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See Inside June/July 2006

Trace of Alzheimer's

Prediction of tissue loss



ALFRED PASIEKA Photo Researchers, Inc.

A new radioactive tracer may one day be used to predict whether a person might develop Alzheimer’s disease.

The brains of Alzheimer’s sufferers are usually shot through with plaques of the protein beta amyloid and so-called tangles of a protein known as tau. Radioactive tracers for beta amyloid plaques exist, but they do not fully distinguish healthy from diseased tissue, says Gary Small, a geriatric psychiatrist at the University of California, Los Angeles. Small and his colleagues conducted positron-emission tomographic scans using a synthetic radioactive compound, FDDNP, that sticks to plaques and tangles. They scanned 60 people, some of “normal” mental status and some with mild cognitive impairment or Alzheimer’s. The greater an individual’s cognitive problems, the more the tracer showed up in the brain, in certain signature patterns.

In follow-up scans of 12 individuals two years later, those whose mental abilities had deteriorated showed greater accumulation of the tracer, suggesting a possible predictive value. The results are encouraging for diagnosing Alzheimer’s and forecasting its progression, says neuroscientist Mony de Leon of New York University. Predicting the onset of the disease may be more complicated, however, because researchers do not know the behavior of plaques and tangles in healthy people or those with other disorders. Siemens AG has licensed FDDNP and is evaluating the technique’s forecasting power, Small says.

Other experiments are identifying factors that could help predict the pace of illness. For example, Nikolaos Scarmeas of Columbia University and his colleagues recently reported on 312 newly diagnosed Alzheimer’s patients whom they followed for an average of six years. The more years of formal schooling the patients had, the faster their memories declined — strengthening the conclusion of less comprehensive studies, Scarmeas says. Although more highly educated people succumb to Alzheimer’s later in life — perhaps because they can more easily compensate for initial impairments — the results indicate the delay may come at the cost of having less in reserve to slow progression once the disease finally kicks in, Scarmeas explains.

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