There are now more than 5 million Americans suffering from Alzheimer’s dementia (AD) at an annual financial cost to the U.S. health care system of $200 billion a year but of course the real cost is the human tragedy that this disease causes as people lose their ability to function and as caregivers, often spouses and other family members, struggle to provide proper care for their loved ones. With the increasing baby boomer population, the number of Americans with Alzheimer’s dementia could skyrocket to 15 million by 2050 at an annual cost of $1.2 trillion.1 The extent of this rapidly developing crisis has not escaped the government, academic research laboratories and the pharmaceutical industry which are pouring significant dollars into research to find a cure for this menace. In order for a safe and effective drug to be developed research scientists must first define a disease on a molecular level. That has not yet been accomplished for AD however the understanding of the pathogenesis of AD has increased greatly since the early 1990s resulting in increasing optimism that better treatments can be developed.2 AD is currently perceived as a protein aggregation disorder and researchers now know that a protein called amyloid-beta (Ab) plays an important role in the pathogenesis of AD. Aggregates of this protein are present in the extracellular plaques that are found in the brains of those with AD and it is now thought to be a toxin that leads to the dysfunction of neurons eventually leading to the extensive neurological damage that is the hallmark of this disease.2 Briefly, Ab is produced when beta amyloid precursor protein is improperly cleaved.3 It is an important step inwhat is referred to as the amyloid cascade hypothesis which researchers are targeting in order to prevent, or at least significantly delay, the ultimate damage
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