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.
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!