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One of the impediements to studying Alzheimer's disease in living brain cells is that the owners of the brains that have Alzheimer's aren't through using them. A breakthrough method, however, allows study of Alzheimer's in a Petri dish.

The ability to observe changes in living brain cells has breathed new life into the old theory that the formation of plaques and tangles causes the symptoms of Alzheimer's, and the prevention of plaques and tangles may prevent the symptoms of the disease. In the laboratory, scientists can clearly observe the following sequence of steps:

  • The formation of beta-amyloid protein in the fatty layers of individual neurons,
  • The accumulation of this "sticky" protein around neurons,
  • Blocking of cell-to-cell transmission of electrical impulses by pieces of plaque, and
  • The collapse of the tau (rhymes with wow) protein around neurons to form tangles.

Changes to tau protein usually accompany what is believed to the final stage of the destruction of a brain cell.

In a healthy brain, tau protein strengthens microscopic tissues that allow for the passage of oxygen, nutrients, and regulatory substances from cell to cell.

Strong tau protein is often compared to railroad tracks, speeding the passage of sustenance for the brain. Degraded tau protein looks a little like wrecked railroad tracks, no longer capable of sending substances where they need to go. Brain cells eventually starve, and those that do not starve lose their connections to the rest of the brain.

Five Thousand Possible Cures Now Testable

This new method of observing brain cells does not provide a way to track interaction of brain proteins with the immune system (yet), but it does allow researchers to measure the effects of medications on this part of the pathology of the disease. Even better, it allows researchers to evaluate the potential of new drugs in just a matter of months, compared to a year for each drug tested in mice, and 20 years or more of observing humans diagnosed with the disease.

Dr. Tanzi plans to test 1,200 Alzheimer's disease treatments already on the market, and up to 5,000 more potential treatments over the next few years. Dr. Sam Gandy of the Icahn School of Medicine at Mount Sinai in New York told a New York Times reporter that the new method is “a real game changer” and “a paradigm shifter," and added, “I’m really enthusiastic to take a crack at this in my lab.”

So, Is a Breakthrough Treatment Coming Soon?

Tanzi and other researchers caution that treatments that work in the lab don't necessarily work in people. One medication got good results in treating cultures of brain cells but was found to be too toxic for people. 

Any medication that works in the lab will still have to be tested on a small group of people before it is released to the public at large.

The new system, however, is not only useful in identifying new drugs that work. It can also be used to study the effects of genetic differences on the course of the disease. Scientists have already started testing brain cells with different APOE genes to see how different genes cause different responses to drugs (and potentially how genetic testing can help doctors prescribe the best drug for their patients). These potential breakthrough drugs probably won't work in absolutely every case of Alzheimer's--some people who have Alzheimer's don't have plaques and tangles--but new drugs that work in many or most cases may be coming in as little as 5 years.

  • Choi SH, Kim YH, Hebisch M, Sliwinski C, Lee S, D'Avanzo C, Chen H, Hooli B, Asselin C, Muffat J, Klee JB, Zhang C, Wainger BJ, Peitz M, Kovacs DM, Woolf CJ, Wagner SL, Tanzi RE, Kim DY. A three-dimensional human neural cell culture model of Alzheimer's disease.Nature. 2014 Oct 12. doi: 10.1038/nature13800. [Epub ahead of print] PMID: 25307057.
  • Kolata, G. Breakthrough Replicates Human Brain Cells for Use in Alzheimer’s Research. New York Times. 14 October 2014.
  • Photo courtesy of Alberta Innovation and Advanced Education by Flickr :
  • Photo courtesy of Carissa Rogers by Flickr :

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