The apoptosis pathway requires the mitochondria to be on… this has been noted since Warburg in 1935 (look up Warburg Effect).
More likely that NR would enable apoptosis to work correctly. Most of the time. Anything can happen with freakin’ aneuploid cells, but that’s how I would bet. Also, try to stop cells from going aneuploid in first place… this came up in the early days of telomerase research. Lengthening telomeres “sounds” like it would increase cancer, but it doesn’t, if it’s just from temporary activation (and I dunno why, but lengthening telomeres lenthens lifespans even in animals like mice with crazy long telomeres and telomerase on in every single cell).
Lengthening telomeres in mid-life actually prevents end-fusion events which can make cells go totally wacky (BTW, I hate using aneuploids like HeLa and then claiming you’ve said something about human cells… I’ve looked at thousands of those things in the cyto lab, and they ain’t even slightly human.)
To be clear, the work I am speaking of is on enhancing the NAD salvage pathway preventing NAD depletion in stressed neurons. This treatment seems to drastically decrease neuron programmed cell death in response to brain injury, neurodegenerative diseases, and hypoxia.
The mose work showed great promise in brain injury and hypoxia and while it doesn’t stop the neurodegeneration from ALS and the like (the underlying damage is being done) the threshold for individual neurons dying is raised, so the mice are healthy for a long time before suddenly falling apart rather than slowly declining.
This is work being done by Calico and by Dr. McKnight. I will provide links when I’m no longer on my phone
The apoptosis pathway requires the mitochondria to be on… this has been noted since Warburg in 1935 (look up Warburg Effect).
More likely that NR would enable apoptosis to work correctly. Most of the time. Anything can happen with freakin’ aneuploid cells, but that’s how I would bet. Also, try to stop cells from going aneuploid in first place… this came up in the early days of telomerase research. Lengthening telomeres “sounds” like it would increase cancer, but it doesn’t, if it’s just from temporary activation (and I dunno why, but lengthening telomeres lenthens lifespans even in animals like mice with crazy long telomeres and telomerase on in every single cell).
Lengthening telomeres in mid-life actually prevents end-fusion events which can make cells go totally wacky (BTW, I hate using aneuploids like HeLa and then claiming you’ve said something about human cells… I’ve looked at thousands of those things in the cyto lab, and they ain’t even slightly human.)
More from Brenner on SARS-CoV-2 and NAD+:
https://twitter.com/CharlesMBrenner/status/1251813463581736961
There is a whole bunch of work on boosting NAD levels to suppress PARP effects on NAD depletion triggering neuron apoptosis...
I did not know that… I can’t spare many neurons, I’d better check it out.
To be clear, the work I am speaking of is on enhancing the NAD salvage pathway preventing NAD depletion in stressed neurons. This treatment seems to drastically decrease neuron programmed cell death in response to brain injury, neurodegenerative diseases, and hypoxia.
The mose work showed great promise in brain injury and hypoxia and while it doesn’t stop the neurodegeneration from ALS and the like (the underlying damage is being done) the threshold for individual neurons dying is raised, so the mice are healthy for a long time before suddenly falling apart rather than slowly declining.
This is work being done by Calico and by Dr. McKnight. I will provide links when I’m no longer on my phone
Thanks!