Share
3,630 Posts.
lightbulb Created with Sketch. 116
clock Created with Sketch. 14/11/18
11:34
Share
Originally posted by skint:
↑
“It used to be thought that stopping the plaques early was ‘primary prevention,’” Tanzi said. “I think primary prevention is stopping the microbes.” Treatment would mean leaving amyloid mostly alone (since it protects the brain from herpes and other viruses) but targeting inflammation, a biological fire that “kills 10 neurons for every one killed by amyloid and tau directly,” he said. “Neuroinflammation is where we’re going to find [Alzheimer’s] drugs. PolicyTanzi chairs the scientific advisory board of AZTherapies, a Boston-based biotech that is recruiting patients with early Alzheimer’s for a clinical trial testing whether inhaling a powdered form of the immune-targeting drug cromolyn reduces dementia. (The nose connects to the brain.)One reviewer of Moir’s latest NIH grant proposal called it “fascinating and innovative,” with “the potential for answering the vital question” of what causes late-onset Alzheimer’s. (The early-onset form is genetic.) Moir, the reviewer said, “has consistently produced creative, thought-provoking work.”Another, however, slammed the proposed research, questioning whether it “will be relevant to understand AD pathogenesis” since, in his view, amyloid formation might not matter in Alzheimer’s. (It’s the disease’s defining trait.)The proposal was turned down in June. “One bad review can sink a new and innovative idea just because it’s new and innovative,” Moir said matter-of-factly. He can’t work up much animosity anymore.
Expand
Prana's PBT2 does not attack the amyloid, but competed with amyloid for transition metals which it could chaperone back to where they are needed. Over 10 years ago Tanzi seemed to be aware that MABs designed to directly attack AB were the wrong way to go. He(and Prana) were so far ahead of the field back then, but that was in the GFC of 2008 and the money had dried up.
