Pretty interesting story in @ScienceMagazine this week on what looks like a serious problem in the senescence field. More than 400 papers apparently used the wrong antibody for p16-INK4a — an antibody that actually recognizes a completely different, unrelated protein (a component of the actin cytoskeleton). This affects work on senescent cell accumulation in aging and disease, and most critically, some of the evidence base for senolytic drug research. What concerns me most is that many of these papers somehow got the "right" answer using the wrong antibody. That's not just an innocent reagent mix-up — it raises real questions about data fabrication or selective reporting in at least some of these labs. I've commented before about how ignoring data that doesn't fit the narrative is a major problem in certain areas of the longevity literature (e.g. sirtuins and NAD), and here a potentially widespread example in senescence. Hopefully journals will investigate and retract as necessary, but based on my experience that seems optimistic. One concrete fix is that journals should flag problematic antibody product codes at submission so reviewers can catch this before publication. Reviewers should absolutely be on the lookout for this going forward. However, these fixes won't address the larger problem. We need to understand how these scientists got the results they wanted and published them over 400 times (!!!): whether through intentional deception, incompetence, accident, or some legitimate explanation. Credit for discovering this goes to @addictedtoigno1 who wrote about it first on his blog: For Better Science science.org/content/article/…?

NAD probably doesn't actually decline with age. This is one of the problems in NAD-world that I've been warning about for years. I'm glad to see it finally reaching publication. nature.com/articles/s42255-0… The myth that NAD levels broadly change with age in humans and other animals has been propagated by some high-profile people in the field, both in the scientific literature (mostly review articles not real data, which should tell you something) and in the pop-sci podcast world. This has generated hundreds of millions of dollars in sales for NAD precursors and hundreds of millions of dollars in grant funding for those investigators. To be clear, NAD biology is real and important. There are likely specific disease states, tissues, or individuals where NAD availability becomes limiting and where interventions targeting NAD metabolism may prove useful. But that is very different from the much broader claim that declining NAD is a universal driver of normal aging in otherwise healthy people. The evidence increasingly suggests that NAD precursors like NR and NMN do not extend lifespan in mice under standard conditions and likely provide limited or no meaningful benefit to the average healthy person. This is a good reminder of how science should work. Strong claims require strong evidence, especially when they become the basis for major commercial industries and public health narratives. Aging biology is complex, and we need to be careful not to confuse plausible mechanisms with demonstrated outcomes.