'Biomarkers' May Help Spot, Track Alzheimer's (HealthDay)

TUESDAY, July 29 (HealthDay News) -- Scientists may be succeedingin the hunt for biomarkers for Alzheimer's disease.

A biomarker -- something that can be measured and that gives anindication of what's going on inside the body -- will help in earlydetection, in testing new therapies and, once doctors have better drugsfor Alzheimer's, with earlier intervention in the disease process.

"If we're going to have any kind of medication that alters or modifiesthe disease, if it's really going to change it rather than treat symptoms,then we need biomarkers that are sensitive to the illness before a personbecomes impaired," explained Dr. Gary Kennedy, director of geriatricpsychiatry at Montefiore Medical Center in New York City. "In Alzheimer's,we need two things: We need to know who's sick and who's not and,secondly, biomarkers should be treatment-sensitive, meaning if you've gotthe right treatment, you watch the biomarker go down, like blood sugar andinsulin. That's the model we want."

One study being presented at the International Conference onAlzheimer's Disease (ICAD) in Chicago found that differences in levels ofCD-69, a protein involved in white blood cell growth and production,allowed researchers to distinguish between people with Alzheimer's, peoplewith 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 falsesignal to divide. The more popular theory holds that a build-up of amyloidplaque (made up mostly of beta amyloid protein) in the brain causesAlzheimer's.

"The alternative theory about Alzheimer's is that the [cell]replication process gets triggered pathologically, and then the cells areprogrammed to die, and that's what's killing the nerve cells, not theamyloid," Kennedy explained. "[This study] all hinges on the theory thatit's a false signal to replicate that starts these neurons down the pathto killing themselves."

But investigators still have a long way to go. "It's one thing todistinguish the sick group from the healthy group and another to see ifyou can predict from the healthy group who gets the disease," Kennedysaid. "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 incerebrospinal fluid (CSF). Beta amyloid 42 is an extra-"sticky" type ofamyloid protein which accumulates and forms plaques. The theory is thatmeasurements of beta amyloid 42 in spinal fluid could serve as a markerfor Alzheimer's disease.

Another study, this time from a team in Ireland and in Germany, foundthat individuals with mild cognitive impairment (MCI), often considered atransitional stage between normal cognitive functioning and Alzheimer's,had elevated levels of beta-secretase (BACE1) activity in the brain whencompared both to healthy people and people with Alzheimer's.

Finally, a fourth study showed that a certain radioactive compound ortracer, 18F-AV-45, may have potential in the diagnosis and early detectionof Alzheimer's when used with PET scans. Trials of the substance,conducted by Philadelphia-based Avid Radiopharmaceuticals Inc., areongoing.

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