This is the current big grift in anti-aging science:
1 - Find a marker correlated with aging across a large sample
2 - Find a medication or supplement that also alters that marker
3 - Do some before and after measurements of the marker with the supplement or medication, and claim that you have reversed aging. Rely on the fact that enough readers won’t look closely enough to wonder if the marker is a true independent variable that represents aging.
High impact journal for an interesting study that is admittedly largely out of my area of expertise. The limitation of it being done in animal models, is of course, noted, but also expected. The question I would ask is how well the underlying background research makes this outcome expected.
You joke, but rodents make great pets, because they are very social and have a range of personalities, but most only live a few years. I knew someone with a pet retired lab rat, and it lived much longer than the average fancy rat, but even then, it didn't even live half as long as the average cat or dog.
If we could breed or treat rodents to live longer, we could keep low-resource pets without as much loss.
TFA reeks of over-sensationalizing. Here is a summary sans hyperbole:
Intranasal Human NSC-Derived EVs Therapy Can Restrain Inflammatory Microglial Transcriptome, and NLRP3 and cGAS-STING Signalling, in Aged Hippocampus[1].
Abstract:
> Neuroinflammaging, a moderate, chronic, and sterile inflammation in the hippocampus, contributes to age-related cognitive decline. Neuroinflammaging comprises the activation of the nucleotide-binding domain, leucine-rich repeat family, and pyrin domain-containing 3 (NLRP3) inflammasomes, and the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway that triggers type 1 interferon (IFN-1) signalling. Studies have shown that extracellular vesicles from human induced pluripotent stem cell-derived neural stem cells (hiPSC-NSC-EVs) contain therapeutic miRNAs that can alleviate neuroinflammation. Therefore, this study examined the effects of late middle-aged (18-month-old) male and female C57BL6/J mice receiving two intranasal doses of hiPSC-NSC-EVs on neuroinflammaging in the hippocampus at 20.5 months of age. Compared with animals receiving vehicle treatment, the hippocampus of animals receiving hiPSC-NSC-EVs exhibited reductions in astrocyte hypertrophy, microglial clusters, and oxidative stress, along with elevated expression of antioxidant proteins and genes that maintain mitochondrial respiratory chain integrity. Moreover, hiPSC-NSC-EVs therapy decreased the levels of various proteins involved in the activation of the NLRP3 inflammasome, p38/mitogen-activated protein kinase, cGAS-STING-IFN-1, and Janus kinase and signal transducer and activator of transcription signalling pathways. Furthermore, in vitro assays using genetically engineered RAW cells and hiPSC-NSC-EVs, with or without targeted depletion of specific miRNAs, demonstrated that miRNA-30e-3p and miRNA-181a-5p, both present in hiPSC-NSC-EVs, can significantly inhibit the activation of the NLRP3 inflammasome and the STING pathway, respectively. Additionally, single-cell RNA sequencing conducted 7 days post-treatment revealed that hiPSC-NSC-EVs induce widespread transcriptomic changes in microglia, including increased expression of numerous genes that enhance oxidative phosphorylation and reduced expression of abundant genes that drive multiple proinflammatory signalling pathways. These changes mediated by hiPSC-NSC-EVs were also associated with improved cognitive and memory function. Thus, intranasal hiPSC-NSC-EVs therapy in late middle age can effectively diminish proinflammatory microglial transcriptome and signalling cascades that drive neuroinflammaging in the hippocampus, contributing to better brain function in old age.
And OCD symptoms, and many also benefit from better impulse control. Its more effective than SSRIs for some.
NAC is one of the only known treatments for trichotillomania, a under discussed but common condition that causes people to uncontrollably pull their hair out.
NAC has also been studied to reduce nicotine and alchohol cravings as well.
Are there any risks associated with NAC supplementation? For example, could long-term usage reduce aptosis and thereby increase risks of developing cancer?
> Therefore, this study examined the effects of late middle-aged (18-month-old) male and female C57BL6/J mice receiving two intranasal doses of hiPSC-NSC-EVs on neuroinflammaging in the hippocampus at 20.5 months of age.
The link to the actual paper was appreciated.
The context of whether findings will generalize outside of mouse models can depend a lot on specifics of the problem.
Many Brain-aging study sample pools are from young folks that died in accidents, aged homeless alcoholics, and individuals that were in declining health.
Most cultures find it taboo to donate their beloved family members bodies for scientific dissection. Thus, people get ingrained "[bigotry] with extra steps" similar to phrenology proponents.
"Reverse brain aging", sure, in the same sense that taking Vitamin C reverses aging.
The nasal spray reduced markers of inflammation in hippocampal microglial cells.
A lot of things reduce inflammation. That is not "reversing ageing".
Of course, "reduces inflammation" doesn't headline very well...
There is a pop theory that aging is just scurvy in slow motion and Vitamin C hypersupplementation actually goes a long way in staving it off.
This is the current big grift in anti-aging science:
1 - Find a marker correlated with aging across a large sample
2 - Find a medication or supplement that also alters that marker
3 - Do some before and after measurements of the marker with the supplement or medication, and claim that you have reversed aging. Rely on the fact that enough readers won’t look closely enough to wonder if the marker is a true independent variable that represents aging.
The article is also heavily ai generated, I call bs on every single bit
I thought the url said temu at first.
Kinda surprised A&M’s letting them use AI to write these things
>>The article is also heavily ai generated
can you please share your methodology for detecting ai please?
c'mon you guys, chill. this is not a vaccine.
AI generated? Not demonstrated.
Whining by humans claiming AI? Predictable. Probable. Indeed LLM "complete the sentence" predictable.
High impact journal for an interesting study that is admittedly largely out of my area of expertise. The limitation of it being done in animal models, is of course, noted, but also expected. The question I would ask is how well the underlying background research makes this outcome expected.
Damn, that’s one hell of a way to say “is this any good though?”. Too many words for such a simple question.
Pretty much, lol. I started to say some other things but decided to say less.
But "how well the underlying background research makes this outcome expected" does not mean "is this any good though".
It's also an actually interesting question.
It's one thing to find some things hard to follow, it's another to be proud of it.
That's exactly what I want: immortal mice!
You joke, but rodents make great pets, because they are very social and have a range of personalities, but most only live a few years. I knew someone with a pet retired lab rat, and it lived much longer than the average fancy rat, but even then, it didn't even live half as long as the average cat or dog.
If we could breed or treat rodents to live longer, we could keep low-resource pets without as much loss.
There is an excellent "This American Life" episode on rats. The first act is about a guy who keeps rats as pets. It's a sweet story.
https://www.thisamericanlife.org/801/transcript
That's a surprisingly underused plot for a sci Fi horror film.
Considering the grand total of experiments we've ran on the little guys, I'm kinda surprised we haven't bred Mousezilla yet
Or Pinky & the Brain
See also: “Flowers for Algernon”
Flowers for Algernon’s Brain
This short story was scarier to me as a kid than anything else I read at the time.
The movie adaptation — “Charlie” — is heartbreakingly good.
TFA reeks of over-sensationalizing. Here is a summary sans hyperbole:
Intranasal Human NSC-Derived EVs Therapy Can Restrain Inflammatory Microglial Transcriptome, and NLRP3 and cGAS-STING Signalling, in Aged Hippocampus[1].
Abstract:
> Neuroinflammaging, a moderate, chronic, and sterile inflammation in the hippocampus, contributes to age-related cognitive decline. Neuroinflammaging comprises the activation of the nucleotide-binding domain, leucine-rich repeat family, and pyrin domain-containing 3 (NLRP3) inflammasomes, and the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway that triggers type 1 interferon (IFN-1) signalling. Studies have shown that extracellular vesicles from human induced pluripotent stem cell-derived neural stem cells (hiPSC-NSC-EVs) contain therapeutic miRNAs that can alleviate neuroinflammation. Therefore, this study examined the effects of late middle-aged (18-month-old) male and female C57BL6/J mice receiving two intranasal doses of hiPSC-NSC-EVs on neuroinflammaging in the hippocampus at 20.5 months of age. Compared with animals receiving vehicle treatment, the hippocampus of animals receiving hiPSC-NSC-EVs exhibited reductions in astrocyte hypertrophy, microglial clusters, and oxidative stress, along with elevated expression of antioxidant proteins and genes that maintain mitochondrial respiratory chain integrity. Moreover, hiPSC-NSC-EVs therapy decreased the levels of various proteins involved in the activation of the NLRP3 inflammasome, p38/mitogen-activated protein kinase, cGAS-STING-IFN-1, and Janus kinase and signal transducer and activator of transcription signalling pathways. Furthermore, in vitro assays using genetically engineered RAW cells and hiPSC-NSC-EVs, with or without targeted depletion of specific miRNAs, demonstrated that miRNA-30e-3p and miRNA-181a-5p, both present in hiPSC-NSC-EVs, can significantly inhibit the activation of the NLRP3 inflammasome and the STING pathway, respectively. Additionally, single-cell RNA sequencing conducted 7 days post-treatment revealed that hiPSC-NSC-EVs induce widespread transcriptomic changes in microglia, including increased expression of numerous genes that enhance oxidative phosphorylation and reduced expression of abundant genes that drive multiple proinflammatory signalling pathways. These changes mediated by hiPSC-NSC-EVs were also associated with improved cognitive and memory function. Thus, intranasal hiPSC-NSC-EVs therapy in late middle age can effectively diminish proinflammatory microglial transcriptome and signalling cascades that drive neuroinflammaging in the hippocampus, contributing to better brain function in old age.
[1]: https://isevjournals.onlinelibrary.wiley.com/doi/10.1002/jev...
How soon until biohackers try this on themselves?
The failure scenarios are fun to imagine, like uncontrollable brain growth or waking nightmares as weird side effect of centuries-old brain.
I take N-acetylcysteine and it helps with brain fog also! Plus it reduces stress and irritability.
And OCD symptoms, and many also benefit from better impulse control. Its more effective than SSRIs for some.
NAC is one of the only known treatments for trichotillomania, a under discussed but common condition that causes people to uncontrollably pull their hair out.
NAC has also been studied to reduce nicotine and alchohol cravings as well.
Are there any risks associated with NAC supplementation? For example, could long-term usage reduce aptosis and thereby increase risks of developing cancer?
What is your dosage?
I take 1200mg a day, when Im taking it. I think standard/reccomended dosage is 600mg.
Story from April;
Some previous discussion: https://news.ycombinator.com/item?id=48288478
When can I snort this?
I knew cocaine had to have an upside.
Prepare a line for me also please
Grab me a bag while your there.
...in mice.
> Therefore, this study examined the effects of late middle-aged (18-month-old) male and female C57BL6/J mice receiving two intranasal doses of hiPSC-NSC-EVs on neuroinflammaging in the hippocampus at 20.5 months of age.
— https://isevjournals.onlinelibrary.wiley.com/doi/10.1002/jev...
That PR piece was brutal to navigate. Undoubtedly punched up by AI, it took far too long to even understand what the treatment entailed.
To be fair though, I think we owe the mice a positive research outcome.
“Congratulations, you get improved brain function while we continue to run other experiments on you!”
The link to the actual paper was appreciated. The context of whether findings will generalize outside of mouse models can depend a lot on specifics of the problem.
Many Brain-aging study sample pools are from young folks that died in accidents, aged homeless alcoholics, and individuals that were in declining health.
Most cultures find it taboo to donate their beloved family members bodies for scientific dissection. Thus, people get ingrained "[bigotry] with extra steps" similar to phrenology proponents.
https://en.wikipedia.org/wiki/Simpson%27s_paradox
"Old age and treachery will always beat youth and exuberance" =3
Mice get all the cool shit first
they get all the worst and most inane tortures too
I even seen a mouse on youtube with it's own tiny EV sports car driving about!
I read a book about a mouse with a motorcycle (https://www.goodreads.com/en/book/show/232109.The_Mouse_and_...) and a different book about a mouse-like child with sailboat. (https://www.goodreads.com/en/book/show/138959.Stuart_Little).
M. Night Shyamalan wrote a screenplay about the latter book, and it was made into a popular movie.
This one?
https://youtube.com/shorts/E74r-ybeQfE
Someone needs to put an octopus in a mini vehicle.
Then they get murdered...
Temu science at Tamu.
I have an AI generated bridge that I can sell you...
Ugh, I thought we were done with the Boomers....looks like they're gonna hang on.