After five years of testing, two more proposed Alzheimer's drugs have failed to improve cognition in test subjects. This is according to an article in the AP. The drugs are solanezumab by Eli Lilly & Co., and gantenerumab by Swiss drugmaker Roche and its U.S. subsidiary, Genentech. (There's a system for coming up with these names, but good luck learning to pronounce them.)
This was not a big surprise, because the mode of action for both drugs is removal of amyloid beta from the brain, and this strategy hasn't lived up to earlier hopes. Of course, aducanumab and BAN2401 may yet show the way to at least slow the advance of Alzheimer's, and this by removal of amyloids. But solanezumab and gantenerumab are out of the running for that job.
According to the AP article, the tests involved about 200 test subjects carrying genes for younger onset Alzheimer's disease. People carrying these genes are almost certain to develop the disease, perhaps in their 40s or 50s. This form of the disease is also often called early onset Alzheimer's disease and familial Alzheimer's disease, but the Alzheimer's Association prefers younger onset Alzheimer's disease. This is because "early onset" gets confused with "early stage."
People carrying the genes for younger onset Alzheimer's disease are good test subjects, because you can be reasonably confident that stabilized cognition or failure to develop the disease are due to your drug, and not just chance.
In my book, "Beating the Dementia Monster," I describe what has occurred since 2015 when I first knew I had memory problems. (You can find it on Amazon.com.) I have experienced remarkable improvement, and I’m certain that I can share valuable information with many others. In this second edition I continue my story to 2020 and provide greater understanding of how Alzheimer's advances and why what I did worked.
Sunday, February 16, 2020
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