Scientist interested in preventing functional decline during aging. Program Manager at ARPA-H. Interests: Crypto, Everton FC and Boxing. Views are my own.

CA
What if we had therapies to extend healthspan and prevent the onset of age related diseases? I’m excited to announce my first @ARPA_H program, PROSPR. The goal is to develop validated surrogate biomarkers, new clinical endpoints and therapies to collectively extend healthspan by 20 years for all Americans.
What if we could predict age-induced health issues before they happen? Our new PROSPR program aims to identify biochemical and physiological markers, paving the way for faster, more targeted aging research. arpa-h.gov/news-and-events/a…
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Andrew Brack retweeted
I’m excited (and definitely a little nervous!) to share that I have started as Principal Investigator and faculty member at the Marcus Institute for Aging Research, a @harvardmed affliate! For the past few years, I’ve been obsessed with a pretty simple question: how do we understand and measure human aging well enough to actually do something about it? That question will be at the heart of what we build next. Our lab will focus on computational geroscience, bringing together AI/ML, multi-omics, and large-scale human data to understand the biology of aging and, ultimately, find ways to intervene on it. A big part of that will be building better biomarkers that can reliably measure aging and tell us whether an intervention is actually working. But I’m equally excited about what comes next: using computational tools to identify causal drivers of aging, discover new therapeutic targets, and help find and prioritize new therapies that could extend healthy lifespan. The bigger goal is to close the loop between measurement, discovery, and intervention, connecting computational work with experiments, human studies, and clinical trials. There is a lot to build, and an even longer list of things I still need to learn about running a lab. But that is probably what I’m most excited about. Building a team, learning from people across geroscience, medicine, computation, and industry, and tackling some interesting questions together. I’m incredibly grateful to everyone at Yale who helped me get to this point, and very excited for what comes next at Harvard ! PS I am definitely looking to hire some smart computational biologists and ML/AI folks so definitely reach out!
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IMO what matters more than the triage percentage is ppl fighting for a proposal that one person tanked for a crap reason
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Andrew Brack retweeted
This is a first-time in history - review by a private board of a novel phase-1+ treatment for medical use The ETRB aims to be highly transparent about its decisions
Montana Experimental Treatment Review Board has completed the review of its first treatment protocol submission. On August 26th the ETRB unanimously voted to approve, with conditions, Parley Neurotech's combination therapy (LOOT) for use at Experimental Treatment Centers in Montana. This is the first treatment protocol approved for use under the Montana SB535 Right to Try pathway. Our Review Decision Letter (RDL) will be published at MontanaETRB.org shortly.
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Andrew Brack retweeted
We have 15 open positions at Astera Neuro! We're hiring experimental and computational neuroscientists and engineers to build a large-scale research effort aimed at understanding consciousness = the brain's internal model of world and self. astera.org/careers/#box=neur… We're looking for: • Experimental Neuroscientists • Computational Neuroscientists • Optical Engineers • Hardware Engineers • Software Engineers • Probe Engineers • and more! I'll share much more about our scientific vision soon. For now: I know we could never have built this in academia. The confluence of talent across different domains, the purposive design of the org structure and open science approach, and the deep, long-term support, all aimed at cracking the brain's internal model, is unprecedented. If you want to understand consciousness, if you sense a huge gap between our internal experience of the world and our scientific understanding of it, if you believe systems neuroscience needs a fundamentally different, collaborative, and scaled up approach, we are building the ideal research environment for you. I've never been more excited in my life. Across Astera Neuro, Astera AI, and Astera Simplex, we're creating a whole new discipline around one question: how does the brain build a world model: a symbolic system that perceives the real world from flickering sensory input streams and can think, plan, and experience? Everyone here is converging on this question from a different direction. The degree of conceptual focus combined with tactical breadth is thrilling. If this sounds like you, come join us. astera.org/careers/#box=neur…
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Andrew Brack retweeted
🚨 BREAKING: Folarin Balogun to SIGN for Everton! 🔵🇺🇸 After failing his initial medical, Everton sought a second opinion from a very experienced American doctor. “I looked at the medical. Perfect medical. Maybe the best medical anyone’s ever seen.” Thanks, Dr. Trump.
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Andrew Brack retweeted
Longevity treatments cannot reach patients if we cannot prove they are working. ARPA-H’s PROSPR program is tackling that bottleneck. A new @nytimes feature explores how PROSPR is using intrinsic capacity — including strength, mobility, cognition, and vitality — to measure healthy aging on a timeline that works for medicine. Through PROSPR, ARPA-H is creating a path for treatments that extend healthy years to reach all Americans. Read the story 👉nytimes.com/2026/08/26/well/…
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Time to stop longevity wokeness and lean heavy on longevity pharma as the minimal first frontier while researching C&G therapy, BCI, replacement and nanoelectronics as the second frontier
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A key component of the pre-clinical drug discovery work in PROSPR is the automated collection of physiological and behavioral measures in mice as they age and receive therapeutic interventions. This is enabled through DOME lids designed and built by @OldenLabs I'm delighted to announce, AUTOMATE, a new @ARPA_H funded project with @OldenLabs that will build new technology to continuously, objectively, and non-invasively measure core domains of intrinsic capacity (cognition, strength, vision, and hearing) in standard laboratory environments. It's a pleasure working with @MichaelFloreaX and team. #PROSPR is building the pre-clinical to clinical validation tool box for Intrinsic Capacity, and we are not done!
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Andrew Brack retweeted
Replying to @JoeSmithai
We're a small team, so we are building in one place for now. We may expand elsewhere in the future, and have a General Interest application for those who want to be on our radar for future roles: ats.rippling.com/openai-foun…
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Awesome opportunities
Some more about these four roles, since I will work closely with everyone we hire into them. (Salary ranges are posted on the job descriptions for these and other roles across the Foundation: openaifoundation.org/careers) First, I am excited to share that, 8 weeks ago, Vidya Vasu-Devan joined the OpenAI Foundation to lead our work in High-Burden Diseases. Before this, Vidya led the investment team for a global health biotech VC fund; before that, she was Chief Strategy Officer at a vaccine company; and before that she was Director of the $2.5 billion portfolio of strategic investments at the Gates Foundation. In an earlier draft of this tweet I wrote two more paragraphs bragging about some of the things Vidya achieved in those roles, but unfortunately for me she doesn’t like being bragged about. Which relates to why you may have a lot of fun working with her if you join our team -- Vidya is unusually humble, has helped protect an unusual number of people from infectious diseases through her work, and most importantly has complementary skills to mine in bar trivia. We are hiring a Program Officer and/or Program Director on High-Burden Diseases. These are open-ended roles with a broad mandate to help solve some of the world's biggest problems in health. They will work with Vidya to figure out: what is newly possible due to AI progress, in tuberculosis drug development? In newborn health, where roughly 2 million infants die each year? In stroke, in hepatitis B, in other diseases facing market failures where we may be able to unlock rapid progress for patients? If you have a scientific or technical background and would like to spend your time thinking about those questions, we would love to receive your application. One of the other two open roles on our team is a Chief of Staff reporting to me. If you've made it this far into a long tweet, that bodes well for your attention to detail, so perhaps you should apply (put "ATN" in the "Anything else?" field on the form). I am looking for someone with excellent judgement and organisational skills who 1) moves fast, 2) is comfortable with ambiguity, 3) takes ownership without waiting to be asked, and 4) enjoys thinking about how teams can operate at their best in the presence of growth + time constraints. I'm open to a range of backgrounds, though some science in your past helps. Vibecoding addiction is a positive too. Finally, we are hiring a Head of AI for Alzheimer's. Our goal is straightforward and extremely hard: help scientists invent new tools to finally prevent and treat Alzheimer’s. We have made some initial investments (openaifoundation.org/news/ai…), but much of what we do next remains deliberately undefined. We are seeking a flexible and highly autonomous leader to help us figure out the path. This role is similar to what Nan Ransohoff describes as a General Manager: nanransohoff.substack.com/p/…. If the role sounds exciting but you are not sure you fit the profile, I recommend reading that essay to see how much you resonate with applying something like it to AI for Alzheimer’s.
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I was delighted to contribute to this @newyorktimes piece on Intrinsic Capacity by Dana G smith The @ARPA_H program, PROSPR has placed a big bet on developing and testing the Intrinsic Capacity framework as a novel clinical endpoint for measuring health changes during aging. ARPA-H programs typically scale and validate early promising technologies with the aim of rapidly impacting human health. PROSPR was built to tackle aging. My thesis is that Intrinsic Capacity is an intervenable proxy of overall health changes based on promising work from @DrJohnBeard, David Furman and @brunovello amongst others. Specifically, PROSPR will build the datasets to ask, can Intrinsic Capacity serve as a novel clinical endpoint on which to assess gerotherapeutics, and can it serve as a predictor of health trajectories for people at home? We are not arm-chair quarter backing; we are doing the work. In less than 5 years, the field will know whether the thesis was correct or not. As David Furman mentioned in the piece "we expect tracking this and intervening early will help people live longer, but we don't have the data yet", which echo's my conclusion: “ we need to do the experiments” to determine it predictive power in clinical trials and in-home. This speaks to the scientific rigor that the team bring to the PROSPR program. I couldn't be prouder of the teams and excited about the journey we are on together. #PROSPR 🖖
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Andrew Brack retweeted
Smart messaging pivot by @bryan_johnson from “Don’t die” to “Don’t disease” The hunt for a cure activates founder mode medicine like nothing else.
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Andrew Brack retweeted
Very excited about Claude Teams for Science! Claude is doing amazing things to help scientists move faster and explore new ways of doing scientific work. It has been totally transformative for my own work! If you’re a PI in academia or a non-profit org, check out this program!
Starting today, 10,000 scientists across every field, from math to chemistry to physics and more, can get Claude through our new Claude Team plan for scientists. Standard seats are free, and premium seats with 5x usage limits are $15 per month, an 80% discount, for one year. Claude is becoming increasingly capable of scientific work, with recent progress on problems from advanced physics calculations to protein design. Alongside that progress, we've been investing in the research community: Claude Science launched in June, and our AI for Science program funds high-impact projects with free credits. Today's expansion builds on both. Principal investigators (or equivalent) at academic and nonprofit research institutions can sign up, then add the researchers in their group. Over the coming months, we plan to extend the program well beyond the initial 10,000 seats. Learn more: claude.com/programs/team-pla…
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Andrew Brack retweeted
From @ashleevance (couldn’t have said it any better!): "This is what makes @AlexJColville refreshing. He's quietly been the most influential longevity investor of the past decade and approaches the field in a pretty sober, rational way." Very well-said. What an honor (and what fun!) to work with this guy. piped.video/watch?v=9OSyjrWv…
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Andrew Brack retweeted
I think @MartinBJensen raises a number of really thoughtful points, and I actually agree with much of the underlying concern. In particular, I agree that responsiveness should not be interpreted as proof that an intervention slowed aging, and that ultimately we need much stronger physiological and clinical ground truths to establish whether changes in these biomarkers represent meaningful changes in human aging. I would just separate that question from what we were trying to establish in the paper. Our goal was not to demonstrate surrogate validity, but to systematically ask which biomarkers are responsive to human interventions in the first place. Until now, clocks have largely been evaluated on their prognostic validity. We see responsiveness as another necessary step on the path toward eventual surrogate validation. I would also be careful about interpreting responsiveness as evidence that the clocks are “unreliable.” Reliability, responsiveness, prognostic validity, and surrogate validity are distinct properties. In fact, our separate work specifically evaluates technical and biological reliability for this reason. I also agree that the x-axis in the commentary figure should not be interpreted as measured longevity. We did not make that figure, and the interventions clearly involve heterogeneous outcomes and populations. Where I think the discussion gets especially interesting is what constitutes the appropriate “ground truth” for human aging. Unlike worms or mice, we do not have a clean experimental measure of lifespan response available on practical timescales. Mortality, disease incidence, functional decline, physiology, and other outcomes each capture different pieces of the biology. That is exactly why I think we need to build the evidence incrementally: prognostic validity → responsiveness → reliability → ultimately surrogate validation against meaningful clinical outcomes. So I think Martin and we are ultimately arguing toward the same destination. The main difference is that our paper was designed to systematically establish one of the intermediate pieces, rather than claim that we have already reached the endpoint.
To say the quiet part: This actually shows that current clocks aren't reliable for detecting intervention effects (yet!). You're thinking that the x-axis is real, measured longevity, but it isn't. The COSMOS trial was entirely negative on health benefits. And the authors of the new study didn't make this x/y plot. What @rv_sehgal et al aimed at was showing which clocks respond to what, which they did thoroughly. But they don't have good data on human physiology effects for most of the interventions. So what we're confident it shows are some clocks go up and down (notably after measuring immune cells only), for mostly unknown reasons, and we don't know what's a correct response. My best guess at what the x-axis of this graph (from a commentary piece) shows is a different kind of 'benefit' for each dot, in different study designs and different populations, none of which are direct measures of longevity. This kind of hand-waving is actively harmful to the goal of using clocks in the clinic, as it prevents real assessment by lumping disparate outcomes and fails to distinguish discrete hypotheses. The truth-seeking path that'll get us real progress is generating ground truth biological effect data to compare (blindly) against clock predictions, and iterating until we have objective robustness. Context: @impetusgrants is funder of the original paper, because robust clocks are hugely important.
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Andrew Brack retweeted
Interested in learning more about @xprize Healthspan and the Finalist teams? The you MUST check out @juliankissa podcast - link below. 👇 This is FIRST combined exclusive with @PeterDiamandis and multiple #XPRIZEHealthspan finalists captured at our award events!
Our @xprize special with @j_n_justice, @PeterDiamandis and many more longevity superstars is out! Watch now: linktw.in/XVmvdX
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Andrew Brack retweeted
As to how the biotech and pharm world have done pre-AI, 15 years ago we did not have : 1. High-efficacy incretin therapy (semaglutide on...) 2. CAR-T therapy 3. modern cytokine-blockade: anti: IL-4/13, IL-17, IL-23 4. mRNA vaccines 5. Anti-Ebola antibodies (Cont'd)
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Andrew Brack retweeted
The mixture of arrogance and complete ignorance in this post is truly impressive. If you compare where we were 30 years ago to where we are today, biotech and pharmaceutical companies have done quite an impressive job. But sure, try it with zero knowledge of biology. Let's see.
dario's right that most human diseases are solvable in 5-10 years, but nobody has done the thinking on how: - biologists especially are sooo lost in the details. it's better to not learn biology at all than to learn the standard version, our understanding is that far off - injecting dumb drugs into a system this complex is the wrong level of abstraction - we should be taking @drmichaellevin far more seriously. the cells already know how to build things, we just don't know how to talk to them
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Andrew Brack retweeted
My comments on a recent editorial in Nature Medicine James is a dear friend, colleague, and fellow LBA Board member, and I strongly agree with the argument he makes here—with one point I would emphasize even further. What should qualify as a true gerotherapeutic? I believe it should meet four criteria: 1. It targets fundamental hallmarks of aging and helps shift older cells and tissues toward a more youthful, resilient state. 2. It extends both healthspan and lifespan in animal models. 3. In clinical studies, it prevents or delays multiple age-related diseases, not simply one disease at a time. 4. Ultimately, it reduces all-cause mortality. When we apply these criteria, several classes of drugs that are already FDA-approved stand out as particularly compelling gerotherapeutic candidates: SGLT2 inhibitors, GLP-1 receptor agonists, metformin, and bisphosphonates. That matters because these drugs provide something geroscience urgently needs: real-world examples suggesting that interventions can influence multiple aging-related outcomes rather than a single disease in isolation. Yet too few physicians and patients recognize the broader geroscience implications of these medications. And the therapies we have today should be viewed as a beginning, not an endpoint. They give us proof of principle—and a strong rationale for developing more powerful gerotherapeutics and, ultimately, personalized combinations that target multiple mechanisms of aging simultaneously. If the practical upper range of human lifespan is around 115 years, a figure that remains debated, there is already an enormous gap between our biological potential and the roughly 80-year life expectancy seen in many high-income countries. The goal of geroscience is not simply to add years to life. It is to enable far more people to reach their 90s and beyond healthy, functional, and resilient. James’s vision can help move us closer to that goal and truly transformative gerotherapeutics may eventually allow us to go further than we currently imagine.1. nature.com/articles/s41591-0…
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