Aussi at Harvard. Moir., page-2

“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.
This month, however, he got an unheard-of email from NIH: The agency had found some extra money lying around in its budget. Would he please respond to the reviewers and resubmit his proposal? An over-the-moon Moir did. He expects to hear back in a few weeks.