February 21, 2012
Alzheimer’s Drugs Acting Like a Bad Electrician?
(Ivanhoe Newswire) -- Recent research has shown that Alzheimer's drugs, which are in clinical trials still, have adverse side effects.
The drugs are designed to prevent BACE1, the enzyme Robert Vassar originally discovered that promotes the development of clumps of plaque associated with Alzheimer's. BACE1 cuts up and releases proteins that form the plaque, making those who developed the drug believe that by blocking the enzyme the development of Alzheimer's disease might slow down.
The study that was performed on mice shows that the drugs act as a bad electrician, meaning neurons are ℠wired´ wrong and interfere with their ability to send messages to the brain. BACE1 was found to map out the location of the wires that connect neurons to the brain and the rest of the nervous system (called axonal guidance). In the study, BACE1 was genetically removed from the mice and researchers discovered that the animals' olfactory system that is used for the sense of smell was wired incorrectly, BACE1 being the key role in axonal guidance.
When the axons are not properly connected to the olfactory system, the problem most likely will exist in the brain or the nervous system. The hippocampus, the part of the brain that is involved with memory, could be vulnerable to BACE1 blockers because of the neurons population being continuously reborn. It is imperative that the neurons grow new axons that must connect them with new targets.
"It's like a badly wired house. If the electrician doesn't get the wiring pattern correct, your lights won't turn on and the outlets won't work. It's not all bad news, however. These BACE1 blockers might be useful at a specific dose that will reduce the amyloid plaques but not high enough to interfere with the wiring. Understanding the normal function of BACE1 may help us avoid potential drug side effects," professor of cell and molecular biology at Northwestern University Feinberg School of Medicine, Robert Vassar, was quoted as saying.
SOURCE: Molecular Neurodegeneration, February 2012