While similar to senile dementia, Alzheimer’s disease is a progressive form of presenile dementia that usually starts in the 40s or 50s. Its first symptoms are impaired memory which is followed by impaired thought and speech and finally complete helplessness.

This inevitable progression toward helplessness makes Alzheimer’s a frightening prospect for anyone diagnosed with the disease. It has always been the equivalent of a death sentence. Approximately 4.5 million Americans alone are afflicted by the disease which is steadily increasing as the population ages.

Now, however, a study headed by Dr. Karen Ashe, a neurologist at the University of Minnesota, suggests the possibility exists that this dreaded disease may be reversible in its early stages.

The study which is published in this week’s issue of the journal Science found that certain neurons (brain cells) affected by Alzheimer’s are not dead but are being poisoned by a mutant protein known as tau.

The theory is that blocking the production of the protein may allow a sufficient number of affected neurons to recover. The process worked in demented mice that rapidly regained memory. This finding made it clear that tau plays some role in the disease process.

Currently, there are no medications to block tau. Most of the research with respect to finding a treatment for Alzheimer’s is focused on another protein known as beta-amyloid. The study should have the effect of making tau a target of increased attention.

The importance of the study is that it raises the prospect of returning some brain function where, previously, none was believed to be possible.    

Although the cause of the disease remains unknown, one interesting theory is that some factor stimulates the growth of beta-amyloid which then forms sticky coatings on brain cells which kills them.

The mice used in the study were specially engineered to mimic the build up and tangling of beta-amyloid in order to see if the process was a cause or a symptom of the disease.

As these mice aged, more tangles built up and more brain cells died. The mice suffered significant memory loss. Tests were devised to demonstrate this fact.

When the production of tau was blocked by an antibiotic which turned of the gene involved, the memory lose was not only halted, it was actually reversed to some extent.   

While the recovery was only a partial one, since dead brain cells cannot be restored, the results showed that memory was improved to about 50% of the pre-dementia level. Brain cell death was also halted.

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