Link between Alzheimer's, leukemia found

A molecule known to play a role in a rare form of leukemia also appears to have a hand in Alzheimer's disease, Long Island scientists have found in the first investigation to show how this well-known component of cancer in the blood can also lead to dementia.

Dr. Peter Davies and colleagues at the Feinstein Institute for Medical Research in Manhasset have made a landmark discovery, unmasking a protein molecule known as c-Abl. They found it in the morass of plaques and tangles that define the damaged brain tissue of people with Alzheimer's disease.

For decades, c-Abl has been known as the active component in chronic myeloid leukemia -- CML. The protein so adversely affects patients' white-cell population, known as B-cells, that some scientists have likened it to a light switch: when it is flipped on, it can lead to CML.

Its newly defined presence in Alzheimer's disease is a story that has been unfolding for more than two decades, said Davies, director of the Litwin-Zucker Center for Research in Alzheimer's disease.

"We first saw c-Abl 25 years ago in the brains of patients with Alzheimer's disease," Davies said Thursday. "There were signs that nerve cells were trying to divide, which of course they shouldn't be doing because adult brain cells don't divide. But now we know that c-Abl is responsible for this."

Davies emphasized that his discovery does not mean that Alzheimer's is a form of cancer but that the two unrelated conditions share an aberrant molecule. His discovery is outlined in greater detail in a study published online Thursday in the Journal of Alzheimer's Disease.

Dr. Creighton Phelps, director of the Alzheimer's program at the National Institute on Aging in Bethesda, Md., said the research was intriguing and that multiple Alzheimer's triggers are likely to be found.

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Phelps said he would like to know precisely where c-Abl fits in the rogues' gallery of molecular suspects. "It may not be in the main pathway" that leads to the disease, Phelps said, "but it may be affecting other players in the main pathway."

Davies and his team, meanwhile, have begun investigating medications that can switch off c-Abl for Alzheimer's. The blockbuster medication Gleevec, approved a decade ago for CML, would not work, he said, because it won't cross the blood-brain-barrier, the tight network of capillaries shielding the brain.

They are working on several medications similar to Gleevec that can potentially evade the brain's defenses.