Alzheimer’s hope in form of wine and tea
15 Mar 2013 by qwbdchbctt.d qwbdchbctt.d
Substances found in green tea and red wine may disrupt a key step of the Alzheimer’s disease pathways, according to researchers at the University of Leeds.
The scientists, whose findings are published in the Journal of Biological Chemistry, identified the process which allows harmful clumps of protein to latch onto neurons, causing their death. They were then able to disrupt the pathway using purified extracts of Epigallocatechin gallate (EGCG) from green tea and resveratrol from red wine.
“This is an important step in increasing our understanding of the cause and progression of Alzheimer’s disease,” said lead researcher Professor Nigel Hooper of the University’s Faculty of Biological Sciences. “It’s a misconception that Alzheimer’s is a natural part of ageing; it’s a disease that we believe can ultimately be cured through finding new opportunities for drug targets like this.”
Alzheimer’s is characterised by a build-up of amyloid protein tangles in the brain. These amyloid oligomers latch onto the surface of neurons by attaching to prion proteins on the cell surface.
“The prion protein is a key receptor on the nerve cell surface for amyloid. Binding of the amyloid to prion activates a series of reactions in the cell which ultimately can lead to cell death,” Hooper told Laboratory News.
The researchers formed amyloid oligomers in a test tube and added them to cultures of human and animal neurons. When the team added the extracts from red wine and green tea, the amyloid balls became distorted in shape and could no longer disrupt cell function.
“We wanted to investigate whether the precise shape of the amyloid balls is essential for them to attach to the prion receptors, like the way a baseball fits snugly into its glove,” said co-author Dr Jo Rushworth.
The team also discovered that when amyloid balls stick to prion, it triggers the production of even more amyloid in a vicious cycle.
The next stages of the research are to understand exactly how the amyloid-prion interaction triggers neuronal cell death.
“I’m certain that this will increase our understanding of Alzheimer’s disease even further, with the potential to reveal yet more drug targets,” said Hooper.
