Stanford Alzheimer's Research Pinpoints Antibodies That May Prevent Disease
July 7, 2009
Adapted from Stanford University School of Medicine
Antibodies to a wide range of substances that can aggregate to form plaques, such as those found in Alzheimer's patients, have been identified in the blood and cerebrospinal fluid of healthy people. Levels of these antibodies decline with age and, in Alzheimer's patients, with increasing progression of the disease.
These findings by Stanford University School of Medicine researchers and outside collaborators, described in a paper published on July 6, 2009 in the journal Proceedings of the National Academy of Sciences, raise the possibility that many of us are carrying antibodies in our blood that could be playing a role in staving off or slowing the progression of Alzheimer's disease. This seems to be true even when we are young and healthy and would presumably have had little or no exposure to the substances that build up in the brain to cause this disorder.
Alzheimer's disease is characterized by the build-up of amyloid plaques in the brain. These are large aggregations of a protein breakdown product, or peptide, called A-beta. Many experiments have shown that immunization with A-beta can reduce the formation of amyloid plaques. Clinical trials now underway are exploring whether this can safely produce cognitive benefits in Alzheimer's patients, while other trials are treating patients directly with antibodies to A-beta.
The study's lead author, Tony Wyss-Coray, Ph.D., reports that the methods used in this research could lead to improved monitoring of clinical trials that are using immunotherapeutic treatments for Alzheimer's disease.
Alzheimer's Disease Research, a program of the BrightFocus Foundation, is proud to have Dr. Wyss-Coray as part of its Scientific Review Committee.
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