This is totally improper reporting of the study.

When enough words, framing, and unstated important premises are omitted, it crosses over from the realm of incomplete or misleading into plain outright lying in my worldview.

They claim "Reverses advanced AD in mice." What they did is reverse symptoms in genetic models.

They claim to "Restore NAD+ homeostasis," ignoring that NAD might not even be causally related to Alzheimer’s, just a side effect. It’s like saying we cured a house fire because we efficiently removed the ashes after the fire. It’s the Tau thing all over again.

The claim: "Conservative molecular signatures" when in reality, 5xFAD mice are poor predictors of human clinical success to such a degree that it’s statistically more common for mice studies to NOT transfer to human biology than to do so.

They also make unsupported claims like "Safer than NAD+ precursors (supplements)," when this is a pre-clinical assumption. No human toxicity trials are mentioned in this context, and there are always MASSIVE differences when switching to real human studies. It might be correct, but there’s no basis to say that based on this study.

Also, the senior author owns the company. The paper has the hallmarks of a "pitch deck" for the drug.

In short, it seems to me that the claim of "Full Neurological Recovery" is misleading to patients. It fails to prove that fixing NAD+ in humans will stop the disease, only that it works in mice engineered to have the disease, and only by assuming that their specific measure is a 1-to-1 with the clinical presentation of the disease. The results are likely the "best case scenario" presented to support the commercialization of P7C3-A20.

Here is the COMMON SENSE question peer-reviews should have asked. Is low NAD+ the fire, or just the ashes?

Why should we believe this works in humans when the last 500 'cures' in 5xFAD mice failed?

Are you regrowing a brain, or just cleaning up a dirty one?

How does one molecule fix five unconnected problems simultaneously? The Context: The drug fixed inflammation, blood-brain barrier, amyloid/tau (protein folding), and memory (neuronal signaling). Drugs rarely hit four distinct biological systems with 100% success....

Where is the toxicology report that proves 'safer than supplements'?

You're asking good questions, but it's unreasonable to expect one paper to answer all of them. Probably the article should have emphasized more strongly that mouse models are imperfect, but they do show efficacy in two different mouse models, which counts for something.

> It fails to prove that fixing NAD+ in humans will stop the disease, only that it works in mice engineered to have the disease

This in particular is just not possible without clinical trials in humans. But you can't have a clinical trial without evidence of efficiency, so you need to start with mouse models, even if they are imperfect. Sadly we don't know if any of the existing mouse models are any good, but it's the best we've got.

> the senior author owns the company

Unfortunately, the moment I saw reference to NAD+ I started looking for this. Thank you.

I can't upvote your comment enough.

Please... people, do not get your hopes up over this one PR pump piece released on Christmas Day. This is not a legit study. (It might, perhaps, somehow, still be correct, perhaps... even broken clocks are right twice a day... but it's still not a legit study.)

Well, NAD+ kinda has the potential to fix multiple things at once if those things are caused by energetic imbalance/deficit. Re-balancing NAD+ could just fix multiple failing systems that were running low on energy and not doing their job properly as a consequence.