UCLA researchers report promising therapeutic approach for Alzheimer's disease
For decades, researchers have been trying, without success, to develop drugs that slow or prevent Alzheimer's disease. Now UCLA investigators suggest that these studies have the right target, but are missing the bulls-eye for Alzheimer’s disease. The target Alzheimer’s research is amyloid-beta; however, the UCLA scientists note that the substance is the correct protein to focus on, what is needed is to direct a drug to a very specific location, which they have discovered on that protein. They reported their findings in the January 23 issue of the Journal of Molecular Biology.
The researchers note that Alzheimer’s disease is the most common cause of late-life dementia and is thought to be caused by a protein known as the amyloid-beta protein, or Abeta, which clumps together in the brain, forming plaques that are thought to destroy neurons. This destruction has an early onset; it can presage clinical signs of the disease by up to 20 years. For decades, researchers have been trying, with limited success, to develop drugs that prevent this clumping. Such drugs require a “target,” a structure they can bind to, thereby preventing the toxic actions of Abeta.
UCLA neurology professor David Teplow and colleagues focused on a particular segment of a toxic form of Abeta and discovered a unique hairpin-like structure that facilitates clumping. “Every 68 seconds, someone in this country is diagnosed with Alzheimer’s,” noted senior author Dr. Teplow, the principal investigator of the NIH-sponsored Alzheimer’s Disease Research Center at UCLA. He added, “Alzheimer’s disease is the only one of the top 10 causes of death in America that cannot be prevented, cured or even slowed down once it begins. Most of the drugs that have been developed have either failed or only provide modest improvement of the symptoms. So finding a better pathway for these potential therapeutics is critical.”