A team of researchers led by Dennis J. Selkoe, professor of neurology at the Harvard Medical School, has come closer to unraveling the deadly secrets behind Alzheimer's disease (A.D.).

Selkoe and his colleagues published their findings last month in the journal Nature Medicine, confirming that mutations in two genes previously known to be connected with early-onset familial A.D., presenilin one and two, do in fact stimulate production of a protein believed to be an important indicator of Alzheimer's.

Scientists have known previously that mutated forms of these genes were found in A.D. patients, but were unsure how they affected the brain.

"This research establishes the genotype to phenotype relations or, in layman terms, how [the gene] does...its dirty work," Selkoe said.

Selkoe says his research found that the mutations in the genes cause the formation of neuritic plaques in the brain which are characteristic of A.D.

"We believe these plaques of amyloid beta short circuit nerve cells, not allowing them to communicate," says Selkoe, co-director for the Center for Neurologic Diseases at Brigham and Women's Hospital.

He says the protein is a common link among Alzheimer's patients.

"We know that 100 percent of Alzheimer's patients have the abnormal buildup of...the amyloid beta protein," Selkoe says.

Consequences of the Disease

Alzheimer's affects an estimated four million Americans, costing more than one hundred billion dollars a year, making it the third most expensive disease to treat in America, according to the Alzheimer's Association of America (AAA).

The disease affects 10 percent of people over 65 and 50 percent of people over 85. It is the fourth leading cause of death in the United States today, said the AAA.

A.D. attacks and destroys neurons in the brain, causing such symptoms as loss of reasoning and memory, triggering the inability to perform simple tasks such as brushing teeth or fixing meals.

After being diagnosed, an Alzheimer's patient lives an average of eight years until dying.

Selkoe says that although they have identified some of the genes which are responsible for A.D., scientists have yet to determine whether the disease is entirely genetic or caused by an outside factor, such as natural radiation.

Selkoe says the plaque is formed by the Amyloid beta (A. beta) protein in the brain, but its formation may serve solely as an indicator of the onset of the disease.