Scientists believe that utilizing biomarkers will offer potential for early detection of Alzheimer's.
One study being presented at the International Conference on Alzheimer's Disease (ICAD) in Chicago found that differences in levels of CD-69, a protein involved in white blood cell growth and production, allowed researchers to distinguish between people with Alzheimer's, people with Parkinson's-related dementia and those who were cognitively normal.
The study, from researchers at the University of Leipzig in Germany, was based on a theory that Alzheimer's occurs when neurons get a false signal to divide. The more popular theory holds that a build-up of amyloid plaque (made up mostly of beta amyloid protein) in the brain causes Alzheimer's.
"The alternative theory about Alzheimer's is that the [cell] replication process gets triggered pathologically, and then the cells are programmed to die, and that's what's killing the nerve cells, not the amyloid," Kennedy explained. "[This study] all hinges on the theory that it's a false signal to replicate that starts these neurons down the path to killing themselves."
But investigators still have a long way to go. "It's one thing to distinguish the sick group from the healthy group and another to see if you can predict from the healthy group who gets the disease," Kennedy said. "That's the real proof of the pudding."
A second study, from researchers at Washington University in St. Louis, confirmed previous findings: that the more amyloid there is in the brain (as measured by PET scans), the less beta amyloid 42 there is in cerebrospinal fluid (CSF). Beta amyloid 42 is an extra-"sticky" type of amyloid protein which accumulates and forms plaques. The theory is that measurements of beta amyloid 42 in spinal fluid could serve as a marker for Alzheimer's disease.