Chemicals in green tea and red wine may block the brain damage caused by Alzheimer's disease, an early-stage study suggests.
Scientists targeted a process that allows harmful clumps of protein in the brain to kill off neurons.
Using purified extracts of the chemicals EGCG in green tea and resveratrol in red wine, they were able to stop nerve cells from being harmed. The findings, published in the Journal of Biological Chemistry, could pave the way for new drugs to treat Alzheimer's, say the researchers.
Lead scientist Professor Nigel Hooper, from the University of Leeds, said: "This is an important step in increasing our understanding of the cause and progression of Alzheimer's disease. 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-beta protein in the brain which clumps together to form toxic, sticky balls. The amyloid balls latch on to molecules called prions on the surface of nerve cells. As a result, the nerve cells start to malfunction and eventually die.
"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 Dr Jo Rushworth, another member of the Leeds team. "And, if so, we wanted to see if we could prevent the amyloid balls binding to prion by altering their shape, as this would stop the cells from dying."
Previous research had shown that the red wine and green tea compounds are able to reshape amyloid proteins. When they were added to amyloid balls in a test tube, the toxic clumps of protein no longer harmed human and animal brain cells.
"We saw that this was because their shape was distorted, so they could no longer bind to prion and disrupt cell function," said Prof Hooper. "We also showed, for the first time, that when amyloid balls stick to prion, it triggers the production of even more amyloid, in a deadly vicious cycle."
The next step for the team is to uncover exactly how the amyloid-prion interaction destroys neurons. Prof Hooper added: "I'm certain that this will increase our understanding of Alzheimer's disease even further, with the potential to reveal yet more drug targets."
Dr Simon Ridley, from the charity Alzheimer's Research UK which part-funded the study, said: "Understanding the causes of Alzheimer's is vital if we are to find a way of stopping the disease in its tracks. While these early-stage results should not be a signal for people to stock up on green tea and red wine, they could provide an important new lead in the search for new and effective treatments. With half a million people affected by Alzheimer's in the UK, we urgently need treatments that can halt the disease. That means it's crucial to invest in research to take results like these from the lab bench to the clinic."