Red Wine and Green tea Polyphenols: Blocking Beta Amyloid

One of the principle ways in which Alzheimer's disease causes destruction in the brain is via accumulation of beta amyloid proteins. It is the presence of these proteins (via several different methods) that results in the death of neurons. New research sheds light on one of the possible pathways by which beta amyloid causes Alzheimer's disease. This study also demonstrates that the polyphenols found in green tea and red wine may be able block this particular pathway.

The study from the Journal of Biological Chemistry (1) demonstrated in a cellular model how the beta amyloid present outside of neurons could bind with surface receptors in order to be drawn into the cell. The continuous internalization of  beta amyloid results in functional deficits and eventually the death of the neuron. This perpetuates a positive feedback loop that leads to disease as explained in my previous post "Why Alzheimer's Disease happens: Targets for slowing, stopping and reversing Alzheimer's disease."

In addition to analysing the process of beta amyloid binding and internalization, the study also examined what would happen if green tea (EGCG) or red wine (resveratrol) extracts were added in with the beta amyloid and neurons. The results demonstrated that EGCG and resveratrol could bind to and change the configuration of the beta amyloid protein. This had the effect of reducing the ability of the beta amyloid to bind to the neuron surface and become internalized. In essence these extracts removed beta amyloid toxicity.

The anti-alzheimer's effects of green tea have been talked about already here, here and here. This study advances our understanding of how it may interact with beta amyloid. Resveratrol has not been covered in this blog but is now an exciting prospect for further comment. As usual though this study was only conducted in cells in the lab. Whether EGCG and resveratrol actually have this effect within the human brain will not be known until tests to examine this are conducted.

1. Prion protein-mediated toxicity of amyloid-β oligomers requires lipid rafts and the transmembrane LRP1. Jo V. Rushworth, Heledd H. Griffiths, Nicole T. Watt and Nigel M. Hooper. (2013) Journal of Biological Chemistry