14 DAY TRIAL // In a new investigation conducted on unsuspecting lab mice, researchers have determined that the proteins largely responsible for forming plaques in the brains of people suffering from Alzheimer's diseases may in fact originate in the liver, not the brain.
These findings have important implications for the way research scientists look at the condition. This affliction makes life miserable for about 280 million people worldwide, and any breakthrough in understanding or treating it could have far-reaching implications.
Researchers with the new study say that the protein, called beta-amyloid, may constitute a new target for a future anti-Alzheimer drug. Stopping the liver from producing the molecule would safeguard the brain from the dangers of developing plaques.
In the animal experiments, scientists used a novel drug, that they designed in such a manner it could not exceed the blood-brain barrier. This is a natural obstacle preventing chemicals and microorganisms from passing through to our brains.
The new chemical proved effective at reducing beta amyloid levels, both in the bloodstream and in the brain. This achievement implied that the protein was not produced in the brain. If it were, then the drug would have not affected its concentrations.
Even the science team, which is based at the Scripps Research Institute, in La Jolla, California, was surprised by the discovery. “Everybody has assumed that it’s the amyloid that originates in the brain that causes the brain disorder,” SRI researcher Greg Sutcliffe explains.
“Had I not seen the data, I would have scoffed at the idea that it might come from someplace else. I think it's possible to foresee a day not too far away when Alzheimer's becomes completely preventable,” the expert goes on to say.
The chief medical and scientific officer at the Alzheimer's Association, William Thies, commented that the new finding is a starting point, but that more research is needed to validate the discoveries.
He says that scientists need to determine whether beta-amyloid concentrations produced in the liver are enough to cause Alzheimer's, and whether inhibiting production of this molecule could indeed have a preventable effect on the neurodegenerative disease.
“It may or may not be sufficient to contribute to or allow us a therapeutic pathway for Alzheimer's disease,” explains Thies, quoted by LiveScience.
But the SRI team says its research is solid. “The genetics say that it’s the amyloid that’s produced outside of the brain that's causing the accumulation,” Sutcliffe argues.