Despite the rapid rise of Alzheimer's disease - the Alzheimer's Association predicts as many as 7.7 million cases by 2030 - there are no preventative treatments available, few in the pharmaceutical pipeline, and those drugs being developed all share the same two molecular targets.
Now Rockefeller University researchers report that by targeting a different molecule, a blood-clotting protein called fibrin, they could reduce inflammation in the brains of mice with different models of the disease.
Even as people with Alzheimer's disease begin to lose bits of themselves, their brains are gathering material. Misfolded beta-amyloid (Aâ) proteins build up, coalescing into dense plaques; another misformed protein, tau, aggregates inside neurons and causes visible neurofibrillary tangles. These two
proteins have garnered the most attention and are at the center of most therapeutic research. But in research published this month in the Journal of Experimental Medicine, graduate student Justin Paul and research professor Sidney Strickland, head of the Laboratory of Neurobiology and Genetics, show that a previously unexplored finding - that brains of Alzheimer's patients have increased fibrin levels - could prove a potent method of attack.
Scientists have known for years that Alzheimer's damages the barrier that prevents blood from seeping into the brain, damage that lets fibrin and other blood proteins leak through. But it was a correlation that had gone largely unexamined. So Paul, Strickland and Jerry Melchor, a former postdoc in the lab, first looked at whether there was a correlation between fibrin and Aâ build-up in the brains of three different mouse models of Alzheimer's. Sure enough, as Aâ accumulated, so did fibrin.