Finding: Scientists from Scripps Research Institute and ModGene, LLC, have made an astonishing discovery that the liver is a source of beta-amyloid protein that forms plaques in the Alzheimer’s disease brain. The researchers treated a presenilin2 mouse model of Alzheimer’s with imatinib (trade name Gleevec, an FDA-approved cancer drug). They found beta-amyloid was reduced not only in the blood, but also in the brain where the drug cannot go. These results may explain why higher expression of presenilin2 in the liver correlates with higher amounts of beta-amyloid deposits in the brain of people with Alzheimer’s disease.
Relevance: These researchers have proposed that Alzheimer’s isn’t just a brain disease, but that it involves contributions from other parts of the body, including the liver. The drug used in this study, Gleevec, is already approved for treating cancer, which will help to accelerate its use in future clinical trials.