Medical Researcher - AMA

>pd-1 inhibitors
hello cancer

Telomere shortening is the basis for cellular aging.
We've coupled this with anti-PD-1 monoclonal antibodies and antioxidants.
Degenerative diseases are a whole other terrain of research, my friend.
What age halting means here is that you won't age at least phenotypically. You're still susceptible to disease or death by accident.
This is what we're aiming for.

GO TO SLEEP PHAGGOT.

>Keep taking OP's drug and a powerful antioxidant to avoid dna deterioration
>go auschwitz mode taking shitloads of methylene blue and rapamycin
>rebuild the body promoting mtor
>repeat auschwitz-rebuild indefinitely
>live forever

Not necessarily. The PD-1/PD-1L pathway is just one of the many routes that converge into cancerous cell genesis, development and progression. So far our trials in chimps have not shown any form of malignant cell related disease.

scratch that, i was thinking PDE

>Gentlemen,

What makes you think it's only men out here, fuckface?

Besides, tumors tend to promote the PD-1/PD-1L pathway in order to survive...

Sweeeet!

Tits or GTFO.

It's the middle of the day in the Continental US. You would know that if you lived in America, which you don't. And never will.

1. Reading the thread if I understand it correctly (no biology experience at all) there is a difference between aging and degenerative diseases that affect us as we age? I'm assuming that these degenerative diseases don't kill us though or whats the point of 'anti-aging'
2. How close are we to at least gene editing embyro's to change kids genes. Like can we splice the european blue eye mutation into an asian as opposed to doing it the old fashioned way.

>source
>needed
>as cumulative DNA damage doesnt equal short telomeres

This thread is retarded. Aging is not simply a function of telomere length. That is just one component of much more complex process. Stopping the telomeres from shortening won't prevent the activation of various genetic programs that result in an aged phenotype.

Of course, it doesn't. DNA repairing mechanisms in the cell are quite efficient. Short telomeres contribute to a decrease in double-strand stabilization, incrementing DNA damage. Furthermore, the shortening of telomeres leads inevitably to cell death by apoptosis. There's enough data on this if you want to do some research on your own.
Constitutive telomerase expression in most cancer cells (the so-called "cancer stem-cells") of most cancer types plays a key role in cancer cell immortality.

Sure, I misunderstood. It's pretty smart then but I fail to see the point in including it unless it's like a preventive measure in case cancers do occur due to removing the Hayflick limit.

1. Yes and no. There are two different things but the first tends to lead to the second.
2. With the new technologies currently at our disposal (such as CRISPR like some user mentioned before) and the ones in development, I'd say probably in about 20-30 years, which is pretty soon from a scientific perspective. This is just a personal opinion though.

It is, as we would be providing one of the many key characteristics of cancerous cells without them even having acquired any related mutation in the telomerase gene coding region.
We've estimated that the risk is minimal though, as cancer cell induction takes way more than just cell immortality.
Tests in chimps will hopefully confirm our hypothesis in a few years.
We've also considered the possibility of adding anti-CTLA-4 monoclonal antibodies to the mix, but the costs go way up, and so do the side-effects.

Why do you need telomerase when somatic stem cells already produce telomerase?
Also, all the premature aging diseases have some mutations in DNA repair proteins.

I've thought about this subject and I think that the best shot would be creating ultraprecise DNA repair proteins (assuming that they haven't reached their full potential because natural selection selects for variants that don't kill you when you're 30 instead of variants that keep you alive into the 100's) and then introducing them via. gene therapy.

I'm an undergrad interested in going into this seem exact thing you're working on...How do I get in on this shit? Can I come see how/what you guys do and stuff? I'm getting my undergrad in biochemistry.

Your cocktail is impractical. Constitutive expression of telomerase is tumorigenic. Delivery systems to whole animals are poor. Good luck though.

How does it taste and how much will you sell it for?

Bump

I fucking hate aging!

have fun with tumours faggot

>Tfw you will forever be a 90yo senile pant shitting pain in the ass to your eternal midlife crisis dumb children

>Telomeres have mantained its lenght on subsequent divisions on multiple cell cultures.
Did I miss something or has it been proven that telomerase shortening is what drives ageing in humans? Or is it one of those borderline fradulent things like that startup Elizabeth Parrish runs? How would that help with mitochondrial mutations accumulating or intracellular junk accumulation or billion other things that happen when you age?

so my brain won't get old?

you cant beat entropy

No youre not. Nice larp though. Do you know why we age?

>starts off with grandiose statements
>refuses to give anything that would prove that they're a medfag at all, let alone a researcher
I believe you purely because you say things I want to hear, even though you're probably a fraud

Shit wears down over time from constant cell divisions
this does not mean however that those cells cannot be regenerated, rejuvenated, or repaired
only reason we haven't done it already is because it's complex as fuck and is outstandingly difficult to not fuck shit up

Radiation

This. Despite the obvious telltales, I actually got duped into posting a serious reply to this guy. Guess he's really laughing at us all now.

> It's a really hard thing to do
> It's hard for many reasons
> The only reason we haven't done it is because it's hard
I'm sure you know all the details though and you're just keeping them to yourself