

LA JOLLA, Calif., March 4 (UPI) -- The liver, not the brain, may be the source of the amyloid that deposits as brain plaques associated with Alzheimer's disease, U.S. researchers suggest.
Study leader Greg Sutcliffe of Scripps Research Institute and colleagues at ModGene LLC described the findings as "unexpected" and said they could completely alter scientists' ideas about Alzheimer's disease.
Sutcliffe said the researchers used a mouse model for Alzheimer's disease to identify genes that influence the amount of amyloid that accumulates in the brain and they found three genes that protected mice from brain amyloid accumulation and deposition.
The study, published online in The Journal of Neuroscience Research, found one of the genes that encodes presenilin -- a cell membrane protein believed to contribute to the development of human Alzheimer's -- was produced in the liver.
"The product of that gene, called Presenilin2, is part of an enzyme complex involved in the generation of pathogenic beta amyloid," Sutcliffe said in a statement. "Unexpectedly, heritable expression of Presenilin2 was found in the liver but not in the brain. Higher expression of Presenilin2 in the liver correlated with greater accumulation of beta amyloid in the brain and development of Alzheimer's-like pathology."
The finding suggests significant concentrations of beta amyloid might originate in the liver, circulate in the blood and enter the brain, the study said.
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