"This was the first study to show an age-related decline in the levels of these antibodies," said Britschgi. A follow-on experiment showed that the same antibodies, whether from Alzheimer's patients or healthy controls, were able to protect freshly cultured in vitro mouse neurons from destruction by A-beta, which is typically highly toxic to these neurons.
The researchers also studied samples from vervet monkeys who, like humans, develop A-beta-derived brain plaques as they age. The Stanford team obtained blood samples before and after immunization. They observed significant post-immunization increases in levels of several different antibodies.
Wyss-Coray said, "With our microarray, you could easily look for antibodies to hundreds of different peptides. It would be possible to see whether certain types of antibodies correlate better with cognitive benefits than others do."
Another possibility, said Wyss-Coray, is to try immunizing Alzheimer's patients with peptides that have amino-acid sequences unlike any of those occurring naturally ? but that, by virtue of their three-dimensional similarity to A-beta as they begin to aggregate, generate antibodies to A-beta oligomers as well. This would reduce the possibility of an autoimmune reaction to such a vaccine, which resulted in the halting of an otherwise promising clinical trial several years ago.
SOURCE:
Proceedings of the National Academy of Sciences, July 6,
2009
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