Winning the race against Alzheimer's disease

Barry Reisberg, M.D., professor of psychiatry at the New York University School of Medicine and clinical director of NYU's William & Sylvia Silberstein Institute for Aging and Dementia, commented, "We don't know the cause of Alzheimer's disease. From a clinical perspective, in terms of my own work, Alzheimer's disease reverses the course of normal human development in remarkable ways. That's true not only in terms of the functional progression of the disease but also cognitively and in terms of neurological reflexes. And why this is the case is still something of a mystery."

AD, a progressive neurodegenerative disorder, is the most common cause of dementia. Over a period of three to 20 years from its onset, it affects an increasing number of nerve cells, impacting learning, memory, thinking, judgment, behavior, and finally control and coordination of movement. AD ultimately leads to death. Treatments thus far approved by the Food & Drug Administration only slow the progression of the disease. Reisberg underscored, "Nothing we have stops the progression of the disease"-but the operative word in looking at the number of drugs in trials may well be yet.

Two drugs, in phase III trials at press time, target beta-amyloid, a known pathology of AD that leads to a buildup of plaque. If these drugs prove successful and attain FDA approval, they are expected to dramatically alter the AD market.

Decision Resources, a leading research and advisory firm, predicts the launch of Alzhemed (NC-758, Neurochem) and Flurizan (MPC-7869, flurbiprofen, Myriad Genetics) will be the primary drivers that grow the dementia treatment market by 11% annually over the next 10 years. Decision Resources also predicts their advent will reshape the market, with the acetylcholinesterase inhibitors, including donepezil (Aricept, Eisai), rivastigmine (Exelon, Novartis), galantamine (Razadyne, Janssen Pharmaceutica), and N-methyl-D-aspartate receptor antagonist memantine (Namenda, Forest Laboratories), declining significantly between 2009 and 2014.

In clinical trials, both Alzhemed and Flurizan appear to offer an advantage over existing therapy. Data suggest each drug may be able to improve cognitive function, though improvement, measured by some scales, is small. Alzhemed has been demonstrated to have a dose-dependent inhibitory effect on both the deposition of cerebrovascular beta-amyloid and its plasma concentration.

Flurizan is the first in a class of drugs known as selective amyloid beta-42-lowering agent (SALAs). Data from a phase II follow-on study of Flurizan in patients with mild AD presented at the November 2005 Society for Neuroscience meeting in Washington, D.C., showed participants improved as a group, regaining cognitive ability in 12 to 18 months.