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Alzheimer’s: A New Theory

New research appears to upend our current understanding of the causes of Alzheimer’s disease, and may lead to a whole new approach to finding a cure for the devastating dementia.

The controversial new theory gaining traction in the scientific community is that in Alzheimer’s disease the brain is destroyed not by sticky plaques—long held to be the culprit—but by free-floating clumps of protein.

In fact, the sticky plaques that surround the brain cells of those with Alzheimer’s may be the body’s way of protecting against these toxic clumps.

For the last 20 years, following the prevailing theory that sticky plaques cause Alzheimer’s disease, drug developers have been targeting those plaques in their search for a cure.

But recently published studies on mice and rats may prove to be the tipping point that takes research in a new direction. Many scientists now believe clumps of amyloid beta protein called oligomers are the main players in the rogue process that attacks the brain.

“Plaques are no longer where the action is,” says Sam Gandy, M.D., of the Alzheimer’s Disease Research Center at Mount Sinai School of Medicine in New York.

Gandy’s work builds on several years of research that has been moving toward this new theory. And if the theory is correct, then drugs that target plaques—as many of the most promising medications have done in the past few years—may not help people who have the disease. They could even make them worse. This research is key. About 5.1 million Americans have Alzheimer’s, and that number will grow as boomers age.

Gandy’s work with specially engineered mice—which developed Alzheimer’s though they had only clumps of the oligomers and no plaques in their brains—“is the final experiment that’s making the whole field turn around,” says Andrew Dillin, a scientist who studies aging and the brain at the Salk Institute of California. The role amyloid beta plays in the development of the disease was a hot topic at the international Alzheimer’s conference in Hawaii this summer.

While the development is exciting, William Thies, the Alzheimer’s Association’s chief medical officer, cautions that the leap from mice to men is a long one and that Gandy’s experiments need to be duplicated by other scientists in other labs before drug companies invest billions of dollars to create new medicines that target the oligomers.

Gandy’s new study looked at the most basic science of the disease in a very different way.

“Alzheimer’s seems to be caused by the buildup in the brain of clumps of material that are formed by the breakdown of protein,” Gandy says.

He now thinks the oligomers, not plaques, cause the loss of memory and reason that characterize Alzheimer’s. Gandy and colleagues published their work in the Annals of Neurology in April.

Dillin, of the Salk Institute, started pursuing the oligomer theory several years ago. Then, the idea was so controversial, Dillin says, that some scientists would walk out of the room when he made his presentation at conferences. Now, he says, many of the top researchers in the field are convinced.

Compelling experiment

Alzheimer’s disease is characterized by two main elements—the sticky plaques that form outside the brain cells, and tangles of another protein, tau, that twist around the inside of the cells. Both are thought to play a role in the progression of the disease.

Scientists noticed the buildup of the sticky plaques in the brains of people with Alzheimer’s disease 100 years ago. And although there has been some debate, the prevailing science has held that sticky plaques and tau tangles cause the damage.

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