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The Claude Wischik Interview (Page 1 of 2)

An Interview with Claude Wischik

Claude Wischik Interview

Professor Claude Wischik is board certified in psychiatry and Professor of Old Age Psychiatry at the University of Aberdeen, Scotland. A pioneer in tau research, Prof. Wischikís work on tau pathology began in 1985 in the laboratory of Sir Martin Roth, who was the first to correlate tangles with Alzheimerís dementia, and later he worked with Sir Aaron Klug (Nobel Laureate) at Cambridge University.

Gary Barg: Dr. Wischik, what is the current state of the science of determining the cause and possible treatment for Alzheimerís disease?

Claude Wischik: For the last twenty years or so the field has focused almost exclusively on the amyloid hypothesis. (Ed. note: The amyloid theory describes how an increase in secreted beta-amyloid peptides leads to the formation of plaques eventually resulting in the death of brain cells.) I think that view has been severely dented by repeated trial failures.

The main alternative is the theory that weíve backed since the mid-80s. And that is the tau theory. This builds on Dr.Alzheimerís original discovery. Dr. Alzheimer discovered a lesion in the brain called the tangle, which are abnormal fibers forming inside nerve cells. These nerve cells are the ones critical for all communication from one part of the brain to the other. We found that the amount of aggregated tau protein going into these tangles is really driving how demented people are.

Gary Barg: Is there a single target potentially identifiable for treatment of the disease? Or is it inherently more complicated?

Claude Wischik: I think tau plays an important role, but probably tau is also not the whole story. Itís just that tau is a better story than the amyloid. If I can put it in simple terms: as nerve cells age, their garbage disposal machinery becomes less and less efficient at handling bits of junk that form during the normal wear and tear of the cells. Once that process is initiated, it acts as a seed on which the tau aggregation can begin. And once tau aggregation begins, it just goes on and on, sucking more and more of the normal tau protein into these toxic aggregates.  And whatís worse is that this process spreads from one nerve cell to the next. I do sincerely believe that a tau based treatment will provide a way forward in the near term. Not just that, it may well be the only story thatís going to break in the next seven years for a potential successful treatment.

Gary Barg: Can you discuss the value of considering clinical trials for Alzheimerís caregivers?

Claude Wischik: Caregivers have to weigh a very simple odds calculation. Theyíve got to do this risk analysis. One, itís a dead certainty that if I have the disease, itís going to progress and at some point, Iím going to end up, or the person I care for is going to end up, in a nursing home. On the other hand, you have the possibility, but by no means the certainty, that a certain experimental treatment will delay or stop or protect from that outcome. Itís a very simple risk calculation to say youíre much better off trying an approach that may give hope versus the dead certainty of just staying where you are.

So for the caregiver and the patient, itís in their own selfish best interests that they participate in clinical trials. Then thereís the more altruistic thing which is that their participation in the trials will hasten the day when treatments can actually help. From a patient caregiver point of view, the odds are very simpleócertainty versus the possibility of a way out.

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