Toggle light / dark theme

There are two ways of dealing with this public health problem. One is to devise a comprehensive strategy to combat social inequality that will prevent disease before it happens. Another way is to develop a pill that treats the wear and tear of stress and toxins on the body.

Believe it or not, there are experiments on such pills underway.

Candidates include dasatinib, quercetin, metformin, rapamycin and fisetin among many others. These drugs may slow or even reverse aging in anyone, but they hold the greatest promise for improving America’s health because they disproportionately help the disadvantaged. This population bears the greatest burden of disease by far, so even small health gains in this population can go a long way.


Americans would much prefer a pill or a vaccine over a contentious policy battle.

Coronary Artery Disease (CAD) is the most common cardiovascular disease worldwide, threatening human health, quality of life and longevity. Aging is a dominant risk factor for CAD. This study aims to investigate the potential mechanisms of aging-related genes and CAD, and to make molecular drug predictions that will contribute to the diagnosis and treatment.

We downloaded the gene expression profile of circulating leukocytes in CAD patients (GSE12288) from Gene Expression Omnibus database, obtained differentially expressed aging genes through “limma” package and GenaCards database, and tested their biological functions. Further screening of aging related characteristic genes (ARCGs) using least absolute shrinkage and selection operator and random forest, generating nomogram charts and ROC curves for evaluating diagnostic efficacy. Immune cells were estimated by ssGSEA, and then combine ARCGs with immune cells and clinical indicators based on Pearson correlation analysis. Unsupervised cluster analysis was used to construct molecular clusters based on ARCGs and to assess functional characteristics between clusters. The DSigDB database was employed to explore the potential targeted drugs of ARCGs, and the molecular docking was carried out through Autodock Vina.

Ora Biomedical, in partnership with Rapamycin Longevity Lab, announces the successful funding of the first subproject under its ambitious initiative to conduct a rapid lifespan analysis of 601 mTOR inhibitors in roundworms.

With $50,000 secured, Ora Biomedical will now commence the next phase of the first subproject. This will be a high-throughput screening of 301 mTOR inhibitors using its cutting-edge WormBot-AI technology. This milestone marks an important step toward identifying next-generation compounds that could be more effective than rapamycin, which is currently seen as the golden standard because of its good longevity effects in multiple species.

Mitchell Lee, CEO of Ora Biomedical, emphasized the importance of this research by stating: “The potential of targeting aging to broadly improve healthy lifespan is clear from decades of studies with compounds like rapamycin. However, even for well-validated molecular targets like mTOR, we still don’t know the best interventions. We at Ora Biomedical are proud to partner with Rapamycin Longevity Lab to advance our understanding around targeting mTOR and related kinases for maximizing healthy lifespan. None of this work is possible without support from visionary donors and organizations like the Lifespan Research Institute, the nonprofit behind Lifespan.io, with whom we have partnered to create pathways for donations to advance longevity science. To all those involved, thank you again, and we are excited to get to work!”

Anjie Zhen & team show rapamycin reduces HIV-mediated chronic inflammation and T cell exhaustion, delaying viral rebound and reducing viral reservoir in mice.


2UCLA AIDS Institute and the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, David Geffen School of Medicine at UCLA, Los Angeles, California, USA.

Join us this episode as we explore how a cutting-edge, high-throughput screening platform can identify lifespan-extending compounds in diverse model organisms, with Dr Kevin Perez, co-founder of Epiterna and Junior Group Leader at Charité Universitätsmedizin Berlin, and host Prof Brian Kennedy, Director of the Centre for Healthy Longevity at #NUSMedicine.

Register for upcoming #HealthyLongevity #webinar sessions at https://nus-sg.zoom.us/webinar/register/2117367621680/WN_g5RF29EWQf65KDFfpVLjFA

Disclaimer: The opinions and advice expressed in this webinar are those of the speakers and do not represent the views and opinions of the organizers and National University of Singapore or any of its subsidiaries or affiliates. The information provided in this webinar is for general information purposes only as part of a general discussion on public health. The information is not intended to be a substitute for professional medical advice, diagnoses or treatment; and cannot be relied on in place of consultation with your licensed healthcare provider. All Rights Reserved.

All of the proceedings of this webinar, including the presentation of scientific papers, are intended for limited publication only, and all property rights in the material presented, including common-law copyright, are expressly reserved to the speaker or NUS. No statement or presentation made is to be regarded as dedicated to the public domain.

Any sound reproduction, transcript or other use of the material presented at this course without the permission of the speaker or NUS is prohibited to the full extent of common-law copyright in such material.

For decades, scientists assumed that neural stem cells (NSCs) only occur in the brain and spinal cord. A new international study, led by Hans Schöler of the Max Planck Institute for Molecular Biomedicine in Münster, has now refuted this assumption and discovered a new type of neural stem cell outside the central nervous system (CNS) that opens up enormous possibilities for the development of therapies for neurological diseases. The study is published in the journal Nature Cell Biology.

In 2014, an article titled “Stimulus-triggered fate conversion of into pluripotency” was published in Nature. This publication initially caused quite a stir because it opened up a simple way to obtain . The induction of pluripotent stem cells without the need for viral vectors, as Shinya Yamanaka had done and for which he received the Nobel Prize, would have been too good to be true.

Although the laboratory of Schöler at the Max Planck Institute for Molecular Biomedicine, like many others, tried to repeat the experiment that described the “stimulus-triggered acquisition of pluripotency” (STAP) based on treating somatic cells with low pH. However, the generation of pluripotent cells failed regardless of the culture conditions and tissues used—and the corresponding paper was eventually retracted several months after publication.

Previous studies have suggested that microRNAs are critical for brain development, but their specific role in differentiation—the process of stem cells maturing into specialized cells—remained unclear.

“When neurons develop, they need to at some point decide what subtype they will become, but we really didn’t know much about the blueprint that instructs this differentiation,” says the author. “There was a lot of evidence suggesting that microRNAs might have a very important role here, but because the tools were not good enough, we couldn’t really nail down that question until now.”

The team focused on Purkinje cells, which comprise less than 1% of cells in the cerebellum. Purkinje cells integrate information from different parts of the brain and body, enabling us to make smooth, controlled movements. They are some of the largest brain cells and have a tree-like appearance—a single axon “trunk” that supports a system of “branches” known as the dendritic arbor. Purkinje cells are also surrounded by structures called climbing fibers that wrap around the cells’ dendrites and deliver information from other parts of the brain.

To attain their large size and elaborate arbor, Purkinje cell development involves prolonged periods of growth and branching. In mice, the long process of Purkinje cell development is complete around four weeks after birth.

To investigate how microRNAs are involved in neuron differentiation, the team developed new tools that temporarily turn off microRNA function during specific developmental windows. They found that microRNAs are critical during two phases in Purkinje cell development: inhibiting microRNAs during the first week after birth resulted in Purkinje cells with less complex dendritic arbors and smaller cerebellums. In contrast, inhibiting microRNAs during the third week after birth prevented the Purkinje cells from forming synaptic connections with climbing fibers. These findings shed light on how microRNAs control the precise timing of different aspects of Purkinje cell development that were previously thought to happen concurrently.

The team also developed a mouse model to identify which genes the microRNA molecules were targeting. Using this system, they identified two microRNAs critical for Purkinje cell development (miR-206 and miR-133) and four gene targets (Shank3, Prag1, Vash1, and En2). When they compared the Purkinje cell microRNA-target map to a map for pyramidal neurons—a functionally different but similar-looking brain cell—they showed that the two cell types follow very different microRNA blueprints during development.


How will AI shape our understanding of our creativity and ourselves?

In February, artist and technologist K Allado-McDowell delivered a fascinating Long Now Talk that explored the dimensions of Neural Media — their term for an emerging set of creative forms that use artificial neural networks inspired by the connective design of the human brain.

Their Long Now Talk is a journey through the strange valleys and outcroppings of this age of neural media, telling a story involving statistical distributions, anti-aging influencers at war with death itself, and vast quantities of “AI Slop,” the low-quality, faintly surreal output of cheap, rapidly proliferating image models.

Yet even in this morass of slop Allado-McDowell sees reason for optimism. Referring to the title of their 2020 book Pharmako-AI, which was co-written with GPT-3, Allado-McDowell notes that the Greek word pharmakon could mean both drug and cure. What may seem poisonous or dangerous in this new paradigm of neural media could also unlock for us new and deeper ways of understanding ourselves, our planet, and all of the intelligent networks that live within it.

This talk was presented February 25, 02025 at the Cowell Theatre in San Francisco. The event livestream is here: https://www.youtube.com/live/AsCGRjl3zac?si=KBfIfkqatLwdMr8M

Episode notes: https://longnow.org/ideas/neural-media/

Join us on Patreon! https://www.patreon.com/MichaelLustgartenPhD

Discount Links/Affiliates:
Blood testing (where I get the majority of my labs): https://www.ultalabtests.com/partners/michaellustgarten.

At-Home Metabolomics: https://www.iollo.com?ref=michael-lustgarten.
Use Code: CONQUERAGING At Checkout.

Clearly Filtered Water Filter: https://get.aspr.app/SHoPY

Epigenetic, Telomere Testing: https://trudiagnostic.com/?irclickid=U-s3Ii2r7xyIU-LSYLyQdQ6…M0&irgwc=1
Use Code: CONQUERAGING

NAD+ Quantification: https://www.jinfiniti.com/intracellular-nad-test/