(Ivanhoe Newswire). ? Researchers at Stanford University School of Medicine studying the blood and spinal fluid of healthy people have identified antibodies to substances that can form plaques, such as those found in Alzheimer's patients.
These findings raise the possibility that many of us are carrying antibodies that could be playing a role in staving off or slowing the progression of Alzheimer's. 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, which form aggregations of a peptide called A-beta. But A-beta is a slippery character, and is prone to modify, mutate or metabolize into different forms. Researchers believe it may be smaller aggregations of a few A-beta molecules, called oligomers, which are most toxic to brain neurons ? more toxic than the plaques themselves.
"Other studies have found antibodies against A-beta, but nobody has ever done a large-scale analysis using hundreds of different samples and almost a hundred different peptides to look for what's already in people's bodies," the paper's first author, Markus Britschgi, PhD, a researcher in the laboratory of Tony Wyss-Coray, PhD. is quoted as saying. Wyss-Coray, associate professor of neurology and neurological sciences, is the paper's senior author.
Britschgi, Wyss-Coray, and their colleagues used a technology developed in a neighboring lab in which a large number of different peptides are affixed to pixels on a microchip, which signals binding of those peptides by antibodies. The investigators customized microarrays, each containing close to 100 different peptides.
The researchers incubated these chips with blood samples from more than 250 individuals between 21 and 89 years old, some with Alzheimer's and others without. They observed antibodies targeting many forms and aggregation-states of A-beta in both healthy and diseased subjects' blood. They then showed that overall levels of these antibodies decline with age and, in those with Alzheimer's, with advancing stages of the disease.
