Researchers: Alzheimer's might start in the liver
Using mouse models for Alzheimer's disease, Scripps researchers evaluated the effect of three different genes on the presence of amyloid-beta plaques in the brain. To their surprise, they discovered that lower gene activity in the liver was associated with greater protection in the brain. One of those genes, called Presenilin2, is similar in both mice and humans. It is associated with increased production of amyloid-beta plaques in the liver, as well as early-onset Alzheimer's disease in humans, according to researchers.
Using a drug that prevents amyloid plaques created in the liver from entering the brain through the bloodstream, researchers were able to dramatically reduce the levels of amyloid-beta plaques in the brains of healthy mice. While more research is required, scientists speculate that humans may have a similar response to this method of treatment, which would make the treatment and prevention of Alzheimer's disease relatively simple. The study was published online in last Thursday's edition of The Journal of Neuroscience Research.