A new hypothesis, published in today's Nature, suggests that Alzheimer's may be caused by a normal prenatal developmental process gone awry in the adult brain.

Before you cast aside years of beta-amyloid research or proclaim a cure is imminent, relax - the results are only from lab and mouse studies. The research indicates that beta-amyloid precursor protein "and DR6 are components of a neuronal self-destruction pathway, and suggests that an extracellular fragment of APP, acting via DR6 and caspase 6, contributes to Alzheimer's disease."

When prenatal brains are developing, some fine-tuning takes place and excess neurons are killed off via N-APP. In adult brains, the research shows that APP is possibly taking an unknown pathway - not through beta-amyloid - to trigger apoptosis, resulting in Alzheimer's. This could explain why some people have accumulated beta-amyloid deposits but not dementia.

Despite the early stage of research, drug companies are already jumping on the hope bandwagon. In fact, the corresponding author, Marc Tessier-Lavigne, is the executive vice president of research drug discovery at Genentech. And the editor's summary accompanying the article is written by Donald Nicholson, VP and worldwide head of basic research at Merck Research Laboratories.