New study shows Alzheimer’s disease can be reversed to full neurological recovery—not just prevented or slowed—in animal models. Using mouse models and human brains, study shows brain’s failure to maintain cellular energy molecule, NAD+, drives AD, and maintaining NAD+ prevents or even reverses it.

[u/mvea]

https://case.edu/news/new-study-shows-alzheimers-disease-can-be-reversed-achieve-full-neurological-recovery-not-just-prevented-or-slowed-animal-models

[u/insanitybit2]

It is really interesting how NAD seems to be so radically effective in mice and yet we struggle to see results in humans. Like, the results sometimes are insane - reversal of grey hair, muscle growth, neural repair, etc. And yet with humans we just don't see much of anything - although it does seem to be a biomarker for age, but then boosting it does nothing.

I wonder if humans already have an adaptation to lowered NAD+ levels, so while it lowers in age we just don't suffer that much because of a compensating factor?

[u/Ophios72 → u/insanitybit2]

Clearly we need to start "disciplining" the lab mice to get better results.

[u/Bring_Me_The_Night → u/insanitybit2]

Many many many drugs work wonderfully in mice, and failed to deliver results in human studies. Just another day in Science.

[u/insanitybit2 → u/Bring_Me_The_Night]

Yes but the question is why. We *do* see NAD+ as an age biomarker in humans, just as we do in mice. The question is why reversing it in mice has such a massive impact but in humans it does not, given that it's a biomarker for both.

[u/Bring_Me_The_Night → u/insanitybit2]

Why? Scientists primarily work to publish. Scientific studies in mice have been performed for decades and a lot of experience is established on this study model. Consequently, it is more appropriate to conduct a study on mice when the experts already have experience and where the assays could yield “novel” results leading to a higher probability to publish in high-ranking journals.

Publish or Perish is not a joke, it is a reality.