It is not understood how these deposits damage cells, nor do researchers have a clear idea how they contribute to dementia. But even if they turn out not to cause AD directly, they are biological markers of the disease that may help to trace its mechanism. Very early in the course of AD, waxy protein deposits called plaques begin to build up between cells. Most elderly people have some waxy plaque buildup, but in people with AD the plaques are extensive, and they are concentrated in the hippocampus and the cerebral cortex. Cells around the plaques often look abnormal.
Plaques mostly contain protein fragments called beta-amyloid peptide.
Proteins get their instructions from genes, and if the gene suffers a defect, called a mutation, the protein the gene codes for may also be defective. As it matures, the protein is cut in several ways, creating fragments of beta-amyloid protein, a small number of which are toxic. However, mutations in the gene that codes for beta-APP cause something to go haywire in the cutting process and to generate an excess of the toxic form of the protein fragment. But how these mechanisms relate to the dementia of AD is not clear. Moreover, researchers disagree whether plaques cause AD by destroying cells, or whether they result from damage to cells caused by something else.