Beta amyloid, often abbreviated as A-beta, is a protein that builds up in the brains of persons with Alzheimer's disease, collecting in clumps called plaques or senile plaques. While some researchers question whether beta amyloid is the cause of the dementia, most agree that it is involved in the disruption of thinking that is a hallmark of the disease. In some cases of familial Alzheimer's disease, mutations in genes for the proteins called the presenilins lead to increased production of amyloid. Researchers have been looking at how presenilin-1 in particular contributes to the excess buildup of beta amyloid. Presenilin-1 apparently acts to increase the activity of gamma-secretase, an enzyme that changes a normal protein (amyloid precursor protein or APP) into beta amyloid itself. Furthermore, presenilin-1 might be gamma-secretase.