Alzheimer's disease is the most common form of dementia -- a progressive disease in which memory and thought processes become severely impaired.

Senile plaques are typical microscopic features seen in the brain tissue of patients with Alzheimer's disease. They are large aggregates of folded amyloid fibrils.  In 1985 amyloid beta was discovered. It is a chain of about 40-42 amino acids (the building blocks of proteins) linked end to end. Amyloid consists of clumps of this proteinaceous material.  As such, senile plaques have long been considered the primary killers of brain cells in this disorder. They were first discovered by Blocq and Marinescu in 1892. In 1906 Alzheimer first made the connection between plaques and dementia. In the 1970s M. Franke showed their association with dementing disease when the density of plaques in the frontal lobes was greater than 200/cubic millimeter. 

In the minds of researchers, the nexus between senile plaques and Alzheimer's disease became so entrenched that they were believed to actually cause the disease. Based on this theory of causation, medications were developed to remove the plaques. However, during drug trials designed to remove these plaques from the brain (such as the recent study testing bapineuzumab, which decreased plaques by 25%),  the patients' ability to think and reason got no better in spite of the decrease in plaques caused by the drug therapy.

This type of results have demonstrated to researchers that plaques are not the chief toxin responsible for Alzheimer's disease.  Moreover, not only are plaques not the cause of Alzheimer's disease, but it now appears that scientists are beginning to think they are a good thing!

According to Adrian Ivinson, director of the Harvard NeuroDiscovery Center in Boston, plaques actually appear to sequester all that amyloid. He went on to suggest that small particles of amyloid, called oligomers, rather than the large plaques, are the truly toxic substance. So it seems that like the capsule, or surrounding membrane, of a collection of pus, the plaque actually is protective rather than being the causative factor in Alzheimer's disease as has been believed all along. This insight has dramatically changed the way scientists view Alzheimer's disease and what they feel may be the optimal way to treat it.  I guess one take home message is that merely because something happens to share proximity with what causes a disease, it might not be the actual culprit.

It is worth taking a moment, in this context, to consider other diseases where related circumstances may have clouded scientific thinking in a similar fashion. Consider the cholesterol theory of heart disease. According to those who believe it, the build up of cholesterol in the blood somehow damages the arterial wall in very specific locations, in spite of the fact that the concentration of cholesterol is identical throughout the vascular tree. Could there be other factors that are producing injury to the lining membranes of blood vessels and that, once damaged, the cholesterol is deposited secondarily in the blood vessel wall in an attempt to repair the damage. If this is the case, then attention must be paid to other potential causes of vascular disease than cholesterol!