Amyloid plaques are insoluble deposits of beta-amyloid - a protein fragment snipped from a larger protein (amyloid precursor protein = APP).

Although researchers aren’t sure whether these plaques are a by-product of AD or a cause of AD, it is known that changes in the structure of the APP can cause AD.

Scientific research is now focusing on preventing the development of beta-amyloid or inhibiting its deposition into insoluble plaques.

Two other protein molecules, presenilin 1 and presenilin 2, may be associated with the actual clipping of APP into beta-amyloid, stress-related cell death, and the ability of neurotransmitters to travel across synapses - the tiny gaps between neurons.

Mutations in these three genes located on 3 different chromosomes account for almost all cases of Familial AD.