23 replies to this topic

[vibrantguy]

Hey everyone,

 

Excited to meet you all! I’m here to kick off an open-source project to tackle aging. Not sure if anyone’s tried this before, but I’m not talking about supplements or small-scale stuff, so let’s skip that.

 

With AI like ChatGPT getting smarter every day, we can all quickly get up to speed on aging solutions. Open-source work can be powerful, and we can achieve a lot together.

 

After you read my paper, you’ll see curing aging might not be as hard as it seems. I know it’s unusual to talk big in science without hedging, but I’ve got solid evidence to back up my optimism.

 

From what I’ve learned, especially from experts like Dr. Bill Andrews, solving aging isn’t necessarily hard—it just takes time and lots of compound screening. My paper outlines a free method for screening compounds, and with a coordinated open-source effort, we can cut down the time it takes.

 

I’ve attached a Word doc that lays out my thoughts in about 4300 words. Check the considerations section, and use the collapsible headings to navigate easily.

 

I put this paper together in a few days, so it might have minor issues, but it’s a straightforward guide to understanding and addressing aging effectively and safely. I’m inviting everyone to jump in and collaborate. Looking forward to your input!

I am making sure the file has attached.

[vibrantguy]

my github is vibrantguy123 my repo is verbose-barnacle and the doc is age.docx on main

 

https : // github. c o m / vibrantguy123 / verbose-barnacle / blob / main / age.docx

[johnhemming]

In a paragraph of 250 words or less why should anyone engage with you on this as opposed to one of the many other people/groups doing something much the same.

[vibrantguy]

Sure.

 

Disclaimer: I am not a doctor. All my advice/medical advice is for entertainment purposes only do not take it seriously.

 

I am not a scientist, my credentials are a secret, I am just a computer science student.

 

I want to cure aging within 10 years so I can treat myself, my family, and my future family. Along the way if I can help you guys / answer your questions, it would be my pleasure.

 

I want you to ask yourself, who are you to trust in the field of curing aging?

 

Will you go with the mainstream? Will you read countless pubmed articles without a specific goal in mind? Will you scavenge the internet as the time goes by? If so, you can ignore the thread.

 

My goal is to use Dr. Bill Andrews research, make it open source, and easy to understand.

 

Basically my current goal is to find the protein structure for two proteins, then put them on a docking site, then find the best docking sites for inhibition, which can probably be done by using the publicly available ta-65 molecule that can increase telomerase, then use an AI/AGI or randomly test molecules in silico (on a computer for free and quickly) to find the best possible and safest compound for inhibition. If we all collectively find extremely potent compounds, we can send them to maybe Dr. Bill Andrews for confirmation or we could go our own ways and test them ourselves in vitro and in vivo. Why do we want to inhibit two molecules? Because according to the https://patents.just.../patent/7795416 patent, we can activate TERT to 90% activation or even higher, simply from inhibiting these two proteins. And as some of you know, we need to activate telomerase to at least a good fraction of the telomerase expression of Hela cells to make cells become immortal. If you read my paper, you will understand.

 

Obviously, it won't be easy, but it is not something we can't work towards? Who knows, maybe we can feed the paper into chat gpt 5 and it has a detailed plan for it to complete. Something like that is what I am hoping for.

 

Even Dr. Bill Andrews has said he doesn't know how to compounds he uses works to increase telomerase, he simply randomly tests them and whatever produces telomerase, he uses lol.

 

My plan basically serves as a guarantee, because cancer is not publicly cured, although Bill Andrews created the anti-sense for cancer, so what exactly are you placing your hopes in to cure aging before cancer, because isn't your goal to cure aging?

 

Are you all not annoyed after seeing petty thread after petty thread?

 

I want to cure aging, with absolute guarantee. If I had the knowledge of "AGI" I would already have more than enough information to find the cure for aging. As you know, I am not an AGI, but my goal is to "move" like an AGI, use AI/AGI to help with this research. I know the high-end AGIs may not be publicly available but still tools like chat gpt and similar are being updated and I feel that would barely be enough to complete the plan. I feel that we need to massively speed up aging research.

 

 

Bill Andrews has continuously said it would take 1-3 years to find the compound to reverse aging if the funding is right. The funding he means is $1 million a month, however he functions at around $100,000 a month. So perhaps it would take another 10 years at minimum? And would they be able to even use AI to help with their research? If they could/did then there is little need for this thread, and we could all just take that drug and become biologically immortal. This thread serves as a "backup" guarantee.

 

I do not expect help in the beginning as I have to prove myself. Therefore, I will post some goals here and try to accomplish it quickly and if you are interested, you can hop in.

 

Today, I don't think I will be able to do more research as I am busy, but maybe tomorrow I might be able to put in lots of work.

 

Another thing to solidify my point. I am new to the anti-aging circle. I do not know which are the open-source groups working on this same thing. If they are and doing great work, that is awesome, but I haven't seen it, so if you could direct me I would like to see. As Dr. Bill Andrews said, the field of anti-aging is filled with charlattans. For me personally, Dr. Bill Andrews is the only gerontologist I can fully trust. He is getting older, and if something happens not even god can help us. At least that is my opinion

 

 

Here is my opinion for the hallmarks of aging

Loss of Proteostasis - Proteostasis will return to normal by epigenetic resetting or telomere elongation and telomere elongation can activate epigenetic resetting, making this hallmark of aging become youthful again, as in the engineered mouse studies and human skin grown on the back of a mouse studies. There may be bad protein buildup, but these can be cleared by the cell becoming younger, as implied by Dr. Bill Andrews.

Epigenetic Alterations - Controls the expression of genes, telomere relengthening controls this. However modern "age reversal studies" decide that this is the main cause when it is not, because it doesn't extend telomeres, at least according to my knowledge. I have an image that shows epigenetic resetting resets all aging factors except telomere attrition, but I can't upload it as I new here.

 

Telomere Attrition - Main cause of aging. Relatively simple to relengthen in humans.

Genomic Instability - Instability arises because of telomere shortening and it can be promptly reversed. Especially in the primordial germ cells, whose maintenance is affected  by the surrounding somatic cells.

Cellular Senescence - Cells become senescent because their telomeres reach 5000 base pairs. Killing senescent cells via senolytics is bad, especially if you are older, because those cells aren't "dead" they just don't divide, this is why senolytics is bad, according to bill Andrews. Also, your stem cells will become more stressed and their telomeres will further shorten. Stem cells don't even produce telomerase, despite what you may read, according to Dr. Bill Andrews. This is why senolytics targeting isn't an option, despite being mainstream. Telomere relengthening can make senescent cells become normal again.

Mitochondrial Dysfunction - Returns to normal, we don't age by oxidative stress, but by telomere decline. A study on human skin in a petri dish showed that antioxidants did not cause the cells to exceed the hayflick limit, but telomere elongation did, showing that antioxidants are of little concern, as the body can produce more than enough already. However, mice already have long telomeres and constantly produce it, but they age by oxidative stress and mitochondrial dysfunction, so adding antioxidants to the mice cells made them exceed the hayflick limit. Not to say that antioxidants aren't important, they are for cellular energetics, keeping proper functioning, and protecting telomeres from further damage. Did you know mitochondria are able to do "fusion" to repair damage?

Deregulated Nutrient Sensing - Nutrient sensing, blood health levels and such return to normal, as implied by the studies.

Altered Intercellular Communication - The intercellular communication returns to normal following telomere reextension, as implied by the studies.

Stem Cell Exhaustion - Stem cells are harbored in special niches where they are exposed to little damage, but they are not able to divide anymore because telomeres shorten. This can lead to a cascade of events.

Extracellular matrix Dysregulation - As seen in the human skin and mouse models, the extracellular matrix becomes normal following telomere re-extension.

 

 

Please reply if you have any concerns.

[vibrantguy]

By the way, I already found one of the two proteins with 99.9% accuracy https://www.ebi.ac.u...pl?pdbcode=A4sc . The other protein is similar to it, but it is going to take me some time, since I don't have the amino acid sequence for it.

[joesixpack]

Sure.

 

Disclaimer: I am not a doctor. All my advice/medical advice is for entertainment purposes only do not take it seriously.

 

I am not a scientist, my credentials are a secret, I am just a computer science student.

 

I want to cure aging within 10 years so I can treat myself, my family, and my future family. Along the way if I can help you guys / answer your questions, it would be my pleasure.

 

I want you to ask yourself, who are you to trust in the field of curing aging?

 

Will you go with the mainstream? Will you read countless pubmed articles without a specific goal in mind? Will you scavenge the internet as the time goes by? If so, you can ignore the thread.

 

My goal is to use Dr. Bill Andrews research, make it open source, and easy to understand.

 

Basically my current goal is to find the protein structure for two proteins, then put them on a docking site, then find the best docking sites for inhibition, which can probably be done by using the publicly available ta-65 molecule that can increase telomerase, then use an AI/AGI or randomly test molecules in silico (on a computer for free and quickly) to find the best possible and safest compound for inhibition. If we all collectively find extremely potent compounds, we can send them to maybe Dr. Bill Andrews for confirmation or we could go our own ways and test them ourselves in vitro and in vivo. Why do we want to inhibit two molecules? Because according to the https://patents.just.../patent/7795416 patent, we can activate TERT to 90% activation or even higher, simply from inhibiting these two proteins. And as some of you know, we need to activate telomerase to at least a good fraction of the telomerase expression of Hela cells to make cells become immortal. If you read my paper, you will understand.

 

Obviously, it won't be easy, but it is not something we can't work towards? Who knows, maybe we can feed the paper into chat gpt 5 and it has a detailed plan for it to complete. Something like that is what I am hoping for.

 

Even Dr. Bill Andrews has said he doesn't know how to compounds he uses works to increase telomerase, he simply randomly tests them and whatever produces telomerase, he uses lol.

 

My plan basically serves as a guarantee, because cancer is not publicly cured, although Bill Andrews created the anti-sense for cancer, so what exactly are you placing your hopes in to cure aging before cancer, because isn't your goal to cure aging?

 

Are you all not annoyed after seeing petty thread after petty thread?

 

I want to cure aging, with absolute guarantee. If I had the knowledge of "AGI" I would already have more than enough information to find the cure for aging. As you know, I am not an AGI, but my goal is to "move" like an AGI, use AI/AGI to help with this research. I know the high-end AGIs may not be publicly available but still tools like chat gpt and similar are being updated and I feel that would barely be enough to complete the plan. I feel that we need to massively speed up aging research.

 

 

Bill Andrews has continuously said it would take 1-3 years to find the compound to reverse aging if the funding is right. The funding he means is $1 million a month, however he functions at around $100,000 a month. So perhaps it would take another 10 years at minimum? And would they be able to even use AI to help with their research? If they could/did then there is little need for this thread, and we could all just take that drug and become biologically immortal. This thread serves as a "backup" guarantee.

 

I do not expect help in the beginning as I have to prove myself. Therefore, I will post some goals here and try to accomplish it quickly and if you are interested, you can hop in.

 

Today, I don't think I will be able to do more research as I am busy, but maybe tomorrow I might be able to put in lots of work.

 

Another thing to solidify my point. I am new to the anti-aging circle. I do not know which are the open-source groups working on this same thing. If they are and doing great work, that is awesome, but I haven't seen it, so if you could direct me I would like to see. As Dr. Bill Andrews said, the field of anti-aging is filled with charlattans. For me personally, Dr. Bill Andrews is the only gerontologist I can fully trust. He is getting older, and if something happens not even god can help us. At least that is my opinion

 

 

Here is my opinion for the hallmarks of aging

Loss of Proteostasis - Proteostasis will return to normal by epigenetic resetting or telomere elongation and telomere elongation can activate epigenetic resetting, making this hallmark of aging become youthful again, as in the engineered mouse studies and human skin grown on the back of a mouse studies. There may be bad protein buildup, but these can be cleared by the cell becoming younger, as implied by Dr. Bill Andrews.

Epigenetic Alterations - Controls the expression of genes, telomere relengthening controls this. However modern "age reversal studies" decide that this is the main cause when it is not, because it doesn't extend telomeres, at least according to my knowledge. I have an image that shows epigenetic resetting resets all aging factors except telomere attrition, but I can't upload it as I new here.

 

Telomere Attrition - Main cause of aging. Relatively simple to relengthen in humans.

Genomic Instability - Instability arises because of telomere shortening and it can be promptly reversed. Especially in the primordial germ cells, whose maintenance is affected  by the surrounding somatic cells.

Cellular Senescence - Cells become senescent because their telomeres reach 5000 base pairs. Killing senescent cells via senolytics is bad, especially if you are older, because those cells aren't "dead" they just don't divide, this is why senolytics is bad, according to bill Andrews. Also, your stem cells will become more stressed and their telomeres will further shorten. Stem cells don't even produce telomerase, despite what you may read, according to Dr. Bill Andrews. This is why senolytics targeting isn't an option, despite being mainstream. Telomere relengthening can make senescent cells become normal again.

Mitochondrial Dysfunction - Returns to normal, we don't age by oxidative stress, but by telomere decline. A study on human skin in a petri dish showed that antioxidants did not cause the cells to exceed the hayflick limit, but telomere elongation did, showing that antioxidants are of little concern, as the body can produce more than enough already. However, mice already have long telomeres and constantly produce it, but they age by oxidative stress and mitochondrial dysfunction, so adding antioxidants to the mice cells made them exceed the hayflick limit. Not to say that antioxidants aren't important, they are for cellular energetics, keeping proper functioning, and protecting telomeres from further damage. Did you know mitochondria are able to do "fusion" to repair damage?

Deregulated Nutrient Sensing - Nutrient sensing, blood health levels and such return to normal, as implied by the studies.

Altered Intercellular Communication - The intercellular communication returns to normal following telomere reextension, as implied by the studies.

Stem Cell Exhaustion - Stem cells are harbored in special niches where they are exposed to little damage, but they are not able to divide anymore because telomeres shorten. This can lead to a cascade of events.

Extracellular matrix Dysregulation - As seen in the human skin and mouse models, the extracellular matrix becomes normal following telomere re-extension.

 

 

Please reply if you have any concerns.

You seem to tie all of the hallmarks of aging to telomere shortening, and tie the fix to telomere lengthening.

 

Have you considered the possibility that telomere shortening and some of the other hallmarks might be biomarkers signaling aging is taking place, but are not necessarily the cause of aging?

 

If that is the case, fixing the telomeres won't necessarily stop aging.

[vibrantguy]

Yes, I once quickly put together a paper targeting each hallmark of aging, treating them as if they were all equally responsible for aging, with a main focus on epigenetic resetting. However, this paper, even being around 25,000 words, didn’t resolve the issue in the end.

 

I understood the damage caused over time by each aging factor and came up with a simple plan for this, including thorough cancer curing and targeting diseases like arthritis, which I have done successfully. But, the goal of curing aging was "incorrect".

 

For example, you might read online that adults who made lifestyle changes have seen a 10% increase in telomeres compared to before. This might lead you to wrongly think that eating healthy means telomeres aren't a problem. But this isn’t right. Telomeres will always shorten; lifestyle changes just reduce the oxidative stress to the telomeres. Therefore, the data is incorrect, depending on how you interpret it. Also, telomere tests are very inaccurate, and the websites might just be trying to sell you an expensive telomere-extending drug.

 

Don’t think of telomeres as a biomarker.

 

Imagine an X, and the longer the ends, the more they can bend inwards affecting gene expression and such. There is a memory in cells of being young, probably epigenetic marks, that can be read when telomeres are longer. I always notice, not just for telomeric extension but also for epigenetic resetting, the "return" age to go back to seems to be around 25 years old (the end of growth maturation for humans), even if you are 80-100 years old.

 

This is important because 80-year-old skin cells, when reset at the telomeres, became younger in "every way imaginable", including gene expression, according to Dr. Bill Andrews. We can assume they probably became identical to 25-year-old skin cells, based off the wording.

 

Obviously, there might be minor DNA damage/mutations, but stem cells in special niches can make up for this.

 

Another way to fix this is having AI give you drugs to restore these sequences. But this isn’t a big deal, and AI will be much more advanced by then, especially since we have CRISPR already.

 

Also, if you look at my paper, you’ll see evidence that in vitro human cells with extended telomerase can divide over 250 times(and still dividing normally) past the Hayflick limit of 50, with the cells dividing and functioning normally. There’s no talk of DNA damage/mutations, so we can at least live five times longer at the minimum if we successfully solve the telomere issue.

 

I believe death eventually happens because too many cells become senescent, unable to perform their duty, therefore I don't think dna damage/mutations aren't a big deal, because the trillions of cells can make up for each others lacking and we only use a small part of DNA for each cell type, therefore there is even less burden of accumulated dna damage.

 

To understand what "every way imaginable" means, consider old mice engineered to age by telomere attrition. They had 75% of their brain size, but after genetic telomere extension, they got 100% of their brain size back. Bones will also extend again as bone stem cells will have the necessary telomerase to put cells where they need to be, confirmed by mouse studies. Most body parts have a stem cell, except maybe the eyes. So, if you need more cells in your eyes, you can use embryonic stem cells, differentiate them as needed, and inject them into the eye.

 

[johnhemming]

Please reply if you have any concerns.

 

I don't have any particular concerns.  Your word count was in fact 1,303 which makes me less likely to be inclined to spend any time engaging with your proposal as I asked for a response in 250 words (or less).

 

You are welcome to do what you are doing.  You might find it a better use of your time working with some other group.   In many ways everyone does their own thing, however.  I do my own thing so I should not criticise doing one's own thing.

Have you considered the possibility that telomere shortening and some of the other hallmarks might be biomarkers signaling aging is taking place, but are not necessarily the cause of aging?

 

 

I think this is the case.  hTERT is expressed when cells have a higher energy status indicated by histone acetylation.  It happens that I think histone acetylation is a key target.

[Mind]

Thanks for posting and thinking about a pathway toward successful rejuvenation. You will get feedback here in the forum to help narrow down the plan.

 

I agree with johnhemming in suggesting that you reach out to other groups as well. Are you aware of BioViva/IHS? They have been doing telomere modulation (lengthening through genetic engineering) for a few years now and have done a couple of clinical trials. The founder of BioViva seems to be in good health, 7 years after getting the treatment. BioViva might be interested in helping accelerate the telomere engineering you have described here.

[didierc]

Hello. Interesting discussion. However, on one side, you write "I am starting an open source initiative to cure aging" and then you write "my credentials are a secret".Can you elaborate?

[vibrantguy]

Thanks for the info guys. I made an update. I figured out we don't need two proteins for targeting, but rather one, and that is the human F13 protein. The F13 homolog referred to the animal version of the protein, but we can do in silico and in vivo tests.

 

"The subject repressor proteins are characterized by having TERT repressor activity. Specifically, the subject proteins bind to a repressor binding site present in the TERT minimal promoter. More specifically, the subject proteins bind to a “Site C” repressor binding site present in the human TERT minimal promoter. The human TERT Site C binding site is located in the region −80 to −50, and particularly −69 to −57 of the human TERT minimal promoter, and the subject repressor proteins bind to this site, where the sequence of this site is: GGCGCGAGTTTCA (SEQ ID NO:01). When binding to this site, or a portion thereof, the subject repressor proteins inhibit expression of TERT, where by inhibit expression is meant that expression of TERT is reduced by at least about 50%, usually at least about 75% and more usually at least about 90% as compared to a control system where TERT expression occurs and that is identical but for the absence of the subject repressor protein. The subject repressor proteins may be glycosylated, or modified in alternative ways."

 

To see why we don't need the F13H protein look below in the quotes. Furthermore, there is no other protein that is described in the patent by Bill Andrews to inhibit TERT activation, much less to this extent. Obviously inhibiting other proteins like c-myc can activate telomerase, but that is risky, and I believe Bill Andrews focused on his TAM818 molecule based off targeting this protein. And his TAM818 molecule has no side effects and he essentially said with pictures, that the primordial germ cells that are telomerically immortal, do not have this repressor protein on them, thus they maintain their telomeres, while the rest of the body has this protein.

 

"
In addition to the specific TERT repressor proteins described above, homologs or proteins (or fragments thereof) from other species, i.e., other animal species, are also provided, where such homologs or proteins may be from a variety of different types of species, usually mammals, e.g., rodents, such as mice, rats; domestic animals, e.g. horse, cow, dog, cat; and primates, e.g., monkeys, baboons, humans etc. By homolog is meant a protein having at least about 35%, usually at least about 40% and more usually at least about 60% amino acid sequence identity to the specific human transcription repressor factors as identified above, where sequence identity is determined using the algorithm described supra. One homolog of particular interest is the F13H homolog disclosed herein as SEQ ID NO:11.

"

 

 

 

If you want to see what I mean visually

 

go to https://github.com/v...erbose-barnacle (to download the pdb and mol2 files)

 

then

 

1 go to http://clab.labshare...p/blinddock.php
2 for the protein upload the f13 pdb file
3 for the ligand, upload the cycloastragenol mol2 file
4 experiment with it to see what you can do
5 The goal is to find the crater(s) for near complete inhibition.
6 The cycloastragenol is just for testing, it does not mean some of those craters are the best places.
7 Also, the more negative the vina score, the higher the binding. Each different vina score represents a different potential crater for binding.
8 You can make new molecules in http://www.swissadme.ch/

9 The goal is to find information / an AI that can do this.

10 The difficulties are that we have to determine what exactly are the best binding site(s) for inhibition. As you can see, the cycloastragenol molecule has a flimsy binding connection.

Or we could just wait for AI to advance and use a powerful drug discovery tool / AI and essentially become "script kiddies" and go very fast very hard, and get the compound structure.

chat gpt said it would cost between $2000-$20,000 for chemically sequencing the molecule, but costs could get under $1 if there is a dedicated setup.

 

This is the gist of what Dr. Bill Andrews is doing I think.

 

 

 

for confirmation

look at the patent for the amino acid sequence for F13

https://www.ebi.ac.u...dSequence.pl   (shows a list of proteins that are most identical to it)

https://www.ebi.ac.u...pl?pdbcode=A4sc (clicking the one with 99.9% identity)

https://www.alphafol...uk/entry/Q96AV8 (downloaded this protein)

 

 

As for working with others I am interested in working with BioViva, but I am just an individual and I don't know how advanced they are. But if I could work with them,

 

I would ask them for the compounds that they have tested/ Dr. Bill Andrews has tested regarding the 350,000+ compounds tested and 900+ inducers of telomerase, obviously after the interview is over, and they can send it on their own time.

 

I would ask, just how much is TERC (telomerase is made up of rna TERC and the protein TERT) limited if we can get TERT to 90% activation and if we also need to increase TERC (but everywhere I see, I see that TERC is ubiquitiously expressed)

 

I would ask for a general review of my methods.

 

I would contact Nvidia and ask about applying for early access for their AI https://www.nvidia.c...-cloud/bionemo/ but I would need to be confident in this tool beforehand.

 

I would ask for funding, or if I am very confident I could take out a loan. I do not want to deal with the FDA or anyone at the top.

 

You may wonder, why don't I just leave this up to BioViva? I think it is very important for open source groups to work on this because if companies work on it, how guaranteed are you that they won't keep the compound secret, especially after something happens to the dynamics of the company, like a ceo change?

 

 

[vibrantguy]

Anyways, my plan from now on, is to thoroughly make sure that what I am doing is indeed correct for achieving biological immortality.

 

I don't plan on working with BioViva right now since I am not ready. But in the meantime,

 

• I will refine my paper.
• After that, I will analyze all the best binding sites for inhibition of the protein, crossing out irrelevant parts.
• Use current tools like cb-dock for viewing docking of ligands.
• and I will further support it with machine learning models to improve the binding affinity, as well as predicting off-target interactions using computational methods.
• I will have chat gpt with vision potentially supporting me (lol)

My goal is to end up with less than 100 really strong compounds for activating TERT to 90% activation or higher in the body (which can potentially lead to biological immortality, according to my current knowledge and according to Dr. Bill Andrews. I am not sure how it will fare to reverse aging though, that is something I have to ask) complete with safety screenings already done, then potentially present them to companies like Sierra Sciences and BioViva after leaking the molecule to the world.

 

I could have my computer well set up for this within 2 months.

 

 

[vibrantguy]

So I made updates to my paper https://github.com/v...in/new doc.docx .

 

I completed all sections besides the Methods for Telomere Resetting.

 

My next tasks are to

Assume the goal is to use the cycloastragenol / ta-65 compound and put it on the f13 protein (molecular docking) and make a new compound that is similar to ta-65 but is made out of simpler molecules, so that it is easier to chemically synthesize, this is simple I think.

and

most importantly, to make the ADME properties incredible to the point that just taking this compound would be enough for biological immortality (the method I am assuming is by "sticking" to the protein for an extended period, because we already know that a relatively weak telomerase increaser like ta-65 can still increase telomere length, but the issue probably lies in the ADME.).


so we need machine learning tools to predict the ADME properties and improve them and it is relatively straightforward.

Would this be safe? Well we are adapting from the ta-65 molecule, which has lots of safety data (no reported side effects), and is thus very useful for in silico analysis and machine learning.

[Mind]

Looks like you are heading in the right direction.

 

Just wanted to mention another company that is working on telomere lengthening: Rejuvenation Technologies I know they are not a likely partner due to their private company status and proprietary technology (not open source), but I thought you might like to see their approach as it might spur further ideas in the space.

[vibrantguy]

So I found the exact location on the f13 protein responsible for connecting to the dna and inhibiting it. It is only 1 cavity (awesome). No other part of the protein has anything else that resembles a bind to the dna. If we make a molecule to bind to that cavity, it won't bind to the dna.

 

I have some minor straightforward work to do.

 

Now we have to design an optimal molecule. Should be pretty simple, we only have to deal with this cavity. I've seen the molecules and atoms that make this up. Also chat gpt vision should speed the process up although it is not necessary

[vibrantguy]

Should take me less than 1 week to get 1 optimal molecule, including the ADME, safety predictions, and such. Then I will probably send it to Dr. Bill Andrews because he can test it?

[Mind]

When you find some potential candidate molecules, if you have some trouble contacting Dr. Andrews or others, let us know. Many people here have connections and could possibly help find a lab to test it out.

[vibrantguy]

Let me know if you guys want to see my research. No one is commenting so I don't know if you guys are interested.

[Daniel Cooper]

Is there any Open Source AI engine oriented towards medical research out there?

 

A ChatGPT of medicine?

[vibrantguy]

Subject: Collaborative Opportunity for Accelerating Biological Immortality Research Using LigBuilder

 

Hello everyone,

 

I'm currently engaged in an exciting project using LigBuilder, and I'd like to share some insights and invite collaboration.

 

The Challenge: We have 50 computational tasks to run, each ideally requiring a dedicated CPU for optimal efficiency. Running this on a standard laptop with 4 CPUs could take an estimated 20 months. However, according to LigBuilder's guidelines, these tasks require approximately 1,000 to 5,000 CPU hours in total. This means with a collective effort of 50 CPUs, we could potentially reduce the time to just 20-100 hours.

 

The Process: The task execution is straightforward and easy. We can distribute the tasks among us, each running a task(s) independently. A task is best run per cpu.

 

The Potential Outcome: Successful completion of these tasks could yield strong candidate molecules for biological immoratlity. We can then analyze these molecules, synthesize the most promising ones for testing, and refine them further if needed. This process is simple. LigBuilder is adept at designing molecules with both optimal functionality and ease of synthesis.

 

My Experience: I attempted this computation at my university but got kicked on the second day.

 

Comparative Analysis with Dr. Bill Andrews' Work:

• Dr. Andrews' approach, while similar, is less computationally focused and involves more empirical testing and iterative improvement of molecules. His method is expensive and less efficient. In one of his podcasts, he said that a secret is that he mostly randomly tests the molecules to find hits and iteratively improves those molecules. He said he doesn't know how the molecules work to inhibit the molecules. Although it may be an over exaggeration, it is important to note. This is not an optimal approach.

 

• His patented molecule (US20090143451A1) shows promising results but is complex to synthesize (7 step synthesis process which would be very very expensive to synthesize). According to Dr. Bill Andrews, it is 16% effective compared to the hela scale, although we may not need 100% as the hela scale divides much faster than normal cells, we may need only 50% of the hela scale. His molecule only leads to 2.5 more cell divisions, while no amount of antioxidants increases the amount of cell divisions, which you guys always talk about . His molecule leads to a reversal of all aging biomarkers, but it is not that effective yet, because the molecule itself is not that effective, even though the method to biological immortality for this is completely sound. It may be that the molecule does not bind optimally to the protein or that its absorbption,distribution, metabolism, excretion, toxicity properties are not optimal, although it has no toxicities.
• The 3D structure of the target protein was only available in 2021, and the molecule in the patent was available in 2008, which means it is really not optimized, especially considering that molecule requires a 7-step synthesis process which is very difficult to synthesize and is only likely to get more complex, if they continue with their methods.

The Call to Action: I'm reaching out to this community for support. Running these tasks on Google's virtual CPUs would be costly (around $2,000 or more), and collaboration could significantly expedite our progress.

How You Can Help:

1. Learn about the project: Familiarize yourself with LigBuilder and its capabilities. It is very simple. Also learn about the theory in a short document that is divided into parts for easy understanding for a beginner. 1.docx
2. Participate in task execution: I'll provide guidance on how to run the tasks. It is very easy. method.docx
3. Contribute and Collaborate: Visit our GitHub repository at verbose-barnacle(github.com/vibrantguy123/verbose-barnacle) for all the necessary information and to share your results. If you want permission to upload/fork ask me. I am new to github so if I am doing something incorrectly or you can give me advice please do so.
4. Ligbuilder folder: I will upload tomorrow to the google drive.

Reference: Yaxia Yuan, Jianfeng Pei, Luhua Lai, "LigBuilder 2: A Practical de Novo Drug Design Approach", J. Chem. Inf. Model., 2011, 51 (5), pp 1083–1091.

 

Together, we have the opportunity to make significant strides in the field of longevity research.

 

Any assistance you can provide would be greatly appreciated.

 

Thank you for considering this collaborative effort.

 

[vibrantguy]

Is there any Open Source AI engine oriented towards medical research out there?

 

A ChatGPT of medicine?

Yes, that is what I am using. Although simple analysis will have to be done by us, since we are human.

I am going to set appointments tomorrow with bioviva/sierra sciences for this.

[vibrantguy]

why is this method so hype?

 

In a lab in human cells, telomere extension has made human cells divide normally/youthfully/healthy like normal cells for 250 divisions and counting.

 

A mice that has been engineered to age by telomere shortening, even though they normally age by oxidative stress and mitochondrial dysfunction (lifespan can be extended with antioxidants and NOT telomere extension), they aged like humans do when their telomeres became shorter, and when their telomeres were reextended in their old age, their brain that was 75% of its original size, became 100% again, and the mouse became like a young mouse again by every method of aging imaginable according to dr. bill andrews.

 

80 year old human skin that was grown on the back of a mouse with their telomeres extended, resembled a young skin cell, in every way imaginable. It doesn't revert it to an embryo cell or anything, it makes it younger and doesn't reverse its age into a baby, it just takes them to the optimal cellular age which is around 20-25. and this is likely to be true for every other cell too, all of this is what dr. bill andrews said.

 

Dr. Bill andrews has invented skin creams and a spray under the tongue that can make you younger in every way, fix your eyesight, etc etc.

[vibrantguy]

In the meantime, while I wait for you guys to help me.

 

What I plan to do next is to take the sulfur atom(from the patent) and put it on the protein 1.png in my github on nglviewer.

 

The purpose is so I can see where it connects and whether it is optimal especially for longer binding times. And I really don't have much choice but to use chatgpt 4 to design optimal molecules based on this.

[rikelme]

vibrantguy, I just saw you deleted the files from the github (luckily there's a commit history so one can obtain the files that way).
Is this what you are asking:

The Challenge: We have 50 computational tasks to run, each ideally requiring a dedicated CPU for optimal efficiency. Running this on a standard laptop with 4 CPUs could take an estimated 20 months. However, according to LigBuilder's guidelines, these tasks require approximately 1,000 to 5,000 CPU hours in total. This means with a collective effort of 50 CPUs, we could potentially reduce the time to just 20-100 hours.

 

?

Thanks