See YouTube, they have (or are in the process of uploading of all videos from the conference). Post the videos you think are specifically very good or relevant (or translatable to action). Note, there are errors in some of the links to supporting papers in the transcript summaries below - I’ll be updating these over the next day or two.
I’ve tried to identify the videos that I think would appeal to the broadest audience below.
David Dodick, Mayo Clinic, presents at the 27th Aging Research and Drug Discovery meeting: Cognitive Longevity: Unlocking the future of brain health today
David Dodick argues that cognitive decline is not an inevitable consequence of aging and that current estimates of dementia preventability (45%) are significant underestimates.
Dr. Gregory Day posits that the “longevity boon” will be a failure if cognitive lifespan does not match physical lifespan. He highlights a critical “imagination gap” in medicine, where cognitive decline is treated as an inevitable age-related decline rather than a modifiable pathological process. Currently, 1 in 3 adults over 85 suffer from Alzheimer’s Disease (AD), with women facing a 20% lifetime risk.
The core thesis is that dementia prevention is significantly more achievable than the 45% figure cited by the Lancet Commission. By expanding modifiable factors beyond the Commission’s 14—to include sleep, shingles/flu vaccinations, and hormone replacement therapy (HRT)—Day suggests 47% to 73% of cases are potentially preventable. He emphasizes “precision longevity,” noting that interventions like Metformin or Rapamycin may have divergent effects based on genotype (e.g., APOE4 or TREM2 variants).
Day advocates for a “life course approach,” where brain health is treated as a recursive process starting in childhood. He presents emerging evidence for aggressive risk reduction: hearing aid use can reduce 3-year dementia risk by 48%, and specific vaccinations (shingles/flu) show a dose-response relationship with reduced neurodegeneration. He also highlights the transition from traditional evidence-based medicine to “evidence-informed, risk-adjusted care,” allowing for the use of emerging therapies like GLP-1 agonists, hyperbaric oxygen therapy (HBOT), and mesenchymal stem cells in high-risk patients before full clinical validation is complete.
The presentation concludes by identifying proteomic organ clocks (especially brain and immune clocks) as the future of diagnostics, outperforming chronological age in predicting mortality and disease. He calls for a deeply phenotyped, integrated clinical model that moves from one-on-one medicine to scalable public health interventions.
| Claim from Video | Speaker’s Evidence | Scientific Reality (Best Available Data) | Evidence Grade | Verdict |
|---|---|---|---|---|
| Hearing aids reduce dementia risk by 48% | Cites specific 3-year risk reduction figure | ACHIEVE Trial (2023) showed this effect only in high-risk older adults. General population effect was null. | B (RCT - Subgroup) | Plausible (High Risk) |
| Shingles vaccine reduces dementia risk by 32% | Recombinant vaccine naturalistic study (200k people) | Taquet et al. (2024) confirmed Shingrix is associated with 17% more time lived diagnosis-free vs. older vaccines. | C (Large Cohort) | Strong Support |
| p-tau217 blood test is >90% predictive | FDA-cleared test metrics | ALZ-NET data confirms p-tau217 accuracy rivals PET scans for amyloid/tau. | B (Diagnostic Validation) | Strong Support |
| GLP-1s reduce dementia risk by 33-53% | Observational studies in diabetics | Meta-analyses of RCTs show promise, but primary outcomes for dementia in non-diabetics (EVOKE trials) are pending. | C (Cohort) | Plausible |
| Estrogen/HRT preserves “youthful” brain | Organ-aging proteomic study (Wisay-Coray) | The KEEPS trial showed neutral effects on cognition, though “Timing Hypothesis” suggests early initiation is key. | C (Proteomic/Cohort) | Plausible (Emerging) |
| Stem cells preserve hippocampal volume | Longeveron (Lomecel-B) Phase 2 trial | Phase 2a data showed safety and some volume preservation, but sample sizes are small (). | B (Small RCT) | Speculative |
| Metformin/Rapamycin may harm APOE4/TREM2 | Mechanistic speculation / cohort variance | Pre-clinical data suggests Rapamycin affects microglia; human evidence for APOE4-specific harm is currently low-grade. | D (Mechanistic) | Translational Gap |
The presentation relies heavily on the Wisay-Coray Organ Aging Model. This technology utilizes large-scale proteomics (SomaScan or Olink platforms) to measure thousands of proteins in plasma. By identifying protein subsets highly expressed in specific organs (e.g., GFAP or NEFL for the brain), researchers can calculate an “organ age.”
Next Step: Would you like me to perform a specific deep-dive into the upcoming EVOKE trial results (Semaglutide for Alzheimer’s) or retrieve the full paper on Plasma Proteomics Organ Aging?
I see Andrea Maier gave a talk, and it was mostly about NUS’s AKG clinical trial results!:
The results were interesting. They didn’t really see much of an effect, exact when it came to people who were “physically active”. In that population they saw quite a large percent that had 1.5 year drop in DNAm change in the AKG group compared to placebo – and at all three testing points, mid-intervention, end-of-intervention, and follow-up. The p-values, however, could have been better; and the last one (follow-up) failed to reach statistical significance; the other two were p = 0.04 and p=0.0335.
It’s possible, though, that I’m just misinterpreting it.
Omg now I have to hold off watching them so I have something to watch next time I’m bedridden (eg from retatrutide overdose) or on the commuter rail…
This transcript features Max Unfried, a computational biologist or evolutionary researcher (associated with Singapore’s NUS research foundation), presenting on the mathematical and molecular mechanisms governing maximum lifespan across mammalian species.
The presentation addresses a fundamental biological question: Why is maximum lifespan right-skewed across almost all animal classes, and what stochastic processes govern its evolution? Max argues that lifespan evolution is not a random walk (Brownian motion) but is best modeled by the Ornstein-Uhlenbeck (OU) process, which incorporates a “stabilizing force” that pulls traits toward an evolutionary optimum.
Key research findings include a quadratic scaling law: longer-lived mammalian families (like whales) exhibit significantly higher variance in lifespan than shorter-lived ones, suggesting that evolution permits greater “aging diversity” and multiple adaptive paths to longevity in long-lived species.
On a molecular level, the speaker utilizes a lipidomic dataset of 34 mammalian species to demonstrate that a subset of approximately 100 lipids (grouped into 5 Principal Components) can predict not only maximum lifespan (explaining 60% of the variance) but also developmental milestones like sexual maturity and gastrulation. By applying multivariate OU processes to this lipid data, Max identifies two distinct regimes:
Max proposes that PC6 (Phosphatidylcholines) represents the “sweet spot” for intervention—moderately constrained but with enough drift to be targetable. The talk concludes with the announcement of a large-scale evolutionary drug discovery project aimed at building a biobank of 250+ species to identify the radical tweaks evolution utilized to extend lifespan beyond 120 years.
| Claim from Video | Speaker’s Evidence | Scientific Reality (Best Available Data) | Evidence Grade | Verdict |
|---|---|---|---|---|
| Lifespan follows OU process evolution | AIC metric comparison (OU vs Brownian Motion) | Widely accepted in comparative biology; OU models better account for selective constraints on traits like body size and lifespan. | C (Computational Modeling) | Strong Support |
| Lipidome predicts Max Lifespan (60% variance) | PC analysis of 34 species (Gorbunova/Seluanov data) | Supported by Jaeger et al. (2015)and others; lipid membranes are key longevity determinants (Membrane Pacemaker Theory). | C (Observational/Omics) | Plausible |
| PC6 is the “Sweet Spot” for intervention | OU parameter modeling (α vs σ) | Theoretical. No current RCT or human data supports PC6 modulation specifically for maximum lifespan extension. | D (In silico/Mechanistic) | Speculative |
| Cardiolipins are highly stabilizing/conserved | Lipidomic evolutionary drift analysis | Well-supported; cardiolipin is essential for mitochondrial cristae and energy production. Mutations are usually lethal/severe (e.g., Barth Syndrome). | D (Mechanistic) | Strong Support |
| Lifespan/Development link is a “Program” | Correlation with sexual maturity/gastrulation | Consistent with “Pleiotropy” and “Developmental Theory of Aging.” High correlation between maturity rate and lifespan is a known biological rule. | C (Cohort/Species) | Strong Support |
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In the context of this talk, the OU process is used to distinguish between neutral drift and adaptive selection.
This transcript features Jaron Rabinovici, a gynecologist and longevity specialist at the Sheba Medical Center in Israel, discussing the transition of Hormone Replacement Therapy (HRT) from a symptom-management tool to a robust geroprotective intervention. The speaker argues that estrogen is a master regulator that influences all 12 hallmarks of aging and that its decline during menopause triggers systemic decay.
The presentation redefines menopause not as a natural transition to be endured, but as a state of hormonal deficiency that accelerates biological aging. The speaker posits that Estradiol (E2) is a true geroprotector because it extends healthspan, delays age-related diseases, and modulates all 12 hallmarks of aging.
A central pillar of the talk is the “Timing Hypothesis”: HRT initiated during the perimenopausal window (ages 50–59) provides significant cardiovascular and neuroprotective benefits, whereas late initiation (post-age 60) may be ineffective or even harmful due to established atherosclerotic plaques. The speaker aggressively critiques the Women’s Health Initiative (WHI) study, labeling it a “killer of women” for misrepresenting HRT risks by focusing on an older, unhealthy demographic.
The analysis concludes that transdermal estradiol combined with micronized progesterone is the optimal longevity protocol. This regimen has been shown to reduce all-cause mortality by 30% over five years. The speaker advocates for universal screening and “precision” HRT based on blood level monitoring to maximize the “hormonally balanced menopause.”
| Claim from Video | Speaker’s Evidence | Scientific Reality (Best Available Data) | Evidence Grade | Verdict |
|---|---|---|---|---|
| HRT reduces mortality by 30% | 5-year study on transdermal HRT | Supported by Danish Osteoporosis Prevention Study (DOPS), showing long-term mortality benefits when started early. | B (RCT) | Strong Support |
| Estrogen affects all 12 Hallmarks | Mechanistic list of receptor interactions | Highly plausible mechanistically. Reviews in Nature Aging confirm E2’s impact on telomeres, proteostasis, and inflammation. | D (Mechanistic) | Plausible/Strong |
| HRT reduces Dementia risk | Cites “Timing Hypothesis” | ELITE-Cog trial confirms no harm, but primary prevention of dementia is still debated in literature; timing is critical. | B (RCT) | Plausible (Early) |
| Transdermal E2 has zero clot risk | Comparison to oral estrogen | Large observational studies show transdermal E2 does not increase VTE risk, unlike oral E2 which has first-pass liver effects. | C (Cohort) | Strong Support |
| 17-α Estradiol extends life in males | Cites rodent studies | Interventions Testing Program (ITP) data confirms 17-α-E2 extends lifespan in male mice by ~19%, but human safety data is absent. | D (Pre-clinical) | Translational Gap |
The speaker emphasizes that estrogen’s geroprotective power lies in its genomic and non-genomic signaling.
By stabilizing the Extracellular Matrix (ECM) through fibroblast stimulation, HRT not only improves skin appearance but maintains the structural integrity of blood vessels and joints, addressing the “Compromised ECM” hallmark.
Sophia Liu, Ragon Institute of MGB, MIT, and Harvard, presents at the 25th Aging Research and Drug Discovery meeting: Architectures of immunological aging and regeneration
This transcript features Dr. Sophia Liu, a researcher who started her lab in 2023, presenting on the intersection of spatial transcriptomics, long-read sequencing, and immunological aging. She argues that the decline of the immune system is a better predictor of cancer and infectious disease than the mere accumulation of somatic mutations.
Dr. Liu’s research focuses on the Thymus, the primary lymphoid organ responsible for T-cell production. Unlike other organs, the thymus undergoes involution (shrinking) starting as early as age 16 in humans, with a half-life of 16 years. This early-onset aging leads to a drastic reduction in T-cell diversity and an “immune escape threshold” where pathogens and cancers evade detection.
The technical core of the talk introduces Slide-seq combined with long-read sequencing. Dr. Liu identifies a major technological gap: standard short-read sequencing (Illumina) misses novel isoforms and splice variants that are functionally critical for aging. By applying these tools to a 20-point longitudinal mouse study, her team discovered that:
Crucially, Dr. Liu demonstrates that simply increasing thymic size (a common startup goal) is insufficient if the internal organization (Cortex vs. Medulla) and functional diversity are not restored. Her work suggests that macrophage restoration can regenerate thymic size and that targeting specific novel proteins identified through spatial data offers a new frontier for immunotherapeutics.
| Claim from Video | Speaker’s Evidence | Scientific Reality (Best Available Data) | Evidence Grade | Verdict |
|---|---|---|---|---|
| Immune decline drives cancer more than mutations | Cites mathematical modeling paper | Palmer et al. (2018) supports that declining T-cell surveillance explains the exponential rise in cancer risk better than mutation accumulation. | C (Modeling) | Plausible |
| Thymic involution begins at age 16 | Longitudinal human/mouse size data | Well-established in classic immunology; the thymus starts replacing functional tissue with fat (adipose) post-puberty. | B (Clinical/Obs) | Strong Support |
| Standard RNA-seq misses novel aging proteins | Discovery of novel isoforms in spatial data | Supported by recent long-read advances (e.g., Oxford Nanopore/PacBio); 30-40% of genes have unannotated isoforms. | B (Technical) | Strong Support |
| Notch signaling loss causes B-cell aggregates | Receptor-ligand interaction maps (Slide-seq) | Mechanistically sound; Notch is the “master switch” for T-cell fate. Recent studies confirm B-cell accumulation in aged thymi. | D (Mechanistic) | Strong Support |
| Endothelial cells drive the “aging clock” | Aging clock analysis of 20 time points | Consistent with “inflammaging” and vascular aging theories, though causal proof for thymic involution is still emerging. | C (Omics) | Plausible |
Dr. Liu emphasizes that Slide-seq provides a bridge between single-cell data and histology.
The Mechanism of CDR3 Sequencing: The T-cell receptor (TCR) is formed by the random recombination of Variable (V), Diversity (D), and Joining (J) genes. The CDR3 region is the specific sequence that contacts the antigen. Short-read sequencing often cuts this region off.
The Notch/B-cell Switch: In the youthful thymus, the ligand Dll4 binds to Notch1 on incoming progenitor cells. This interaction inhibits the B-cell program and activates the T-cell program. As the thymus ages, the loss of this spatial interaction (visualized by Liu’s receptor-ligand maps) leads to the accumulation of B-cells in what should be T-cell-only zones.
This transcript features Lars, a representative from the McKinsey Health Institute (MHI), presenting at a major longevity conference. He provides a macro-level, “size of the tent” analysis of the longevity field, aimed at accelerating the transition from a niche scientific community to a mainstream global industry.
Lars presents a critical view of the current state of longevity: while lifespan has increased since 1960, every year of life extension is currently bought at the cost of six months of poor health, a “terrible deal” for humanity. McKinsey identifies a massive gap between scientific potential and institutional investment. Currently, the total global burden of age-related disease is 600 million DALYs (Disability-Adjusted Life Years)—one-third of the global total and 2.5 times larger than oncology.
Despite a 400% increase in biotech investment over the last decade, the field remains nascent, with investment levels 200 times smaller than oncology. Lars identifies seven key “unlocks” required to scale the industry, including standardized terminology, global data sharing, and consensus on surrogate endpoints for clinical trials. He introduces “Health Span Science” as a more palatable public health term and emphasizes that the field’s growth is currently throttled by a “talent shortage” and the lack of established regulatory pathways.
| Claim from Video | Speaker’s Evidence | Scientific Reality (Best Available Data) | Evidence Grade | Verdict |
|---|---|---|---|---|
| Aging is 1/3 of global disease burden | McKinsey Health Institute analysis | Global Burden of Disease (GBD) studies generally support that NCDs (Non-Communicable Diseases), mostly age-related, dominate global DALYs. | B (Statistical Analysis) | Strong Support |
| Longevity investment is 1/200th of Oncology | Internal McKinsey benchmarking | Generally accurate; while “Longevity” as a buzzword is high, true Geroscience-focused R&D is a fraction of the $200B+ annual oncology market. | C (Industry Analysis) | Plausible |
| 60% of consumers are interested in longevity | Global consumer survey data | Consistent with recent market research showing a $1.8T wellness market with a focus on longevity. | C (Survey) | Strong Support |
| Every year of life adds 6 months of sickness | 1960–present healthspan trends | WHO data confirms that “Healthy Life Expectancy” (HALE) has increased slower than total Life Expectancy. | B (Global Health Data) | Strong Support |
Lars focuses on DALYs (Disability-Adjusted Life Years) as the primary metric for defining the field’s value.
DALY=YLL(Years of Life Lost)+YLD(Years Lived with Disability)
James Kirkland, M.D., Ph.D, presents at the 25th Aging Research and Drug Discovery meeting: Clinical Trials and Future Directions of Gerotherapeutics
This transcript features a prominent geroscience leader discussing the operational and clinical landscape of the Translational Geroscience Network (TGN). The speaker shifts the focus from theoretical lifespan extension to the practical, regulatory-friendly world of treating and reversing specific diseases driven by fundamental aging processes.
The presentation outlines a pragmatic framework for moving geroscience into the clinic. The speaker argues that primary prevention trials for lifespan are currently impossible due to their duration and cost. Instead, the TGN focuses on repurposing drugs and interventions to treat acute and chronic conditions where no good treatments exist—such as idiopathic pulmonary fibrosis (IPF), preeclampsia, and childhood cancer survivorship.
A major theme is the use of senolytics to clear senescent cells, which the speaker identifies as “root cause” contributors to morbidity across the lifespan, even starting before conception. The TGN utilizes a “parallel trial” approach, running 87 clinical trials simultaneously across the US, Europe, and Canada. These trials prioritize academic exploratory outcomesand surrogate biomarkers over traditional drug registration.
The talk also highlights a shift toward innovative trial designs (Adaptive trials, N-of-1 trials) and novel biomarkers(mitochondrial DNA in urine, viscoelastic properties of cells). A groundbreaking frontier mentioned is organ rehabilitation, where senolytics are used to “refresh” kidneys and hearts from older donors, potentially solving the global organ shortage.
| Claim from Video | Speaker’s Evidence | Scientific Reality (Best Available Data) | Evidence Grade (A-E) | Verdict |
|---|---|---|---|---|
| Senolytics improve physical function in IPF | 2019 Phase 1 open-label trial | Justice et al. (2019) showed improved 6-minute walk distance, but the study was small (N=14) and lacked a control group. | C (Pilot RCT) | Plausible (Early) |
| Aging begins before conception | Maternal PTSD affects offspring aging | Pre-clinical and cohort data suggests epigenetic “weathering” can be transmitted, though direct “aging” is hard to define in utero. | C (Cohort) | Plausible |
| Senolytics rehabilitate donor organs | Cold-perfusion experiments by Stefan Tulius | Pre-clinical work shows clearing senescent cells in donor kidneys reduces post-transplant inflammation. | D (Pre-clinical) | Strong Support (Experimental) |
| Alpha-Klotho is a geroprotective factor | Restored in 20/20 subjects in senolytic trial | Extensive literature supports Klotho as a longevity protein that declines with age and kidney disease. | B (Human/Animal) | Strong Support |
| Electrical impulses kill senescent cells | Interim analysis of Phase 2a trial | Highly novel and largely unpublished. Relies on the distinct physical/electrical properties of senescent vs. healthy cells. | E (Anecdote/Interim) | Speculative |
The speaker introduces a shift from chemical to physical properties of senescent cells. Cellular Senescence is characterized by the SASP (Senescence-Associated Secretory Phenotype), which poisons neighboring cells.
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Evelyne Yehudit Bischof, Sheba Longevity Center, presents at the 25th Aging Research and Drug Discovery meeting: Healthpan Protocol in the Clinical Practice
This transcript features Dr. Evelyne Bischof, a leading physician in healthy longevity medicine, discussing the clinical application of longevity diagnostics and interventions across diverse patient populations. She advocates for a “reciprocal pathway” where longevity medicine works in tandem with traditional curative medicine (oncology, cardiology, internal medicine) to optimize healthspan for everyone, not just the “healthy.”
Dr. Bischof’s presentation focuses on the integration of Healthy Longevity Medicine into the hospital setting (specifically Sheba Medical Center). She defines the “longevity population” as essentially everyone—excluding only the terminally ill or severely cognitively impaired—with a focus on measuring and achieving **“Healthspan Optimization”**for specific individuals over time.
Key findings from the SHARP (Sheba Healthy Longevity Prospective) study include:
| Claim from Video | Speaker’s Evidence | Scientific Reality (Best Available Data) | Evidence Grade | Verdict |
|---|---|---|---|---|
| Biological age predicts TAVI outcomes | Retrospective study of 380 patients | Supported by studies showing that “frailty” and “biological age” outperform age in predicting surgical recovery. | C (Retrospective) | Strong Support |
| Sarcopenia is predominant in cancer survivors | Baseline DEXA data from SHARP cohort | Well-documented. Chemotherapy-induced sarcopenia is a major cause of disability in survivors. | C (Observational) | Strong Support |
| Bio-clocks (ECG/Echo/Blood) have low overlap | Direct comparison of 3 clocks in SHARP | Emerging research suggests “organ-specific” aging means one person might have an “old heart” but “young blood.” | C (Pilot Data) | Plausible |
| Subjective feeling > Testosterone for andropause | Correlation matrix of QAM vs. serum levels | Controversial. While subjective symptoms are critical, serum levels remain the clinical gold standard for diagnosis. | C (Observational) | Plausible/Experimental |
| Digital brain training reduces reaction time | Longitudinal training data (400+ users) | Systematic reviews show brain training improves specific tasks (reaction time), but “far-transfer” to general life is debated. | B (Prospective) | Strong Support (for specific task) |
Dr. Bischof highlights that in the TAVI (Transcatheter Aortic Valve Implantation) study, the Biological Age Delta was the key predictor of clinical outcomes.
Nir Barzilai, Albert Einstein College of Medicine, presents at the 25th Aging Research and Drug Discovery meeting: From Pathways to Patients: Translating Geroscience into Gerotherapeutics
This transcript features Dr. Nir Barzilai, a prominent figure in geroscience, discussing the repurposing of FDA-approved drugs to target the hallmarks of aging. He argues for a shift from treating individual diseases to optimizing healthspan and lifespan using “gerotherapeutics.”
Barzilai posits that repurposing existing drugs is the most practical path forward because their safety profiles and long-term data are already established. He proposes a 12-point scoring system (6 preclinical, 6 clinical) to identify true gerotherapeutics.
The following drugs were highlighted for their ability to target multiple hallmarks of aging and reduce all-cause mortality in human data:
| Drug Class | Scoring | Key Geroscience Insight |
|---|---|---|
| SGLT2 Inhibitors | 12 / 12 | The only drugs to receive a “perfect” score. They reduce all-cause mortality by ~31% and are considered powerful “calorie mimetics.” |
| Metformin | 11 / 12 | High pedigree for targeting metabolism and immunity. Data suggests it reduces “Long COVID” by 60% and lowers hospitalization rates. |
| Bisphosphonates | 11 / 12 | Originally for osteoporosis, these show a staggering ~59% reduction in ICU mortality. They may act by modulating stem cell populations in bone marrow. |
| GLP-1 Agonists | High | High-impact calorie mimetics; human data shows up to a 43% decrease in overall mortality in certain cohorts. |
The debate persists regarding “preventative” vs. “therapeutic” timing. While the Harvard colleague in the transcript suggested starting before age 50, Barzilai maintains that starting trials in younger populations is currently financially and practically unfeasible.