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Article:
New Hope for Alzheimer's Treatment by: Boris Predovich There is now widespread agreement among research scientists and medical professionals that Alzheimer's Disease (AD) is a problem quickly growing to vast proportions. As the life expectancy of Americans continues to rise, increasing the percentage of the population over 65 years of age, so does the number of Alzheimer's cases. It is currently estimated that people over 65 years of age have a 10% chance of developing Alzheimer's, while those over 85 have a 50% likelihood of developing AD, making it the leading cause of dementia among older people. Though the disease is associated primarily with memory loss, its effects also comprise a number of other severe disabilities, including changes in personality, disorientation, difficulty with speech and comprehension, and a lack of ability to move normally. Consequently, most Alzheimer's patients require a great deal of care, costing society close to $100 billion annually. According to Christian Fritze, Ph.D., Director of the Antibody Products Division at Covance Research Products, 'The impact of Alzheimer's Disease on our society will only increase as our population ages. The prevalence of the disease and disabling effects on the patient are significant by themselves. In addition we are becoming increasingly aware of the far-reaching effects on families, care-giver networks and the economics of our health care system. The drive for progress towards effective treatments by the research and drug development community is growing stronger every day.' A New Consensus But recent developments in the medical research community do provide some hope. During the last two years, there has been a growing consensus among Alzheimer researchers about the cause of Alzheimer's disease, providing focus for scientists exploring the new treatment options. The focus is on amyloid beta oligomers, a new wrinkle on an older hypothesis called the 'amyloid cascade hypothesis'. Widespread acceptance of this new conclusion is something of a milestone in the history of Alzheimer's research. As Dr. Fritze says, 'The decades old quest for the causative agent in Alzheimer's Disease has recently focused on the precursors of amyloid plaques. These precursors are part of a bewildering array of processed (APP) Amyloid Precursor Protein) variants, Tau isoforms and secretase components that play a role in neuronal cytotoxicity and subsequent brain dysfunction.' Amyloid plaques are sticky protein deposits in the brain containing amyloid beta peptide. Researchers have associated the buildup of this plaque with Alzheimer's disease since its discovery in 1907. But despite the clear correlation, scientists were not sure what, exactly, spurred the onset of Alzheimer's Disease. The hypothesis that amyloid beta accumulation in the brain is the major cause of Alzheimer's Disease1 has been the focus of much attention over the past decade. Although this hypothesis was the leading explanation for the cause of AD, it had several weaknesses. The most obvious problem with the theory was the fact that the buildup of amyloid beta peptides did not necessarily correspond with the severity of Alzheimer's symptoms. However, in 19982 and in '20023
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