New Hope for Alzheimer’s Treatment By Boris Predovich, Covance Research ProductsThere 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.
This new focus provides one more spur to action for Alzheimer’s researchers, and underscores
need for further advancement. “The AD field demands sophisticated, highly-sensitive research tools to track these components and quantitate
existence of monomeric, oligomeric and fibrillar amyloid forms present in
progression of Alzheimer's disease,” says Dr. Fritze.