> Horvath used four different epigenetic clocks to assess each patient’s biological age, and he found significant reversal for each trial participant in all of the tests.
Presumably the "epigenetic clocks" are correlated with age, but it's not clear if changes to the epigenetic clocks causes aging, or aging causes changes to the epigenetic clocks. (Maybe it's both?) Is this like overhauling the engine in an old car to make it function like new, or is it more like rolling back the odometer to make it seem new?
'The FDA’s eventual decision to ignore the advice of its advisory committee and approve the drug, it says, was based on aducanumab’s ability to lower levels of amyloid plaques in the brain — protein clumps that some scientists think cause Alzheimer’s.'
...
With aducanumab, the agency has shown that it is willing to push the paradigm to a broader set of people. One reason that decision has attracted criticism is that decreased levels of amyloid plaques are an unvalidated and contentious marker of a drug’s activity.
In large trials of other Alzheimer’s drug candidates, amyloid lowering has not led to cognitive benefits, and this has made it a sticking point for researchers.' [0]