Jun 18, 2010

No End to Dementia

Ten years ago people talked confidently of stopping Alzheimer’s disease in its tracks. Now, they realise they have no idea how to do that.....
By Bob DeMarco
Alzheimer's Reading Room

I just finished reading an interesting article on The Economist about Alzheimer's and dementia. It is easy to get frustrated about the lack of any new treatments since Namenda in 2003. About 11 clinical trials aimed at discovering a treatment for Alzheimer's have failed.

Increasing discussion are taking place about the dominant theory of the last 20 years beta-amyloid -- the plaque theory. Have scientist been looking in the wrong place?

The Economist is a major international publication. The simple fact that they are bringing light on to the issues and the drops in funding for Alzheimer's research is a positive.

Recently researchers have agree to share 4,000 profiles of patients from the 11 trials. This is also a big positive. The sharing of intellectual capital and collaboration is a big step in the right direction.

Is it possible that a subset of all Alzheimer's patients could benefit from drugs that are failing? Could we learn more by dividing Alzheimer's patients into subsets and defining their characteristics?

Hopefully new and innovation appproaches will be discovered through sharing and collaboration.

Beta testing

The problem of what causes Alzheimer’s is profound. The physical manifestations of the disease that Alois Alzheimer noticed in 1906 are sticky plaques of one type of protein, now known as beta-amyloid, and nerve-cell-engulfing tangles of a second type, called tau protein. Since 1991 the smart money has been on the hypothesis that the disease is caused by the plaques, and that the tangles are mere consequence. For the past two decades, therefore, most attention has been given to developing drugs that will remove amyloid plaques from an affected brain. Five drugs that do this are on the market, but they only delay the onset of dementia. Once their effectiveness has run its course, memory loss and cognitive decline progress unimpeded, and sometimes even accelerate.

Partly as a consequence of this, the plaque theory is waning. Most researchers still believe beta-amyloid is the culprit, but the idea that free-floating protein molecules, rather than the proteins in the plaques, are to blame is gaining ground. This idea is supported by a study published in April in the Annals of Neurology, which showed that mice without plaques, but with floating beta-amyloid, were just as weakened by the disease as mice with both. If that is true in people, too, many more drugs now in clinical trials may prove to be ineffective.
To read the entire article at The Economist -- go here.

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Bob DeMarco is the editor of the Alzheimer's Reading Room and an Alzheimer's caregiver. Bob has written more than 1,565 articles with more than 8,000 links on the Internet. Bob resides in Delray Beach, FL.

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Original content Bob DeMarco, the Alzheimer's Reading Room