At least three of the large anti-amyloid trials will be adding tau imaging to the existing protocol, Dr. Buckholtz added.
Preclinically, he said, the induction of pluripotent stem cells into neurons with an aging phenotype was a very important step in creating in vitro models of human aging (Cell Stem Cell. 2015 Dec 3;17[6]:705-18). Before this discovery, stem cell–induced neurons didn’t re-create human aging; in fact, induction somehow seemed to rejuvenate them, even if the progenitor cells were from an elderly person.
“Making these neurons with an aging phenotype is going to be very important as we look at aging – the biggest single risk factor for Alzheimer’s,” Dr. Buckholtz said.
Sleep is another emerging story, he said. “The relationship between sleep and beta-amyloid is fascinating. Some studies indicate that amyloid disrupts slow-wave sleep, which is needed for memory formation.”
And, despite the decades-old knowledge that the apolipoprotein E epsilon-4 allele confers various levels of Alzheimer’s risk, little is known about the mechanics of that relationship. Dr. Buckholtz hopes that will change in the near future.
Finally, work continues on what he called one of Alzheimer’s Holy Grails: a validated, blood-based biomarker. “The search hasn’t gone as well as we hoped it would. We still don’t have a reliable one, but no one is sure if that’s because there are just so many things that affect blood proteins or because we simply don’t have a good way to look at it. I’m hopeful, though. An accurate blood-based biomarker would bring Alzheimer’s screening into the primary care office. It would be an enormous step.”
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