The idea that aging research is being stifled by patent law (or any other mechanism) is ridiculous. Aging and neurodegenerative disease already receive an exorbitant amount of funding from the government (see: the NIA). The aging billionaire class is also more than happy to fund aging research that works for them (see: Altos Labs as the most recent example, The SENS Research Foundation, and tech life sciences offshoots like Calico). The argument that you "can't patent naturally occurring proteins" may be technically true, but there are plenty of ways around this which often improve the performance of the native proteins as therapeutics (see: insulin, among many others).
"Leapfrogging ahead of these research institutes with a practical demonstration has been Harold Katcher. Katcher’s method is proprietary."
Wow, a proprietary method that outdoes decades of scientific research? Haven't heard that one before. I understand that there has been little progress in this space, but that's because no one knows what causes aging (or if it can be halted at all). There's no single smoking gun, and there is likely no single easy solution. I also understand that our scientific institutions aren't perfect–and that the big ship of science can sometimes take a while to turn away from a tantalizing hypotheses, like the amyloid hypothesis-but that doesn't mean that you should trust Harold Katcher instead.
Presumably, longer proteins require more splicing, so impaired RNA splicing could account for a deficit of longer proteins as we age.
Why is this "presumably true"? Intuitively, impaired splicing would produce longer proteins, because introns aren't excised as effectively. Even this take is far too simplistic–there are innumerate feedback and control mechanisms involved in mRNA splicing. I'm sure the author has a better grasp on molecular biology than this hot take suggests based on his credentials, but the treatment of this topic by the author is concerning.
As an aside, wow, that preprint spent over three years in review, and the figures and text are way different. A lot of work and stress must have gone into it.
I suspect that the impaired splicing leads to a multitude of premature stop codons and stretches of RNA that don't lend themselves well to transcription and/or translation. Longer proteins, have more introns and are therefore more likely to suffer from this issue, at least that is my guess.
"Leapfrogging ahead of these research institutes with a practical demonstration has been Harold Katcher. Katcher’s method is proprietary."
Wow, a proprietary method that outdoes decades of scientific research? Haven't heard that one before. I understand that there has been little progress in this space, but that's because no one knows what causes aging (or if it can be halted at all). There's no single smoking gun, and there is likely no single easy solution. I also understand that our scientific institutions aren't perfect–and that the big ship of science can sometimes take a while to turn away from a tantalizing hypotheses, like the amyloid hypothesis-but that doesn't mean that you should trust Harold Katcher instead.
Presumably, longer proteins require more splicing, so impaired RNA splicing could account for a deficit of longer proteins as we age.
Why is this "presumably true"? Intuitively, impaired splicing would produce longer proteins, because introns aren't excised as effectively. Even this take is far too simplistic–there are innumerate feedback and control mechanisms involved in mRNA splicing. I'm sure the author has a better grasp on molecular biology than this hot take suggests based on his credentials, but the treatment of this topic by the author is concerning.
As an aside, wow, that preprint spent over three years in review, and the figures and text are way different. A lot of work and stress must have gone into it.