Today is “International Alzheimer’s Day”. Given my interest in Alzheimer’s disease (AD) and my role at Pfizer to investigate the safety and efficacy of a potential therapy in AD patients, this seemed like an especially appropriate day to blog. AD is second only to cancer as the most feared disease in the United States. It is a particularly cruel disease, given the progression of the dementia over an 8-10 year period (dementia is the loss of intellectual and social abilities severe enough to interfere with daily functioning).
The greatest risk factor for developing AD is advancing age. The risk doubles every five years from about the age of 65 onward. Age, of course, is not a risk factor that we can do anything about. Nor is our genetic make-up: do we have one (or two) Apo E4 genes, do we have a first degree relative with AD, etc…On the other hand, there are other risk factors that are at least, in part, within our control: do we have a heart healthy lifestyle, do we exercise regularly, do we keep an eye on our weight, blood pressure and cholesterol? All of these factors can contribute to whether (and when) we are ever diagnosed with AD. By looking at these risk factors, it’s clear that, in general, what is good for the heart is good for the brain, and vice-versa. It is also becoming increasing clear that AD is a disease that can begin years, probably decades, before individuals (and those who regularly interact with them) notice that there are significant problems in the ability to think, reason, remember and follow through with a task. What this means is that the brain, like all other organs in the body (lungs, liver, kidneys, etc…) has some resiliency or reserve. Thus, for a while, there may be compensatory mechanisms that still allow individuals to function at their baseline level. However, at some point, the brain can no longer fully compensate and the difficulties in thinking and memory begin to become evident.
I believe that we are making great strides towards understanding what causes AD. Two proteins, called amyloid (Abeta) and tau are made in excessive amounts in the brains of individuals who have been diagnosed with AD. We now have experimental (not FDA approved yet) drugs that appear to have the capability of actually determining how much amyloid is in a person’s brain and thus to make a good inference as to whether they have AD. There are many different promising drugs that are targeting these two abnormal proteins, but none of them are approved for the treatment of AD at this time. I work on an antibody program that targets the amyloid protein. Antibodies can ‘capture’ certain proteins and thus render them incapable of performing their action (good or bad). Antibodies can be very specific for a certain protein (monoclonal antibody) or target several or many proteins (polyclonal). The one I am investigating is very specific for amyloid. We are currently studying this anti-amyloid antibody in patients who have AD to determine its safety and efficacy.
Of course, there are many other approaches besides targeting the abnormal amyloid or tau proteins and no one is sure about which approach is the best one or if we might even need more than one approach! It is an exciting time in Alzheimer’s research and I am delighted that Pfizer has committed significance resources to finding improved medicines to treat this dreaded disease.




