AD is the most common dementia, affecting over 944,000 people in the UK.
Researchers from the University of Sheffield’s Institute of Translational Neuroscience (SITraN) and scientists from the UK Dementia Research Institute, Cambridge, have uncovered how a protein interaction hallmark of Alzheimer’s disease (AD) increases the risk of developing AD.
Published in a journal NatureThe findings of this study open up the possibility of new therapeutic approaches to treat neurological diseases.
More than 944,000 people in the UK are affected by dementia, a general term that describes impairment of a person’s ability to think, remember or make everyday decisions.
AD, currently the most common form of dementia in the UK, is caused by a buildup of proteins in the brain that impairs the ability of brain cells to pass messages.
Scientists have investigated how two fundamental processes in Alzheimer’s disease are linked: how the inherited apolipoprotein E (APOE) gene is linked to the development of the disease by regulating the accumulation of amyloid beta.
Currently, APOE, the most common risk gene associated with neurodegenerative diseases, has three common forms, APOE2, APOE3, and APOE4, which are significantly increased in AD and are carried by two in five AD patients.
The team found that all forms of the APOE gene interact with amyloid-β during the early stages of its accumulation, but the high-risk APOE4 variant makes amyloid-β more harmful to neurons and accelerates its accumulation compared to other variants of the gene.
“We have identified a specific target: APOE4-Aβ co-aggregates or clumps. By focusing on removing these clumps, we may be able to reduce the damage that Aβ causes to brain cells, promote the clearance of toxic Aβ and slow its accumulation,” explained Dr Suman De, from SITraN at the University of Sheffield.
Selectively removing the harmful amyloid clumps that APOE4 interacts with could reduce neuronal loss and accelerate the clearance of amyloid from the brain, opening up the possibility of new therapeutic approaches to combat AD.
