Slowing the Formation of Beta Amyloid Plaques

Beta amyloid plaques are deposits of abnormal, highly insoluble protein.  They form in the space between cells in the Alzheimer brain, and are one of the characteristic hallmarks that identify Alzheimer’s disease at autopsy. There are drugs being developed to slow the formation of these plaques and to speed the clearance of the beta amyloid deposits. To find compounds that prevent the clumping of beta amyloid, are reasonably nontoxic, and are effective when taken orally has been difficult.

The company did WHAT??

One particularly interesting drug was called tramiprosate. In the laboratory, it attaches to Aβ and stops clumps from forming. But when tramiprosate was tested in North America on volunteers with mild-to-moderate Alzheimer’s, it was not effective. The company developing the drug, Bellus Health, discontinued a similar study in Europe. Instead, in 2008, they released tramiprosate as an over-the-counter neutriceutical (a nutritional supplement or herbal remedy) said to protect memory functions. They called it Vivimind. There was protest from the scientific community over this release, but it was essentially ignored.

Another drug preventing the clumping together of Aβ is called Clioquinol (PBT1). This drug was highly toxic in initial studies, but a new version of it, PBT2, is showing good results in animal studies. It is not uncommon for a drug to be developed in several versions. Small changes in chemical structure that do not significantly change the effect of a drug in the laboratory can make a big difference when that same drug is tested in animals or humans. PBT2 looks promising.

Next time, drugs that clear away amyloid plaques—using the immune system to fight Alzheimer’s!


6 thoughts on “Slowing the Formation of Beta Amyloid Plaques

  1. Are Beta Amyloid Plaques slowed by exercise and nutrition or just by drugs? Is just the symptoms that are slowed by exercise and nutrition? What percentage of those diagnosed with Alzheimer’s actually have an autopsy? I personally wish everyone would have autopsy to get a handle on what works, what doesn’t, and how many misdiagnosis.


    • We know that exercise and good nutrition are important in Alzheimer’s, as well as being just plain important for general brain health. Research shows all kinds of benefits to brain cells from exercise! When I finish this long series on drug development, I want to get into brain health. Thanks for the questions! I don’t know what percent of Alzheimer’s victims have an autopsy. Generally speaking, families are receptive to donating brains for research, but only major medical facilities have the personnel (with the training AND the time) to properly prepare and classify brain donations. Thus, I would guess the actual percentage to be fairly small. If I find any stats on this, I will put it in a blog.


  2. my gf has huntingtons disease (juvenile onset) she’s 33 and exhibits few symptoms of the disease so far. having been with her 24/7 for years now, i notice a complete absence of dimensia. some dystonia from time to time, and little to any corea. her speech is often affected, and can be a challenge for her. would pbt2 be a treatment one in such position consider, with any discernable expectations?


    • Hi, Anthony. I am not qualified to comment on Huntington’s or pbt2. I am a neuroscientist whose background is in Alzheimer’s research. What I do is try to help people understand the scientific background of Alzheimer’s, so they can better understand the articles they read about it. I would encourage your girlfriend to ask her doctor about the pbt2 treatment. Or perhaps you could ask your doctor–that would give you two opinions to go on. I hope you succeed in finding the information and advice you are looking for.


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