Andrew Brack

2.4K posts

Andrew Brack

Andrew Brack

@BrackLab

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

CA Joined Nisan 2012
1.1K Following4.2K Followers
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Andrew Brack
Andrew Brack@BrackLab·
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.
ARPA-H@ARPA_H

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-event…

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Celine Halioua
Celine Halioua@celinehalioua·
loyal on 60 minutes this weekend!
Celine Halioua tweet media
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Andrew Brack
Andrew Brack@BrackLab·
A medicine is only helpful if you take it. The benefits of exercise and healthy living are clear. The reality is that far too few people do it. As someone who wants to maximize healthy lifespan for every person we need additional solutions.
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Andrew Brack retweeted
Alexis Ohanian 🗽
Alexis Ohanian 🗽@alexisohanian·
The boxer my father named me after, Alexis Arguello, was the world's first 3-weight world champion before facing an opponent who cheated. Boxing is only great when it's fair, and @jabbr.ai is here to make it so!
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José Luis Ricón Fernández de la Puente
Various ways to think about aging, roughly in order of when they became popular: 1. Longevity 1.0: Target the well conserved pathways (mtor, foxo3, ampk etc) and their regulators. 2. Longevity 2.0 The SENS/Hallmarks view: Remove damage, typically concrete molecular entities or cells, as well as adding back what was lost (like stem cells) 3. Longevity 3.0: Organisms can mostly fix their aging if they tried, they just 'forgot' how to or are "stuck" in some way (information loss (Sinclair), loss of morphostasis (Levin)) so what's needed is to nudge them in the right direction (e.g. reprogramming) and they can sort the rest out. None of these are "true" or "false", they are all incomplete, but I think of them as useful.
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Andrew Brack
Andrew Brack@BrackLab·
@KarlPfleger I was poking fun based on your claim that you had a more accurate measure. I’m good on wherever your analysis places me.
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Karl Pfleger
Karl Pfleger@KarlPfleger·
@BrackLab Sorry to disappoint but it's alphabetical within the large coarse overall scores. So you are one of N people with a score of X whose last name happens to start with B. The ranking is not meant to be a good one. Just to separate out people into generally high vs mid vs low.
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Andrew Brack
Andrew Brack@BrackLab·
YES!!!! I’m 148th on the objective measures longevity list. Hopefully I’ll break top 100 next year😂
Karl Pfleger@KarlPfleger

@Longevity_Now_ Better longer list, much based on objective measures: AgingBiotech.info/people Note: Altman & Kurzweil not even on it despite being 250+ long. Altman funded 1 company w/o being very involved. He's busy w/ AI. Poor pick. Kurzweil had vision long ago but not really in the field.

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Andrew Brack
Andrew Brack@BrackLab·
@RapaNews This points to the selection criteria of why these compounds were tested-when resources are limited. Personally, I’m not surprised at all. Who advocated for these?
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David J Glass MD
David J Glass MD@davidjglassMD·
A very important point is the safety point: this paper shows you can significantly decrease myostatin levels throughout a person’s lifetime, and the result is more muscle, less fat, increased strength, and no noticeable side effects
David J Glass MD@davidjglassMD

Humans with function-disrupting variants in the myostatin gene (MSTN) have increased skeletal muscle mass and strength, and less adiposity nature.com/articles/s4146…

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ARIA
ARIA@ARIA_research·
The search for ARIA’s next cohort of Programme Directors has begun 🚀 As an ARIA PD, you will design and actively manage a ~£50M R&D programme within or around our opportunity spaces with the goal of unlocking scientific and technological breakthroughs that benefit everyone. There is no one way to be an ARIA PD – our existing cohorts come from a range of backgrounds, including academia, entrepreneurship, invention and industry, and have launched programmes in areas ranging from synthetic plants to multi-agent coordination to brain surgery-free neurotechnologies. Full applications will open in August 2026 for a May 2027 start date – over the coming months we’ll be running webinars and in-person events across the UK, Europe, the US and Asia where you’ll get the chance to engage directly with the ARIA team and learn more about the opportunity. Find out more about what it means to be a PD and register your interest to be the first to receive updates on the recruitment process: link.aria.org.uk/pdc3-x
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Andrew Brack retweeted
Adam Auton
Adam Auton@adamauton·
New opportunity at 23andMe Research Institute! We're looking for a new team member to help us build and deliver clinically useful risk prediction models that can be deployed to consumers and clinicians. 23andme.wd5.myworkdayjobs.com/en-US/23/detai…
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Andrew Brack retweeted
Andrew Brack retweeted
Jay Bhattacharya, MD, PhD
Jay Bhattacharya, MD, PhD@NIHDirector_Jay·
At NIH, we’re accelerating the future of medical research, advancing innovation and repurposing existing drugs to deliver new treatments faster for the American people🔬🇺🇸
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Andrew Brack
Andrew Brack@BrackLab·
I think, you and I are aligned on the approach, my point is that we dont have the n of 1 positive control, and im not sure there is such a thing. We need to build a new infrastructure, a US biobank with emphasis on longitudinal collection for RWD. Happy to chat in more detail about building.
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Jason Kelly
Jason Kelly@jrkelly·
@BrackLab @bryan_johnson why low n? I think you can do home blood draws and make it pretty cheap. Bryan would agree with that too -- he's just been doing n of 1 b/c he's been willing to pay for it. But no reason can't make it cheap now.
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Andrew Brack
Andrew Brack@BrackLab·
Thanks for enganging @jrkelly. Agree with you that constant molecular monitoring -longitudinal measures, is going to be a huge unlock, and when combined with long term health outcomes, but we need to build that data layer out. In line with your passion for lab automation, noise and low n is going to limit interpretations. Bryans focus on his own n-of-1 as a standard of which to map against, with interventions of somewhat unknown utility and to monopolize, is why it’s wrong. But happy to chat about automation of the n of 1 for longevity anytime. We are all living our own adaptive clinical trial.😉
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Jason Kelly
Jason Kelly@jrkelly·
hit me! what don't you like? my general theory is we should be doing as frequent as possible measurement of tons of biomarkers in at least blood. Oura ring but for molecular measurement. Then can do various interventions and see what works -- also likely to get early detection signals of various diseases over time if lots of people start doing this. Easy way to get started IMO is frequent blood collection sent to central labs for broad metabolomics, proteomics, etc.
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Andrew Brack retweeted
Norn Group
Norn Group@NornGroup·
Nicolas's review highlights the design variables that determine whether a trial produces actionable evidence or noise: population enrichment, dose and schedule, endpoint construction, and confirming the drug is engaging its target. Joan Mannick and Adam Salmon flagged the same gap to Nicolas independently: baseline mTORC1 activation varies enormously between individuals, and there's no reliable way to confirm engagement in a given person. Endpoint selection for longevity is already hard, and this challenge touches on the three other variables. But things are happening, with multiple trials exploring designs and endpoints (several funded by @NornGroup @impetusgrants): VIBRANT-I is a randomized trial at Columbia testing whether weekly low-dose rapamycin can slow ovarian aging in women in their thirties. It hasn’t fully read out but showing early separation in ovarian reserve. A larger followup, VIBRANT-II, is already being set up. RAPID, Jonathan An's clinical trial at the University of Washington, is testing rapamycin in adults over fifty with periodontal disease, with biological aging biomarkers and microbiome sequencing built into the protocol alongside the clinical endpoints. Kaeberlein et al's survey of 333 off-label users provided the human safety data that made the controlled trial possible. ERAP, a Phase IIa trial out of the Karolinska Institute, tested weekly rapamycin in fourteen early-stage Alzheimer's patients over six months, with cerebral glucose uptake as the primary endpoint. This derisked the design for rapamycin trials in Alzheimer's, with primary imaging endpoints steady or even increased in exploratory regions compared to natural history disease progression. @LammingLab's RAP-PROTECT trial at Wisconsin recruited fifty people who already take rapamycin off-label, drew their blood at home using mobile phlebotomy, and ran it through metabolomic and lipidomic profiling to see which aging biomarkers actually respond to mTORC1 inhibition. Results expected this year. And elsewhere: Marmoset survival data from a 10-year, 66-animal study is incoming. And @BrackLab @ARPA_H just committed up to $144M across seven longevity teams, two of which are mTOR inhibitors. Trial design and infrastructure might finally be catching up to the science...
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