Scientists have long suspected that the protein clumps and tangles identified by Alois Alzheimer in 1907 somehow cause the disease that bears his name, probably by killing neurons. Now some researchers are blaming a much smaller form of protein, one that apparently produces memory deficits merely by binding to neurons and disrupting their ability to transmit signals. The search has begun for an antibody that would destroy these tiny proteins--or ADDLs--thereby preventing the onset of Alzheimer's disease and possibly even reversing the early symptoms.
The discovery of ADDLs explains glaring anomalies in the conventional thinking about Alzheimer's, which holds that fragments of amyloid precursor protein, produced by normal neurons, aggregate into sticky, insoluble plaques that damage neurons. The problem with this theory is that virtually every older person carries some amyloid plaque, but only a few develop Alzheimer's. Conversely, those with Alzheimer's often have relatively few plaques. Another proposed culprit is the presence of tangles of tau protein, which form inside neurons and coincide with the collapse of microtubules that support the cell body and transport nutrients. The tau tangles correlate much better with the disease but tend to appear later, suggesting that they are a consequence, not a cause.