Research Shows We are Behind on Alzheimer’s Advancements
December 18, 2009
By David Gutierrez
Research is emerging that casts serious doubt on the major hypothesis as to the cause of Alzheimer’s disease, raising questions as to whether scientists really understand the disease at all.
The most effective drug currently in use for the treatment of Alzheimer’s is not any of the complex drugs developed or used in the United States or in Western Europe, which slow cognitive decline for only about six to nine months. That honor goes to a Russian antihistamine named dimebolin, which reverses the symptoms of Alzheimer’s for a full year. Although not currently approved for U.S. use by the FDA, dimebolin is shaking up the Alzheimer’s research world.
In a study conducted by researchers from Mount Sinai School of Medicine and presented at the International Conference on Alzheimer’s Disease in Vienna, dimebolin was found to drastically improve symptoms at the same time that it led to a drastic increase in the levels of the beta amyloid protein in brain cells, both in cell-based experiments and in the brains of mice. Yet beta amyloids are the very molecules that most Western researchers have, until recently, believed to be the cause of the disease, by forming sticky plaques in the brain that interfere with neural functioning.
“I would say that conventional wisdom in the field … is that an amyloid benefit would mean amyloid-lowering,” researcher Sam Gandy said. “Certainly, up until now, no one has been looking (intentionally) to treat Alzheimer’s by raising amyloid levels. [So] it was startling to observe that a compound with an apparently beneficial clinical effect on cognition caused acute elevation of amyloid beta levels in three out of three systems, in two labs.”
The pharmaceutical industry has been pouring massive amounts of time and money into drugs capable of lowering amyloid levels directly – efforts that it now seems may do more harm than good. In light of recent findings, some researchers are now suggesting that amyloid plaques might actually function as a toxic waste dump of sorts, sequestering dangerous compounds to defend the brain from further damage. If so, eliminating them might drastically accelerate the progress of dementia.