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ALZHEIMER'S DISEASE BETWEEN THE BETA AMYLOID AND THE TAU. COULD BOTH THEORIES BE TRUE?

Prohost Biotech - Tuesday, November 13, 2012

Many are asking our opinion on the Wall Street Journal’s article on Alzheimer’s Disease. To begin with, we would like to state that we do not believe that the beta amyloid hypothesis has failed with regard to Alzheimer’s Disease (AD), but that clearing the plaques has failed because the treatments were given after the disease has reached the stage of no return, i.e., when  the nerve cells could not be resurrected. That’s why there are still fervent believers in the beta amyloid theory who say that beta amyloid needs to be attacked very early in the disease cycle—perhaps before symptoms begin—for such medicines to work.   

The reason why treatments of beta amyloid could not be given early enough is that there were no diagnostic tests that could pin down the disease or suspect it before the appearance of symptoms. Currently, several diagnostic procedures have been made available, including genetic tests, which enable identifying the disease at very early stages and pinpointing vulnerable people. That is the reason why the U.S. government decided to help fund a $100 million trial of Roche's amyloid-targeted drug crenezumab in 300 people who are genetically predisposed to develop early-onset Alzheimer's. According to the Wall Street Journal article, Dr. Selkoe, one of the authors of the amyloid hypothesis, said that this trial should help provide a "definitive" answer about the theory.” 

The tau theory is not new. Elan (ELN), other drug companies, and academic researchers have already considered tau as part of the problem, yet, without dumping the beta amyloid hypothesis, but adding to it. Some believe tau is part of the pathological process that leads to AD. 

The reasons scientists and investors are turning more attention to tau are the failures of the several drugs targeting beta amyloid. Also, analysts and investors have heard about the offer Roche has made to the Swiss firm AC Immune for the rights to a new type of tau-targeted drug. Roche offered an undisclosed amount to be followed by up to CHF400 million in additional payments if any drugs would make it to market.

What we see here is a situation where a successful treatment could be accomplished through the following:

- Drugs that deal with the beta amyloid to be given at a very early stage in the disease. to prevent plaques from forming. This treatment would be preventive and given only to subjects whose genetic analysis results classify them as vulnerable to developing AD.  

- Tau treatments as being suggested by various developers and scientists. The same rule applies, i.e., the drug should be given very early in the disease, or before the appearance of symptoms

- Beta amyloid treatment and tau treatment administered together.

Trials with drugs that deal with the beta amyloid very early in the disease, even before the symptoms appear have already been scheduled, as cited above. With regard to tau treatments, as mentioned in the WSJ article, Johnson & Johnson invited Dr. Buee, the longtime tau researcher in France and other scientists to a meeting to discuss a range of approaches to fighting Alzheimer's.

So large drug developing firms are now involved in treatments based on the tau hypothesis. With regard to the firm TauRx, established by Dr. Wischik, it is the first company to test a tau-targeted drug against Alzheimer's in a large Phase 3 human clinical trial. WSJ revealed that the man who showed passionate beliefs in the tau hypothesis admitted that he ‘may be just as much a zealot about tau as he accuses others of being about beta amyloid.’ "I may be," he says. "In the end…it's down to the phase 3 trial.”

Inspite of the increased optimism, nobody could predict the outcome of any of the aforementioned clinical trials. Nobody yet knows, which of these approaches would finally conquer Alzheimer’s Disease. The good news in that the genomic revolution enabled identifying vulnerable patients, which allowed treatments to be given before the toxic beta amyloid kills the nerves cells and before the neurofibrillary tangles, the second anatomical hallmark of AD, further twist and tangle, causing the brain cells to become unable to transport nutrients properly and eventually die.

The only speculation we can make now is that scientists have in hand most of what is required to make them close in on Alzheimer’s Disease.

We are optimistic.      

FORWARD-LOOKING: Material presented here is for informational purposes only. Nothing in this article should be taken as a solicitation to purchase or sell securities. Before buying or selling any stock you should do your own research and reach your own conclusion. Further, these are our 'opinions' and we may be wrong. We may have positions in securities mentioned in this article. You should take this into consideration before acting on any advice given in this article. If this makes you uncomfortable, then do not listen to our thoughts and opinions. The contents of this article do not take into consideration your individual investment objectives so consult with your own financial adviser before making an investment decision. Investing includes certain risks including loss of principal.

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