That’s what Rudolph Tanzi, a prominent Alzheimer’s researcher at MGH says about the work of Robert Moir, a member of his team. A story in STAT last week — which ran in today’s Globe – chronicles Moir’s struggle to get funding for a theory that
Alzheimer’s disease is a triggered by microbes in the brain.
“If true, the finding would open up vastly different possibilities for therapy than the types of compounds virtually everyone else was pursuing, ” Sharon Begley writes….
If he and other scientists are right that beta-amyloid is an antimicrobial, that the brain goes on an amyloid-making immune rampage in response to pathogens, and that the rampage ignites neuron-killing inflammation, it suggests very different therapeutic approaches than the 30-year pursuit of amyloid destroyers.
“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.”
Noting the final paragraph. Not sure it applies here, but sometimes just a call from a reporter can move some wheels. (See the Globe’s Fine Print column as an example.)
This month…(Moir) 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.