Cholesterol is a waxy, fat-like substance processed in the liver and other cells. It is necessary for the body to function properly, and needed for the digestion of dietary fats, the building of cell walls and the production of vitamins and hormones. Too much cholesterol leads to a thick, hard deposit build up in the arteries called plaque. The results of too much plaque are narrow arteries that constrict the flow of blood to other parts of the body, and leads to the development of fatty liver and heart disease. A recent study, published in the March 3, 2011 edition of the Journal of Neuroscience, says this plaque build up travels to the brain, and could be the root cause of Alzheimer’s disease.
The Alzheimer’s Association states that nearly half of all Americans 85 years and older have Alzheimer’s disease, and almost 5.1 million Americans are believed to be directly affected by the disease. They believe that figure will rise from 11-16 million people aged 65 and over within the next half century if effective treatments and preventative measures are not found and taken.
In the study, laboratory mice were used to find out which genes influenced amyloid build-up in the brain. They were able to ascertain that three genes were found to protect the mice from the deposits, and lesser amounts of each of these genes reside in the liver, indicated some degree of protection for the brain. One of them is presenilin, also found in the membrane of cells that are believed to promote Alzheimer’s in humans.
Researchers built upon their previous works of large quantities of information to identify the appropriate genes and the identities of inherited modifiers. One gene in the mouse, Presenilin2, is among a group of enzymes involved in generating pathogenic beta amyloids. In addition, Presenilin2 is linked to a gene know to predispose some humans to Alzheimer’s early-onset. They explained that “heritable expression of Presenilin2 was found in the liver but not in the brain, and higher expression of Presenilin2 in the liver correlated with a larger accumulation of beta-amyloid in the brain, and development of Alzheimer’s-like pathology.”
They believe the production of beta-amyloid begins in the liver, and not in the brain, as previously thought, and then transported through the bloodstream. This may change the direction research is being conducted on Alzheimer’s and other forms of dementia. If they are able to get the same results, clinical trials will begin on qualified human candidates to learn more about the production of beta-amyloid in the liver.
This is Ron White, two-time USA Memory Champion. This research looks promising in finding the real source of the development of Alzheimer’s and other forms of memory loss. I will continue to keep you informed as to their progress.
MemoryZine.com – Amyloid Deposits In Alzheimer’s Brain Plaques Begin In The Liver: http://memoryzine.com/2011/03/09/amyloid-deposits-in-alzheimers-brain-plaques-begin-in-the-liver/#comment-514
Journal of Neuroscience — March 3, 2011, DOI: 10.1002/jnr.22603
LiverSupport.com – Simultaneous Support of Heart and Liver Health: http://www.liversupport.com/wordpress/2011/09/simultaneous-support-of-heart-and-liver-health/