Any drug that substantively delayed or stopped Alzheimer's would be an immediate blockbuster, perhaps exceeding sales for Prozac or Lipitor. No such drugs are on the market because investigators are still trying to understand how to alter the underlying mechanisms by which the disease causes dementia.
Drugs that impede amyloid buildup offer a case in point: a number of drug possibilities at various stages of testing can purportedly inhibit amyloid accumulation or foster its clearance. Yet several antiamyloid drugs tested in clinical trials have already failed. (The table below lists major classes of Alzheimer's drugs under development.) Some researchers wonder whether too little emphasis has been placed on interfering with other processes that contribute to the disorder. Among the 100 or so agents under development are prospective drugs that target the cell-damaging tau protein. Some are intended to quell inflammation, boost the functioning of mitochondria, enhance cerebral insulin levels or provide other protection for neurons. One high-profile failure involved Dimebon, a drug that did not target tau or amyloid. As with cancer and HIV, it may be necessary to combine several of these agents to slow or halt Alzheimer's.