The Washington University School of Medicine researchers in St. Louis said such plaques are accumulations of fragments of amyloid beta protein, and are found in post-mortem examinations of the brains of Alzheimer's patients.

Neuroscientists at the school experimentally manipulated the ability of brain cells to take in substances from their surface -- a process called endycytosis. To mice having a disease similar to Alzheimer's, the researchers administered a drug that stops the process of endocytosis. The result was a 70 percent reduction in the production of amyloid beta protein.

In another experiment, the researchers gave the mice a drug that reduced brain cell communication, but did not affect endocytosis. The result was a 60 percent reduction in amyloid beta production.

"Blocking endocytosis isn't a viable option for treatment because cells throughout the body, including brain cells, need endocytosis for healthy function," said John Cirrito, a research instructor and first author of the study. "But we are starting to understand the origins of amyloid beta in more detail now …"

The study appears in the journal Neuron.