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 life expectancy of Americans continues to rise, increasing percentage of population over 65 years of age, so does 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 leading cause of dementia among older people. Though 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 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 disease and disabling effects on patient are significant by themselves. In addition we are becoming increasingly aware of far-reaching effects on families, care-giver networks and economics of our health care system. The drive for progress towards effective treatments by research and drug development community is growing stronger every day."

A New Consensus

But recent developments in medical research community do provide some hope. During last two years, there has been a growing consensus among Alzheimer researchers about cause of Alzheimer’s disease, providing focus for scientists exploring new treatment options.

The focus is on amyloid beta oligomers, a new wrinkle on an older hypothesis called “amyloid cascade hypothesis”. Widespread acceptance of this new conclusion is something of a milestone in history of Alzheimer’s research. As Dr. Fritze says, "The decades old quest for causative agent in Alzheimer's Disease has recently focused on 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 brain containing amyloid beta peptide. Researchers have associated buildup of this plaque with Alzheimer’s disease since its discovery in 1907. But despite clear correlation, scientists were not sure what, exactly, spurred onset of Alzheimer’s Disease. The hypothesis that amyloid beta accumulation in brain is major cause of Alzheimer’s Disease1 has been focus of much attention over past decade. Although this hypothesis was leading explanation for cause of AD, it had several weaknesses. The most obvious problem with theory was fact that buildup of amyloid beta peptides did not necessarily correspond with severity of Alzheimer’s symptoms.

However, in 19982 and in 20023, researchers proposed that it was not amyloid beta plaques themselves that were neurotoxic – and therefore cause of Alzheimer’s – but rather precursors to amyloid beta plaques formed by smaller aggregates of amyloid beta. These new ideas are gaining widespread acceptance among Alzheimer’s research community, creating a consensus that had not existed before.