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Transcribed is your front-row seat to the fascinating world of biotech. Hosted by two curious minds bridging science and business, this podcast brings you insightful conversations with leading voices in biotechnology. Whether you're a student navigating STEM or business, or simply a curious listener, Transcribed delivers practical tools, career advice, and behind-the-scenes stories that make the complex world of biotech accessible and inspiring.
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Every new organism starts young, even though it is made from old cells. How?Dr. Maria Marinova, co-scientific director of the Thalion Initiative, joins Pierre Jacob and Meronn Jacob on Transcribed. We recorded this conversation in person at the Longevity Summit in Dublin.Maria has wanted to work on aging since high school. She did research at Berkeley, EMBL, Cancer Research UK and LMU Munich, then left the bench for venture capital at Apollo Health Ventures and decentralized science at VitaDAO. Now she is building the Thalion Initiative, a new nonprofit that wants to go back to first principles and fund the basic science of aging.Her argument: the field is pouring money into translation while the foundation underneath is not stable enough. She explains why she sees drug development as a biology problem rather than a funding problem, how VitaDAO uses blockchain tokens and IP-NFTs to fund lab research, and why philanthropic money may be the least biased capital in science.We also get to her favorite open question in aging: embryogenesis. Data from the Gladyshev lab suggest that biological age drops after fertilization, reaches a "ground zero" around gastrulation and then starts rising again. What clears the damage, and could we ever learn from it?In this conversation:◼️ Why she left the lab for venture capital◼️ How venture capital works in biotech◼️ The gap the Thalion Initiative wants to fill◼️ Decentralized science and VitaDAO, explained◼️ How embryos reset their biological age◼️ Biology problem or funding problem?◼️ What academia, investors and founders get wrong◼️ Why basic research is hard to fundraise for◼️ What we lose if we only fund applied work◼️ Thalion's goal for the next 10 yearsTranscribed Podcast: in-person interviews with scientists, founders, and industry experts shaping the future of biotech and pharma.New episodes every Tuesday at 16:00 (Europe/Berlin).🎙️ Watch all episodes: https://www.youtube.com/@TranscribedPod📥 Free Biotech Starter Pack: https://transcribedpod.com📸 Instagram: @transcribedpod📧 [email protected]🎵 Jingle composed by Tembeh: https://open.spotify.com/artist/4s9JmadJjVdYQ6YxYtJgja⚠️ Disclaimer: For information and education only. Not medical, financial, investment, tax or legal advice. Guests share their own experiences and opinions, not necessarily those of Transcribed or its hosts. Nothing here is a recommendation to start, stop or change any treatment, supplement or investment; consult a qualified professional about your own situation. Mentions of companies, tokens or products are not endorsements, and Transcribed accepts no liability for decisions based on this content.00:00 Introducing Maria Marinova00:26 Chasing aging since high school01:10 From the lab to venture capital04:13 How venture capital works in biotech05:14 The gap Thalion wants to fill06:27 Decentralized science and VitaDAO09:20 How embryos reset their age10:51 Biology problem or funding problem?11:56 What each world gets wrong13:32 Fundraising for basic research14:10 If we only fund applied work15:22 Thalion's 10-year goal
Is aging a disease we can cure, and could death really become optional by 2045?José Luis Cordeiro, MIT-trained engineer, futurist and founding faculty member at Singularity University, joins Pierre Jacob and Meronn Jacob on Transcribed. We recorded this conversation in person at the Longevity Summit in Dublin.José spent his early career in energy. Then Shinya Yamanaka's 2012 Nobel Prize, which he calls the biggest discovery in history, convinced him to move into longevity. In The Death of Death, the book he co-wrote with David Wood, he argues that aging is the last undefeated disease.He explains why he sees immortal cells and organisms as proof that the problem can be solved, where the 2045 date comes from, how the $101M XPRIZE Healthspan fits in, and what "longevity escape velocity" means. These are José's own forecasts, and many biologists find them hard to believe, which is exactly where we push him.Who gets these therapies first? Why does he insist they will end up free? And why would AI compress decades of biology into a few years? We also cover his run for the European Parliament, what's overhyped in longevity, why doctors, biologists and engineers see these timelines so differently, and whether life still has meaning without death.In this conversation:◼️ Why he calls aging the last undefeated disease◼️ Where the 2045 date comes from◼️ From the energy industry to longevity◼️ Who gets rejuvenation therapies first?◼️ Three bridges to immortality◼️ Why he argues the therapies will be free◼️ The case for a European anti-aging agency◼️ How the longevity field has accelerated◼️ XPRIZE Healthspan and the AI race◼️ What's overhyped in longevity◼️ Can AI really cure all disease?◼️ Doctors vs. biologists vs. engineers◼️ Does life need death to have meaning?Transcribed Podcast: in-person interviews with scientists, founders, and industry experts shaping the future of biotech and pharma.New episodes every Tuesday at 16:00 (Europe/Berlin).🎙️ Watch all episodes: https://www.youtube.com/@TranscribedPod📥 Free Biotech Starter Pack: https://transcribedpod.com🌐 https://transcribedpod.com📸 Instagram: @transcribedpod📧 [email protected]🎵 Jingle composed by Tembeh: https://open.spotify.com/artist/4s9JmadJjVdYQ6YxYtJgja⚠️ Disclaimer: For information and education only. Not medical, financial, investment, tax or legal advice. Guests share their own experiences and opinions, not necessarily those of Transcribed or its hosts. Nothing here is a recommendation to start, stop or change any treatment, supplement or investment; consult a qualified professional about your own situation. Mentions of companies or products are not endorsements, and Transcribed accepts no liability for decisions based on this content.#TranscribedPodcast #Longevity #Aging #Immortality00:00 Introducing José Luis Cordeiro00:46 Why call aging a disease?03:46 Why 2045?06:13 From energy to longevity10:17 Who gets the therapies first?12:37 Three bridges to immortality13:57 Why he says it will be free18:44 A European anti-aging agency21:52 How fast is the field moving?24:18 XPRIZE Healthspan and the AI race26:10 What's overhyped in longevity28:34 Can AI really cure all disease?31:54 Doctors, biologists and engineers33:57 Meaning without death36:30 The first thing he'd do
Can a few drops of blood tell you how fast you're aging, and what to eat about it?Dr. Berit Hippe, nutrition scientist and co-founder of HealthBioCare in Vienna, joins Pierre Jacob and Meronn Jacob on Transcribed. We recorded this conversation in person at the Longevity Summit in Dublin.Berit's team brought one of the first biological age tests to the German-speaking market in 2014, combining telomere length, DNA methylation and inflammation markers. Last year they published MiRNA-3Age, a clock built on just three microRNAs measured from finger-prick blood.She explains why she bets on microRNAs when methylation clocks had the head start, why her company doesn't hand customers a single biological age, and why she puts the split at 70% lifestyle, 30% genetics. Then we get practical: how a home test works, what she changed in her own diet after her PhD on butyrate, and why measuring only makes sense if you actually plan to change something.We also cover 15 years of building a company without a sales team, whether biological age checks will become as routine as blood pressure, wearables vs. blood tests, AI-lab timelines for curing all disease, and what's overhyped in longevity (hint: hyperbaric chambers) vs. what's underrated (nutrition).In this conversation:◼️ From nutrition science to a biological age company◼️ What a biological clock actually measures◼️ Why microRNAs instead of methylation◼️ The MiRNA-3Age model◼️ Why biological age tests disagree◼️ How a home blood test works◼️ How much of aging is lifestyle vs. genetics◼️ 15 years without a sales team◼️ Will age tests become routine?◼️ Wearables vs. blood tests◼️ Can AI cure all disease in 10 years?◼️ The fiber she added to her own diet◼️ Overhyped vs. underrated in longevityTranscribed Podcast: in-person interviews with scientists, founders, and industry experts shaping the future of biotech and pharma.New episodes every Tuesday at 16:00 (Europe/Berlin).🎙️ Watch all episodes: https://www.youtube.com/@TranscribedPod📥 Free Biotech Starter Pack: https://transcribedpod.com🌐 https://transcribedpod.com📸 Instagram: @transcribedpod📧 [email protected]🎵 Jingle composed by Tembeh: https://open.spotify.com/artist/4s9JmadJjVdYQ6YxYtJgja⚠️ Disclaimer: For information and education only. Not medical, financial, investment, tax or legal advice. Guests share their own experiences and opinions, not necessarily those of Transcribed or its hosts. Nothing here is a recommendation to start, stop or change any treatment, supplement or investment; consult a qualified professional about your own situation. Mentions of companies or products are not endorsements, and Transcribed accepts no liability for decisions based on this content.00:00 Introducing Dr. Berit Hippe00:23 From nutrition science to a company01:23 What her biological clock measures02:22 Why microRNAs instead of methylation03:34 The MiRNA-3Age model04:37 Why biological age tests disagree06:12 How the home test works06:48 Lifestyle vs. genetics: 70/3007:18 Building the business for 15 years08:09 Will age tests become routine?08:48 Wearables vs. blood tests09:36 AI timelines for curing disease11:04 What changed in her own diet12:33 Why measure at all?12:59 Overhyped vs. underrated in longevity13:55 Her 10-year goal
Can you supplement your way to a longer life?Dr. Eric Verdin, president and CEO of the Buck Institute for Research on Aging, joins Pierre Jacob and Meronn Jacob on Transcribed. We recorded this conversation in person at the Longevity Summit in Dublin.Eric trained as an MD in endocrinology, became a virologist at the start of the HIV epidemic, and his lab went on to clone the HDACs, a family of enzymes he describes as some of the first epigenetic regulators. That road led him to aging.He explains why NAD+ levels fall as we age, why topping them up is like pouring water into a leaky sink, and why he thinks parts of the longevity field are running ahead of the science. Then we get practical: why lifestyle still beats any supplement, how the hallmarks of aging are linked to each other, and why results in lab mice may overstate what will work in humans.We also cover GLP-1 drugs as possible geroprotectors, how AI went from almost nothing to a third of the work at the Buck, the one human trial he would run with an unlimited budget, his reaction to "longevity escape velocity" timelines, and why he races old cars with no power steering.In this conversation:◼️ From a childhood microscope to HIV to aging◼️ Running an independent aging institute◼️ What people get wrong about NAD+◼️ The leaky sink: fix the leak, don't pour more water◼️ Why lifestyle still beats supplements◼️ The hallmarks of aging are connected◼️ Racing cars, fitness and community◼️ From academic discovery to patients◼️ GLP-1s: aging biology's aha moment?◼️ Four days for one protein, one hour for 5,000: AI in biology◼️ Why mice may mislead us about human aging◼️ Longevity escape velocity claims◼️ The metformin and rapamycin trials we should have run◼️ Advice for people in their 20s entering the fieldTranscribed Podcast: in-person interviews with scientists, founders, and industry experts shaping the future of biotech and pharma.New episodes every Tuesday at 16:00 (Europe/Berlin).🎙️ Watch all episodes: https://www.youtube.com/@TranscribedPod📥 Free Biotech Starter Pack: https://transcribedpod.com📸 Instagram: @transcribedpod📧 [email protected]🎵 Jingle composed by Tembeh: https://open.spotify.com/artist/4s9JmadJjVdYQ6YxYtJgja⚠️ Disclaimer: For information and education only. Not medical, financial, investment, tax or legal advice. Guests share their own experiences and opinions, not necessarily those of Transcribed or its hosts. Nothing here is a recommendation to start, stop or change any treatment, supplement or investment; consult a qualified professional about your own situation. Mentions of companies or products are not endorsements, and Transcribed accepts no liability for decisions based on this content.00:00 Introducing Dr. Eric Verdin00:29 From a childhood microscope to medicine01:37 From HIV to aging biology04:18 Running the Buck Institute05:19 What people get wrong about NAD+07:51 The leaky sink08:41 Lifestyle beats supplements10:41 The hallmarks of aging are connected13:21 Racing cars and longevity16:03 From academic discovery to patients18:11 Why the Buck's collaborative model works19:34 GLP-1s and the case for basic research21:57 AI and biotech24:03 Do mouse results translate to humans?29:21 AI CEOs and longevity escape velocity30:23 The one human trial he would run32:11 Advice for people in their 20s
Why do old cells refuse to die, and should we get rid of them?Professor Lynne Cox, a biochemist and biogerontologist who spent nearly three decades at Oxford studying where aging begins inside the cell, joins Pierre Jacob and Meronn Jacob on Transcribed. We recorded this conversation in person at a longevity conference in Dublin.Lynne explains cellular senescence from the ground up: why cells stop dividing, how these "zombie cells" pile up with age, and how their inflammatory signals (the SASP) can push neighbouring cells into senescence too. She also shares the finding that surprised her most: senescence is essential to building the placenta. In her words, "We are only mammals because of cell senescence."Then we get practical. When does it make sense to clear senescent cells? What did senolytics do in mice and in early human studies? Why might quieting senescent cells be smarter than killing them all? And why is it so hard to run a clinical trial for something that isn't officially a disease?We also cover what Werner syndrome, a rare premature aging disorder, reveals about normal aging, whether epigenetic clocks are ready to serve as trial endpoints, the part of aging Lynne thinks is badly under-researched (the extracellular matrix), and her view on AI leaders' predictions about doubling human lifespan.In this conversation:◼️ What cellular senescence is, and why cells stop dividing◼️ Zombie cells and the SASP◼️ The placenta, and why senescence made us mammals◼️ Senolytics vs. senomorphics: kill or quiet?◼️ From mice to people: COVID and pulmonary fibrosis◼️ Why "aging is natural" isn't an argument against treating it◼️ What rejuvenation really means◼️ Lessons from Werner syndrome◼️ Epigenetic clocks: useful, but only part of the story◼️ Sense of safety and cognitive resilience◼️ The overlooked extracellular matrix◼️ AI and the "double lifespan in five years" claim◼️ Advice for people in their 20s entering the fieldTranscribed Podcast: in-person interviews with scientists, founders, and industry experts shaping the future of biotech and pharma.New episodes every Tuesday at 16:00 (Europe/Berlin).🎙️ Watch all episodes: https://www.youtube.com/@TranscribedPod📥 Free Biotech Starter Pack: https://transcribedpod.com📸 Instagram: @transcribedpod📧 [email protected]🎵 Jingle composed by Tembeh: https://open.spotify.com/artist/4s9JmadJjVdYQ6YxYtJgja⚠️ Disclaimer: For information and education only. Not medical, financial, investment, tax or legal advice. Guests share their own experiences and opinions, not necessarily those of Transcribed or its hosts. Nothing here is a recommendation to start, stop or change any treatment, supplement or investment; consult a qualified professional about your own situation. Mentions of companies or products are not endorsements, and Transcribed accepts no liability for decisions based on this content.00:00 Introducing Professor Lynne Cox00:31 What is cellular senescence?02:27 Zombie cells and the SASP04:12 Why senescence made us mammals06:46 When should we clear senescent cells?08:37 Kill or quiet? Senolytics vs. senomorphics09:03 Senolytics in mice and in people11:16 Aging isn't a disease: the regulatory problem12:13 "Aging is natural" and the cancer argument13:50 Whack-a-mole medicine14:20 What rejuvenation really means15:31 What Werner syndrome teaches about normal aging17:42 Do epigenetic clocks capture what's happening?20:18 Can clocks be clinical trial endpoints?22:42 Sense of safety and cognitive resilience23:45 Hype vs. truth: reprogramming and the extracellular matrix26:53 AI and "doubling lifespan in five years"29:48 Advice for people in their 20s




