Alzheimer's enzyme important regulator
The enzyme Bace1, which plays a central role in Alzheimer's disease, is also responsible for the myelin covering of nerve fibers. Future Alzheimer's therapies that try to switch off Bace1 could therefore lead to serious side effects, warn researchers led by Riqiang Wan from the Lerner Research Institute.
Alzheimer's disease is characterized by fragments of the protein APP (amyloid precursor protein) accumulating in the nerve cells, which lead to functional failures. Bace1 starts this process by splitting APP. According to the authors, no other functions of the enzyme were previously known.
In genetically modified mice that could not develop Bace1, however, the myelin sheath of their nerve fibers was also underdeveloped. The animals were more sensitive to pain and had less control over their muscles. The scientists therefore assume that the enzyme has a regulatory impact on the myelination process. Myelin wraps the axons, causing the excitation signal to spread much faster. If axons are insufficiently isolated, symptoms typically appear, as observed in the modified laboratory mice.
Should it turn out that Bace1 is not only responsible for the formation but also for the maintenance of already developed myelin sheaths, caution should therefore be exercised when trying to counteract the harmful cleavage of APP by switching off the enzyme.
