KALLEL 🐢 @Kallel_org

Important new Nature paper (Alexander Tyshkovskiy, Vadim Gladyshev lab): universal transcriptomic clocks of aging and mortality across mice, rats, macaques and humans, from more than 11,000 transcriptomes. The aging field has long wanted robust multi-species transcriptomic clocks, this seems to fit the bill. I also liked that their chromatin-modification module clock tracks DNA methylation clocks most closely which hints at a transcriptome-epigenome link. nature.com/articles/s4158…

New in Nature Aging: an open, searchable atlas of how DNA methylation changes with age across 17 human tissues: over 15,000 methylomes. Three things stood out to me: 1) Aging isn't uniform drift. The methylome shows conserved directional change, rising person-to-person variability, AND rising disorder (entropy), three analysis approaches most studies don't measure together. 2) A cell-adhesion hub, PCDHGA1, recurs across organs, while an NAD+ module stands out as one of the few modifiable nodes among otherwise fragile aging networks. Co-methylation modules were built with WGCNA (per tissue). 3) Best of all, the atlas and summary data are open: explore it yourself: bioinformatics.erc.monash.edu/apps/human-agi… Jacques M & Eynon N (2026), Meta-analysis of DNA methylation aging signatures in 17 human tissues. doi.org/10.1038/s43587…

The Biomarkers of Aging Conference at Harvard Medical School. I am speaking on Oct 6 about "The Year in Aging Clocks". What moved in the field this year and what did not? Program here: agingconsortium.org/2026-conference

A wave of epigenetic therapies is offering hope as ways to cure chronic hepatitis, which affects more than 250 million people around the world go.nature.com/4rru4pF

Oocyte aging finally gets a single-cell proteome+transcriptome map. Cao, Wu, Jiang, Hou et al. (Zhejiang, Xudong Fu lab) built a single-oocyte co-profiling pipeline (proteins + mRNA from the SAME oocyte), then compared young vs aged mouse GV and MII oocytes in Nature Communications (Sep 21, 2026). The clean finding: proteome and transcriptome disagree. Post-transcriptional regulation and protein turnover dominate what actually changes as oocytes age. Bulk RNA-seq misses most of it. Their strongest hit: dysregulated lactate metabolism. MCT4 (SLC16A3, the lactate exporter) is one of the top-ranked age-associated proteins. That pins metabolism, not just DNA damage or spindle defects, as an intrinsic driver of the aging oocyte. Why this matters for our field: our work on aging biomarkers (Moqri et al., Cell 2023 and Nat Med 2024) has argued that protein-level readouts are underused vs methylation and transcriptomic clocks. Oocytes are the extreme case, long-lived, post-mitotic single cells where post-transcriptional biology has to carry the signal. This is a proof of principle. Also worth flagging: aging oocytes look nothing like early-life oocytes at the protein level even when the transcriptome looks similar. We need protein clocks for reproductive aging, not just RNA clocks. Paper (open access): doi.org/10.1038/s41467… #aging #longevity #reproductivehealth

Some 3.5 million American men live with prostate cancer, often for many years. A new study suggests that changing the fats they eat might make a significant difference in the health and number of those years. #HarvardHealth buff.ly/QUkfXwR

How do cells die? What used to be thought were 2 ways, now it's >20 nature.com/articles/d4158…

This is cool — of the ~20,000 human proteins, 610 are the targets of approved drugs:

Nature Reviews Drug Discovery @NatRevDrugDisc

2 days ago

The evolving landscape of drug targets nature.com/articles/s4157… rdcu.be/22o1FPpNJ3Ga In the past 25 years, advances in areas such as genomics and the diversification of therapeutic modalities have expanded the drug target landscape, which now includes ~700 targets mapped here

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INSTEAD OF WATCHING AN HOUR OF NETFLIX TONIGHT. This 60-minute Cambridge lecture by Demis Hassabis will teach you more about the future of AI than most people will learn in the next 5 years. Bookmark it and give it an hour, no matter what.

Claude Opus 5.5 is here — and it may mark a new phase for AI Biology. The biggest story is not that AI got better at answering biology questions. It is that AI is starting to execute real scientific tasks. From protein design and binder engineering to drug discovery reasoning and wet-lab troubleshooting, Opus 5.5 shows a shift: From understanding biology → participating in biology. A thread 🧵👇

Claude @claudeai

a day ago

Introducing Claude Opus 5.5, the first model in our new Claude 5.5 family. It performs at the level of Claude Fable 5.1 for most tasks, and costs 40% less to run than Opus 5.

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There’s an interesting theory for why left-handedness wasn’t phased out by evolution: It may have provided a combat advantage. Left-handedness increased from ~3% in the most peaceful to ~27% in the most violent societies.

🚩Cada 90 minutos/semana de entrenamiento de fuerza hace que el ADN de tus células sea 4 años más joven. 📌El entrenamiento de fuerza es el mejor anti-envejecimiento que existe.

BREAKING STUDY: Nattokinase Breaks Down SPIKE PROTEIN, AMYLOID MICROCLOTS, BLOOD CLOTS, and SHRINKS ARTERIAL PLAQUE We assembled DECADES of evidence to uncover the powerful MULTI-TARGET EFFECTS of nattokinase: - Degrades spike protein - Breaks down harmful amyloid proteins - Dissolves abnormal amyloid microclots - Breaks down fibrin blood clots - Boosts the body’s natural clot-dissolving system - Shrinks arterial plaque - Lowers blood pressure - Reduces blood-clotting factors and platelet clumping Our new paper, “Proteolytic Targets and Clinical Benefits of Oral Nattokinase: Spike Protein and Amyloid Degradation, Fibrinolysis, and Cardiovascular Risk Reduction,” was produced through a collaboration between The Wellness Company and the McCullough Foundation. It represents one of the most comprehensive evaluations of nattokinase to date, uniquely integrating its proteolytic, cardiovascular, pharmacokinetic, amyloid, and spike-protein literature into a single paper. After oral dosing, nattokinase-related activity shows up in human blood and changes clotting and clot-breakdown markers within hours. Three independent labs have now shown that nattokinase-related enzymes can BREAK DOWN SPIKE PROTEIN in vitro—including purified nattokinase itself. At higher doses, human imaging studies reported about a 36% SHRINKAGE in carotid artery plaque—suggesting the effective range may begin around 6,000 FU/day. Randomized human trials also show modest BLOOD-PRESSURE reductions with nattokinase, with pooled decreases of about 3.5 mmHg systolic and 2.3 mmHg diastolic. And in long-term population studies, higher natto intake was associated with a 25% LOWER RISK of cardiovascular death and a 32% LOWER RISK of stroke death. Nattokinase has been well tolerated across human studies, with no notable adverse events reported across six randomized trials. Even 10,800 FU/day for 12 months was used in a large observational cohort without reported excess bleeding. This inexpensive, orally available enzyme holds immense promise for cardiovascular risk reduction in the post-COVID era. It now deserves large-scale clinical testing for cardiovascular risk reduction and other post-vaccination injury applications. We plan to launch some of these studies shortly. @twc_health @McCulloughFund @P_McCulloughMD @DrHarveyRisch @DrKellyVictory @jathorpmfm @drdrew @PeterGillooly

📚Jin Q, Wan N, Leaman R, Tian S, Wang Z, Yang Y, et al. Tutorial: guidance on the use of large language models for medical research. 2026. @NatureProtocols 🔗nature.com/articles/s4159… #InteligenciaArtificial #InvestigaciónMédica

Peripheral arterial disease (PAD) affects more than 300 million people worldwide—yet it remains under-recognised, underdiagnosed, and undertreated. A new Series aims to address this major health burden: spkl.io/60187rwOO

Is AI actually speeding up drug discovery? According to new McKinsey research, there are early signs that it is: all of these candidates were AI-enabled, with discovery time cut by ~15-80%. (Incredibly bullish)

Arterial calcification is not just the accumulation of cholesterol. It is an active biological program in which vascular cells begin behaving like bone-forming cells and they start building bone. Could loss of epigenetic information be pushing them to forget what they are?

A Stanford Medicine study found that healthy cells can transfer working mitochondria to diseased cells, revealing how bone marrow transplants could offer a potential treatment for a group of rare genetic diseases. stan.md/46EUNFC

Ferroptosis & aging: Inducing & catalyzing neurodegenerative diseases ▶️ Ferroptosis induces aging-related neurodegenerative diseases & neuronal cell death, triggering disease onset and progression. ▶️ Ferroptosis inhibitors, physical therapies, stem cell treatments, & exosome therapies show great potential for inhibiting ferroptosis in neurodegenerative disease. ovid.com/jnls/nrronline… @Mangan150 @DHPSP Aging & ferroptosis. After aging, neurons undergo iron deposition, increased lipid uptake & synthesis, dysfunction of the antioxidant system, heightened oxidative stress response, downregulation of autophagy, dysfunction of the cytomembrane repair system, & disorders in transcription and translation. All of these changes considerably lower the threshold for the occurrence of ferroptosis, ultimately leading to aging-related neurodegenerative diseases.

Resolving inflammation and preserving membrane fluidity are two powerful ways omega-3s support cardiovascular health. Chronic inflammation is one of the main drivers of atherosclerosis, which is likely why a higher omega-3 index has been associated with up to a 40% lower risk of cardiovascular events in observational studies. This clip comes from my presentation at Expo West earlier this year, where I discussed the many ways omega-3 fatty acids support cardiovascular health.