Has Alzheimer’s Research Been Wrong for 20 Years?

Alzheimer’s is the sixth leading cause of death in the United States. Affecting over 5 million Americans, the disease is incurable and untreatable. Most of the research done to find a cure for Alzheimer’s has revolved around the beta-amyloid protein, but now, some researchers are suggesting the past twenty years of Alzheimer’s research targeting this protein may have been one expensive mistake.

Has Alzheimer's Research Been Wrong for 20 Years?

What is Beta-amyloid?

Beta-amyloid is a protein that was found and identified by Alois Alzheimer in 1906. Most scientists and researchers believe that when beta-amyloid accumulates in the brain, it will cause Alzheimer’s disease. The prevailing theory is that the protein is sticky and forms a plaque which strangles healthy cells in the brain.

For over twenty years, researchers have been implicating beta-amyloid as a leading cause of Alzheimer’s disease. They have reasons to do so which include:

  • The discovery of rare genes that increase beta-amyloid production and almost guarantees the development of Alzheimer’s
  • The observation that mice who develop amyloid plaques also develop behaviors that mimic human dementia and Alzheimer’s
  • Noting that people with Down Syndrome have three copies of the gene that carries that beta-amyloid protein and they often develop Alzheimer’s disease by middle age

Is Beta Amyloid the Wrong Protein?

Despite the evidence that links beta-amyloid with Alzheimer’s, a growing group of scientists are questioning the decades old theory. For two decades, researchers have tried and failed to treat, stop, and prevent Alzheimer’s using drugs that attack the beta-amyloid protein. There have been more than 100 drugs tested that have failed. While it is possible that the drugs weren’t good or were given too late in the Alzheimer’s process to be effective, some scientists think it is because the beta-amyloid protein is not the issue.

One of these scientists is Claude Wischick, founder of pharmaceutical company TauRx. “It’s extraordinary that in the face of these failed trials, the claims for amyloid remain exactly the same as though there haven’t been any failure,” Wischik said. “There’s been no fundamental revision of the thinking.”

What Does This Mean for Future Research?

Wischick and like-minded researchers believe another mechanism may be at fault. In the 1990s, a team of researchers found that the degeneration of tau is more directly linked to the development of Alzheimer’s than beta-amyloid. Tau is another protein in the brain and its main function is to hold cells open to receive nutrients. When tau clumps together, the cells can not get the necessary nutrients they die, resulting in Alzheimer’s disease.

A clinical study, sponsored by Wischick’s company TauRx, is working towards enrolling 1,500 participants to test the tau theory. The study will evaluate the effectiveness of a drug called TRX-015 and data from that trial will hopefully be available in early 2016.

Researchers continue to attack Alzheimer’s from both angles, hoping that one study will lead to a breakthrough that stops the global Alzheimer’s epidemic.

Do you believe the beta-amyloid protein is the main culprit in Alzheimer’s disease? Or should researchers switch gears and do what is necessary to find a cure?

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Please leave your thoughts and comments

  • Nice article!

  • Guest

    The study from the 1990s is old. ABeta is still a big factor and has been shown to appear before tau. Abeta can induce hyperphosphorylation tau, but tau doesn’t induce misfolding of Abeta.

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