12 November 2009
Alzheimer vaccine
Neuropathological analysis ofAD-affected brains reveals extensive atrophy due to neuronal loss, and accumulation of neurofibrillary tangles and neuritic plaques, surrounded by a tract of neuroinflammation (i.e. astrocytosis and activated microglia). Neuritic plaques consist of deposits of variously sized peptides collectively called b-amyloid (Ab), which is widely believed to be the key player in the pathogenesis of AD. Within this context, reducing AD amyloidosis represents one of the main therapeutic strategies under investigation for AD. Examples of this approach include the Ab vaccine (which reduces brain amyloidosis by several mechanisms), inhibitors of secretases, Ab-disaggregants, non-steroidal anti-inflammatory agents, cholesterol-lowering compounds and estrogen, all of which are known to reduce the production and/or accumulation of Ab .
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The Alzheimer vaccine has had a rocky road! The first clinical trial was abruptly ended in 2002: "Within days of announcing that trials of its therapeutic vaccine, AN-1792, had been suspended, the company's share value plummeted by over 70% amid concerns over accounting practices and calls for Elan directors to resign" (Nature). In 5 patients the vaccine seemed to cause intense brain inflammation. Why wouldn't it? If you immunize people against a brain antigen, it seems that you might expect a harmful immune-mediated inflammatory response in the brain. There is still talk of a vaccine but I don't think anyone soon will try again in humans.
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