Prions Mutate, Migrate Throughout Body
Alzheimer’s disease proteins form and accumulate differently in every patient, according to new research. This means that universal treatments may be impossible. With Alzheimer’s disease a protein called amyloid-beta forms fibers that congregate into plaques. These protein formations appear to be toxic and destructive to brain cells. The neurodegeneration associated with Alzheimer’s disease starts years before symptoms of dementia appear.
Alzheimer’s disease is a form of dementia that causes gradual deterioration of the memory and thinking process and, eventually, death. A new study suggests that each person may have a distinct version of the fibers, and that this affects how the disease develops. This was shown from a small study where the A-beta protein was removed from the brain tissue of two women who had died from Alzheimer’s disease.
The women had different symptoms and the disease affected different parts of their brains and the protein took only a very different shape in each of the women. What the researchers found was that one woman’s fibers were long, thin and straight, while the other woman’s fibers were thicker and contained periodic twists. The research was undertaken by the U.S. National Institutes of Health and the findings have been published in the journal Cell.
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Gary Chandler is a prion expert. He is the CEO of Crossbow Communications, author of several books and producer of documentaries about health and environmental issues around the world. Chandler is connecting the dots to the global surge in neurodegenerative disease, including Alzheimer’s disease, Parkinson’s disease, Creutzfeldt-Jakob disease, chronic wasting disease and other forms of prion disease. The scientific name for prion disease is transmissible spongiform encephalopathy. The operative word is “transmissible.” Even the global surge in autism appears to be related.