Investigating how to clear toxic amyloid protein from the brain in Alzheimer’s disease
Award Type
PhD studentshipStatus / Stage
ActiveFunder(s)
Alzheimer's SocietyFunding Amount
£84,900.00Funder/Grant study page
Alzheimer's SocietyContracted Centre
University of BathPrincipal Investigator
Professor K. Ravi AcharyaPI Contact
K.R.Acharya@bath.ac.ukWHO Catergories
Understanding Underlying DiseaseDisease Type
Alzheimer's Disease (AD)CPEC Review Info
| Reference ID | 41 |
|---|---|
| Researcher | Reside Team |
| Published | 12/06/2023 |
Data
| Status / Stage | Active |
|---|---|
| Funder/Grant study page | Alzheimer's Society |
| Contracted Centre | University of Bath |
| Funding Amount | £84,900.00 |
Abstract
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. 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.
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.
Aims
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.