A novel marker of Alzheimer's disease (AD) can predict how rapidly a patient's memory and other mental abilities will decline after the disorder is diagnosed.

Higher levels of the marker, visinin-like protein 1 (VILIP-1), in the cerebrospinal fluid (CSF) of Alzheimer's patients have been linked to a more rapid mental decline in the years that followed.

Scientists at Washington University School of Medicine (St. Louis, MO, USA) studied 60 individuals with a clinical diagnosis of very mild or mild AD and measuring baseline CSF protein levels of VILIP-1, Tau, phosphorylated Tau-181 (p-tau181), and amyloid-beta 1–42 (Aβ42), and these were followed longitudinally for an average of 2.6 years.

Baseline CSF VILIP-1 and VILIP-1/Aβ42 levels predicted rates of future decline in the clinical dementia rating and global composite scores over the follow-up period. Individuals with CSF VILIP-1 equal to or greater than 560 pg/mL progressed much more rapidly than individuals with lower values. CSF tau, p-tau181, tau/ Aβ42, and p-tau181/ Aβ42 also predicted more rapid cognitive decline overtime. Scientists think VILIP-1 serves as a calcium sensor in brain cells. It is released into the cerebrospinal fluid when the cells are injured. CSF samples were analyzed for total tau, p-tau181, Aβ42 using Innotest, (Innogenetics, Ghent, Belgium), and CSF Aβ40 by an enzyme-linked immunosorbent assay. CSF samples were analyzed for VILIP-1 by Erenna, a microparticle-based immunoassay (Singulex, CA, USA).

Rawan Tarawneh, MD, the lead author of the study, said "VILIP-1 appears to be a strong indicator of ongoing injury to brain cells as a result of Alzheimer's disease. That could be very useful in predicting the course of the disease and in evaluating new treatments in clinical trials. These results are intriguing, but we need a larger study to fully understand how the insights provided by VILIP-1 compare to those we can gain from other markers.” The study was published online on February 22, 2012, in the journal Neurology.

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Washington University School of Medicine
Innogenetics
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