Researchers move one step closer to understanding the process of Alzheimer’s disease.

One of the key areas of research for Alzheimer’s is amyloid beta and the plaque that it forms. Researchers believe that a process called endocytosis is involved in the increase of amyloid beta.

John Cirrito, PhD, research instructor in neurology, Washington University School of Medicine, St. Louis, and colleagues, decided to test how significant of a role endocytosis plays in the development of amyloid beta. Using mice genetically engineered for Alzheimer’s disease, researchers used a drug to shut down the endocytosis process and found there was a 70% decrease of amyloid beta.

Researchers believe endocytosis may accidentally be triggering a process that results in the formation of amyloid precursor protein (APP), which eventually breaks down into amyloid beta and leads to Alzheimer’s plaque. In theory, researchers note, that a drug that reduces APP may help reduce amyloid beta production.

Although APP is involved in the process that leads to amyloid beta, researchers believe that APP may be an innocent bystander because there appears no functional reason for APP to participate in the process.