Many scientists believe that Alzheimer’s disease is caused in part by a sticky substance called amyloid that clumps in the brain to cause plaques. But scientists also have posited that the amyloid protein could be causing trouble even before it forms plaques, when it is still floating around in cerebrospinal fluid in its so-called soluble form. (Other theories suggest that other proteins, such as tau , also play a role.) The experimental Alzheimer’s vaccine bapineuzumab, being co-developed by Pfizer and Johnson & Johnson, appears to bind to soluble amyloid and “neutralize” amyloid’s downstream toxic effects, preventing it from binding to neurons, according to research presented today at an Alzheimer’s and Parkinson’s disease conference in Barcelona. So what’s the significance of this finding? Well, in mouse studies there does appear to be a benefit of injecting the therapeutic vaccine, according to Gene Kinney, head of research at J&J’s Janssen Alzheimer Immunotherapy R&D

group. Mice that are prone to forming amyloid plaques and have trouble learning fear (a proxy for cognitive function) were injected with bapineuzumab prior to plaque formation. Those injected were better able to be conditioned to fear–the fear-learning deficit was reversed to a level that was comparable to healthy mice, said Kinney. Though scientifically interesting, whether the vaccine’s binding to soluble amyloid really matters depends on if it translates to actual improvements in symptoms. This question can only be answered when human clinical trials are completed, according to Kinney. It remains to be seen whether bapineuzumab will be effective when given to patients who are in the early stages of the disease. Bapineuzumab, which is late-stage human testing, has shown limited efficacy in earlier stage trials and encountered a setback in terms of safety in 2009 . Image: Associated Press

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Bapineuzumab Might Tackle Alzheimer’s Protein Early On