Alzheimer's disease researchers have long tried to address a key question: Do amyloid plaques cause the disease, or do other disease mechanisms come first? A new study published today (February 6) in Nature reports that plaques form immediately before neurite damage, suggesting that amyloids do play a direct role on the pathway to dementia.

The researchers, led by Bradley Hyman at Massachusetts General Hospital, used an in vivo imaging technique in a mouse Alzheimer's model to observe how and where plaques form over time. They observed that plaques formed very quickly over 24 hours, followed by the recruitment of microglia, which did not clear plaques but prevented any further plaque formation. The group also observed changes in neurites following the formation of plaques; they saw neuritic deformation after two days of plaque formation, and after three to four days neurites began wasting away.

"This is the first study to really look at a time course examination of plaques -- examining them in the cellular setting," George Perry, neuroscientist and dean of life sciences at the University of Texas, San Antonio, who was not involved in the study, told The Scientist. He added that this work shows plaques to be very dynamic -- that is, they can form quickly and be removed quickly. Researchers have previously thought that all plaques are slow to form and long-lived.

The caveat, Perry said, is that these results are based in a mouse model genetically engineered to overexpress amyloid protein. And "we can't assume that plaques will form the same way in the human Alzheimer's brain." In fact, he added, researchers know that mice plaques are core-containing, while human plaques are diffused, and thus inherently structurally different.

"This is an extremely important study and well executed," said Perry, but it still doesn't answer the question of where amyloid plaques come from in the first place.