In people with Alzheimer's disease, Amyloid-beta sticks together to make amyloid fibrils which form plaques between neurons in the brain.
Scientists have designed a new protein that may act as an essential laboratory tool to help understand why nerve cells die in people diagnosed with Alzheimer’s.
The new protein which closely resembles the Amyloid-beta — proteins involved in Alzheimer’s disease — in size and shape, but contains two different amino acids, the building blocks that proteins are made up of.
These changes mean that the new protein does not form amyloid fibres or sticky clumps, and, unlike Amyloid-beta, is not toxic to nerve cells.
“Our study clearly shows that the aggregation of Amyloid-beta into bigger species is critical in its ability to kill cells,” said lead author Karen Marshall from the University of Sussex in Britain.
Further, stopping the protein aggregating in people with Alzheimer’s can slow down the progression symptoms of the disease, said the paper published in the journal Scientific Reports.
“We hope to work towards finding a strategy to do this (stop the protein) in the lab and reverse the damaging effects of toxic Amyloid-beta,” Marshall added.
In people with Alzheimer’s disease, Amyloid-beta sticks together to make amyloid fibrils which form plaques between neurons in the brain.
The build-up of these plaques causes brain cells to die, leading to the decline in mental skills of patients suffering from the disease.
Why this particular protein’s “stickiness” causes cells to die is not known yet, the researchers said.
“Understanding how the brain protein Amyloid-beta causes nerve cell death in Alzheimer’s patients is key if we are to find a cure for this disease,” Marshall said.
“This is a really exciting new tool that will contribute to research to uncover the causes for Alzheimer’s disease and enable tangible progress to be made towards finding targets for therapy,” noted Louise Serpell, Professor at the University of Sussex.