Researchers led by Guojun Bu of the Washington University School of Medicine in St. Louis said their finding could lead to new approaches to treating the disease.

The medical scientists sought to link the function of two known causative Alzheimer factors -- amyloid precursor protein, of APP, and a particular form of the gene for the protein apolipoprotein E, or apoE, that has been linked with higher late-onset risk.

Mutations in APP are known to cause early-onset Alzheimer's when cleavage of the protein produces a short toxic protein that accumulates in the brain, killing cells.

A specific variant of the gene for apoE has been linked with late-onset AD, although how that predisposes individuals to the disease is largely unknown.

"Our results provide important insights into APP biological function and its potential implications for neuronal dysfunction in AD and may lead to the design of better therapeutic strategies to treat this devastating disease," the researchers said.

The study appears in the Oct. 4 issue of the journal Neuron.