Reservatrol from Red Wine May Help Postpone the Onset of Alzheimer’s Disease
Abstracted by Susan Sweeny Johnson, PhD, Biochem, from “Resveratrol Promotes Clearance of Alzheimer’s Disease Amyloid-B-Peptides.” JBC Papers in Press, September 14, 2005, DOI 10.1074/jbc.M508246200. Posted August 25, 2008.
Lots of press has been given recently to the health benefits of moderate red wine or grape juice consumption. Some of the components of red wine and grape juice, specifically resveratrol, quercetin and catechin, are powerful antioxidants. Resveratrol, in particular, protects the nervous system (1) and reduces the risk of developing Alzheimer’s disease. (2,3)
Alzheimer’s disease is characterized by the formation of amyloid-B (AB) plaques or clumps in the brain. These AB plaques are an accumulation of AB peptide. These plaques can be caused by making too much AB, not being able to secrete AB from the cell, or failure to breakdown excess AB.
Researchers recently studied the effect of resveratrol on amyloid-B ( AB) production in mouse nerve cells to see just how resveratrol slows plaque formation. The researchers looked at how much AB was made by the cells with and without the three compounds, resveratrol, quercetin and catechin. They found that only resveratrol reduced the amount of AB made.
By doing various experiments, the research team was able to show that resveratrol did not prevent excretion of AB nor did it interfere with the enzymes that made it. They were able to show that resveratrol actually enhanced the natural breakdown of AB by a component of the cell called a proteasome.
Proteins in a cell are regularly broken down by enzymes called proteases so that worn out proteins can be removed and the building block amino acids can be recycled. Proteosomes are made of a bundle of proteases that look like a short stack of lifesavers with a gate at each end. The gate recognizes proteins tagged for degradation and lets them inside the tube where they are broken down to amino acids.
Once again, the fruit of the vine promotes healthy aging.
References:
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Pharmacol. 141, 997–1005. - Luchsinger, J. A., Tang, M. X., Siddiqui, M., Shea, S., and Mayeux, R. (2004) J. Am.
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