Using the formidable powers of the immune system to attack one of the body's own proteins seems like a risky approach. But this is what nearly all vaccines, or immunotherapies, against Alzheimer's disease aim to do. Their target is amyloid-(3, a tiny protein produced by neurons. Scientists do not know what function amyloid-(3 evolved to have in its ordinary, free-floating form. But they do know that it is unusually prone to sticking to copies of itself, and that this aggregation process seems to be the principal trigger for Alzheimer's disease. The first vaccine against Alzheimer's disease - Dublin-based Elan Pharmaceuticals' AN-1792 - was based on a particularly aggregation-prone form of amyloid-p1 known as A(342. In mice that had Alzheimer s-like deposits, or 'plaques', of amyloid-(3 in their brains, it seemed enormously promising: it provoked a storm of anti-amyloid-(3 antibodies that dissolved the plaques in older mice and stopped plaques from forming in younger ones. But in humans, AN-1792 was a disaster. Elan halted its first large clinical trial in 2002, after patients developed meningoencepha-litis, an inflammation of the brain and its membranes that was apparently caused by rcigue immune cells~1.
展开▼
