In the first hypothesis, external proteins called beta amyloid peptides kill nerve cells. A mistake in protein processing produces an abnormal form of the peptide, which then forms aggregates or plaques. The plaques begin to fill in the brain and then damage and kill nerve cells. However, these amyloid plaques have been found in autopsies of people that did not have Alzheimer's disease.
The second hypothesis maintains that the nerve cells are killed by an abnormal form of an internal protein. This protein, called tau, normally functions to maintain protein transport microtubules. Abnormal forms of tau assemble into helical segments that form tangles which interfere with the normal functioning of the nerve cells. Researchers continue to study whether tangles and plaques are causes or effects of Alzheimer's diseases.
Progress has been made in identifying genes that increase the likelihood of developing Alzheimer's and genes that when mutated can cause Alzheimer's disease. However, the genes may not reveal much about Alzheimer's as they do not show up in most Alzheimer's patients, and they cause symptoms that start much earlier than when most Alzheimer's patients show symptoms.
"Hopes Are Rosy on Alzheimer's But Results Slim" by Gina Kolata, The New York Times, July 30, 1996