Some investigators speculate that an imbalance between the amount of amyloid BPP produced and the brain's ability to degrade it may cause the earlier onset of development of plaques. Classical plaques consist of several microglial cells surrounding a center core of amyloid that is fibrillized. Diffuse plaques, on the other hand, contain amyloid deposits with few, if any, amyloid fibrils or abnormal neurons. The process of formation and disintegration of neurological plaques remains controversial. Some investigators believe that diffuse plaques are an early form of classical plaques with amyloid precursor rather than true amyloid.
Current research gives more credence to the first hypothesis.
The deposition of amyloid beta protein in nervous and vascular tissue is known to be an early event in AD, but the appearance of amyloid fibrils seems to be the initiating pathological change in the neurons. A person with Down syndrome may have a long period of time when only diffuse plaques, containing amyloid deposits without fibrillization, are formed and therefore no neuronal degeneration occurs. Furthermore, diffuse plaques are not found exclusively in persons with Down syndrome. They also occur in persons who have sustained a head trauma, critical coronary disease, and other disease processes. The key concept is that both types of plaques may appear in the same individual at the same time, but only classical plaques appear to affect the structure and function of nervous tissues.