What Are The Financial Implications of The Phase IIA Findings Of Elan and Wyeth’s “AN-1792”, (If Successful)?

At the 9th Annual International Conference on A.D. and Related Disorders in Philadelphia, Elan Corporation and Wyeth Pharmaceuticals announced the findings from their Phase IIA clinical trial of AN-1792 and A.D. AN-1792 which has been touted by many in the medical community, specifically those in neurology, neuroscience and neuropsyhology as exciting news.

According to the Alzheimer’s Organization, there are approximately 4 million Americans with A.D. This rate has doubled since the 80’s. Furthermore, it is expected by the year 2048-2050, that the number of individuals with A.D. could be 15 million (Hebert et al, 2003).

A.D. is not a normal part of the aging process and the great risk factor for developing A.D. is increased age. On rare occassions, those < 65 y.o., [primarily bet. ages 30-50] develop symptoms of the early stages of A.D. This is soley based upon genetics.

The formation of amyloid plaques and neurofibrillary tangles are thought to contribute to the degredation of the neurons or (nerve cells) in the brain and the subsequent symptoms of A.D. A.D. is often associated with the accumulation of amyloid plaques between neurons or nerve cells in the brain. Protein fragments are identified as amyloid. This particular fragment of a protein is "snipped" from another protein called amyloid precursor protein or (APP). Healthy brains denotes protein fragments which are already brokend down. In a patient with A.D., these fragments accumulate.

One of the hallmarks of Alzheimer's disease is the accumulation of amyloid plaques between nerve cells (neurons) in the brain. Amyloid is a general term for protein fragments that the body produces normally. Beta-amyloid is a fragment of a protein that is snipped from another protein called amyloid precursor protein (APP). In a healthy brain, these protein fragments would be broken down and eliminated. In Alzheimer's disease, the fragments accumulate to form hard, insoluble plaques (Larsen et al, 2004). This is where this vaccine shows particular promise.

The implications of these Phase IIA findings are significant. If a treatment is discovered, it could possible delay the onset of stage 1 & 2 symptoms, by five years for those already diagnosed. According to the Centers for Medicare Services, the national direct and indirect annual costs of caring for individuals with A.D., are currently at $100 billion. Moroever, A,D, costs American business at least $61 billion a year according to (Alzheimer's Association; Brookmeyer et al, 1998; R. Ernst, 1998).

As we increase our attention to age-demographics in this country, due to the baby-boom generation, any positive news on the drug development [in the area of neuroscience and A.D.] front is welcomed.


Hebert, LE; Scherr, PA; Bienias, JL; Bennett, DA; Evans, DA. “Alzheimer Disease in the U.S. Population: Prevalence Estimates Using the 2000 Census.” Archives of Neurology August 2003; 60 (8): 1119 – 1122.

Brookmeyer, R; Gray, S; Kawas, C. “Projections of Alzheimer’s Disease in the United States and the Public Health Impact of Delaying Disease Onset.” American Journal of Public Health 1998; 88(9): 1337 – 1342.

Larson, EB, Shadlen, M-F, et al. “Survival after Initial Diagnosis of Alzheimer Disease.” Annals of Internal Medicine, 6 April 2004; pp. 501 – 509.

Ernst, RL; Hay, JW. “The U.S. Economic and Social Costs of Alzheimer’s Disease Revisited.” American Journal of Public Health 1994; 84(8): 1261 – 1264.

National Nursing Home Survey. National Center for Health Statistics, 1985; p. 49.

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