Alzheimer's May Not Start in the Brain

Researchers at the University of British Columbia in Canada investigated sharing blood between mice with Alzheimer's and those without.

The neurons of the brain produce the amyloid-β protein in large amounts when a person has Alzheimer's, he said.

After a year, scientists found that the normal mouse had "contracted" Alzheimer's, presumably due to the spread of amyloid beta from its mutated twin.

The findings, published today in Molecular Psychiatry, offer hope that future drug therapies might be able to stop or slow the disease without acting directly on the brain, which is a complex, sensitive and often hard-to-reach target.

The article's senior authors, UBC's Weihong Song, Ph.D., and Chongqing's Yan-Jiang Wang, M.D., Ph.D., emphasized that the Aβ traveled from the genetically modified mice to the brains of their normal partners, where it accumulated and began to inflict damage.

'This study hints that a medical drink could slow the decline of thinking skills in people experiencing mild memory problems, who also have early signs of Alzheimer's disease on a brain scan or a lumbar puncture test.

That is, they surgically attached two mice-one healthy, one modified to carry a gene that produces high levels of amyloid beta-so they share the same blood supply.

The researchers suggest that this is the first proof that amyloid beta produced outside of the brain can in fact contribute to the disease. However, the global team of researchers from the University of British Columbia in Canada, along with colleagues in China's Third Military Medical University in Chongqing, believes that future therapies for Alzheimer's, a major precursor to dementia, may instead target other organs such as the liver or kidneys to provide a more effective treatment.

The normal mice also developed twisted protein strands or tangles that form inside brain cells, killing the brain cells along with other Alzheimer's-related damage including brain cell degeneration, microbleeds, inflammation and an impaired ability to transmit signals involved in learning and memory. Amyloid is created naturally in the blood and muscles, but in Alzheimer's patients it appears to build up in the brain and create "sticky" plaques that clump up and kill brain cells, the researchers wrote in a press release. Until now, scientists have generally believed that deposits of amyloid-beta found in the brain originate in the brain.

"Human study is tough", Song said. The hypothesis is that as we get older more amyloid beta crosses into the brain, amplifying the degenerative aspects of Alzheimer's.

Song, head of UBC's Townsend Family Laboratories, envisions a drug that would bind to amyloid-beta throughout the body, tagging it biochemically in such a way that the liver or kidneys could clear it.