
What does this project involve?
This project will build on our understanding of one of these enzymes, known as neprilysin. Professor Acharya and his team will use several biochemistry and molecular laboratory techniques to gain an in-depth understanding of how the neprilysin enzyme breaks down amyloid beta.
The researchers will also produce altered forms of the enzyme, with the aim of identifying a form which degrades amyloid beta more efficiently.
How will this project help people with dementia?
There is a well-established link between amyloid beta accumulation and the progression of Alzheimer’s disease. One strategy for designing new treatments for Alzheimer’s disease is developing drugs that target amyloid beta and cause it to be broken down.
By investigating how the enzyme neprilysin breaks down amyloid beta protein, this research study could lead discover a new drug target to reduce amyloid beta levels in the brain. It is hoped that by reducing amyloid beta protein build ups, treatments may be able to slow down the progression of Alzheimer’s disease.