David Meyer

Aging clocks delineate neuron types vulnerable or resilient to neurodegeneration and identify neuroprotective interventions - Nature Aging Gallrein et al. pair functional assays with clocks to compare chronological versus biological age of single neuron types in C. elegans, to probe their vulnerability or resilience to neurodegeneration,...

🧠⏰our latest paper is out now: how each neuron ages differently allowed us to define in silico screens for new therapeutic molecules that could prevent neurodegeneration @cecad.bsky.social @unicologne.bsky.social @uniklinikkoeln.bsky.social @meyerdh.bsky.social www.nature.com/articles/s43...

🚨Publication Alert🚨
New work from our #CRC1678 members @bjornschumacher.bsky.social and @meyerdh.bsky.social reveals why some neurons age faster. Using neuron‑specific aging clocks, they identified vulnerable neurons and highlight syringic acid and vanoxerine as promising neuroprotective hits.🧬

Aging clocks based on accumulating stochastic variation - Nature Aging Meyer and Schumacher use simulations to show that accumulation of stochastic variation is sufficient to build clocks that can measure both chronological and biological age, sensitive to changes induce...

And the stochastic clock: www.nature.com/articles/s43... (n/n)

BiT age: A transcriptome‐based aging clock near the theoretical limit of accuracy Using Caenorhabditis elegans RNA seq and lifespan datasets we developed a binarized transcriptomic aging (BiT age) clock with a precision close to the theoretical limit of accuracy that can also be a...

Links to BitAge: onlinelibrary.wiley.com/doi/full/10.... (10/n)

Big thanks to @bjornschumacher.bsky.social for his guidance and all co-authors. This was a great team effort. Paper: www.nature.com/articles/s43...
(9/n)
#aging

Amazingly, these in silico predictions held up in vivo: protective hits delayed degeneration (syringic acid, vanoxerine), while predicted pro-aging/toxic compounds caused neurite deterioration and accelerated degeneration (resveratrol, Bay K8644). (8/n)

We used this discovery to adapt an in silico drug screen and mapped worm neuron-aging signatures onto human perturbation profiles (CMAP) to identify novel compounds affecting neurodegeneration. (7/n)

These trajectories aren't worm specific. Despite millions of years of evolution, the same transcriptomic signature we see in C. elegans aligns with human brain aging, and it flips sign under geroprotective interventions. That argues for conserved neuronal aging programs. (6/n)

Fast-aging neurons are enriched for neuropeptide and protein biosynthesis pathways. These neuron types show earlier structural decline and loss of neuron-specific function. And indeed, pharmacological inhibition of translation prevents degeneration of fast-aging neurons. (5/n)

Critically: fast-aging types show earlier structural degeneration and loss of function in vivo. Remarkably, we can already predict which neurons will degenerate earlier at a late developmental stage. Vulnerability is detectable as an early transcriptomic aging state. (4/n)

We applied two independent clocks (links below): our BitAge (binarized transcriptomic aging clock), and our Stochastic clock (noise-based and data-type agnostic). Both independently rank neuron types as fast- vs slow-aging from their transcriptomes. (3/n)

Selective vulnerability is central to #Alzheimer’s and #Parkinson’s disease, but which neurons age faster is rarely quantified. Transcriptomic clocks let us estimate biological age directly from neuron-type gene-expression states. (2/n)

Why do some neuron types degenerate early while others stay intact?

We used transcriptomic aging clocks for single-neuron-types in C. elegans and found neuron-specific biological age predicts vulnerability.
🧪

www.nature.com/articles/s43...

#Neurodegeneration 🧵👇 (1/n)

A sex-adjusted 7-biomarker clinical aging clock for translational preventative medicine - Scientific Reports Scientific Reports - A sex-adjusted 7-biomarker clinical aging clock for translational preventative medicine

A sex-adjusted 7-biomarker clinical aging clock for translational preventative medicine
www.nature.com/articles/s41...

Happy to share that this is now out in Microbial Ecology 🥳 Huge thanks to the whole team, especially @sultanova.bsky.social 🙌

link.springer.com/article/10.1...

@leibnizfli.bsky.social @uniofeastanglia.bsky.social

1/6 In a new preprint we ask a question:

Why do males and females so often age and die at different rates?

We argue that sex-specific mutation accumulation may be the most parsimonious evolutionary explanation for sex-biased ageing:

ecoevorxiv.org/repository/v...

Thanks to the whole team (not on Bluesky)!

The clock predicts an accelerated age up to 5 years before a chronic disease is diagnosed.
And it stays robust during acute infections, but correlates with CRP.

We built a clinical #aging clock using only 6 routine blood biomarkers + sex on a Southeast Asian dataset that validates well in NHANES and UK Biobank.

Happy to share our recent publication, which grew out of a consulting job I did last year:
www.nature.com/articles/s41...
🧵

New study by our #CRC1678 members @bjornschumacher.bsky.social, @meyerdh.bsky.social and Walter Sandt showing that C. elegans dauer stage decelerates aging and even reverses biological age upon exit, revealing natural gene patterns of rejuvenation. Congratulations! 🎉
#AgingResearch #Longevity

Celebrating excellence: meet the 2025 SIB Bioinformatics Awards laureates Two early career bioinformaticians have been recognized for their mathematical and AI models, along with a collaborative resource for single-cell data analyses. The three 2025 SIB Bioinformatics Award...

🎥 Meet the 2025 SIB Bioinformatics Awards laureates:
⭐ David Meyer @meyerdh.bsky.social, PhD Paper Award
⭐ Michael Skinnider @skinnider.bsky.social Early Career Award
⭐ scverse @scverse.bsky.social, Innovative Resource Award, accepted by Ilan Gold
Watch their award ceremony talks👇& congrats to all!

Age Deceleration and Reversal Gene Patterns in Dauer Diapause The dauer diapause is a naturally occurring extraordinarily long-lived alternative C. elegans larval stage that, upon dauer exit, lives a normal adult life with full reproductive capacity. Here, we d...

🚀 🚀 🚀 Our latest paper is out now: Age Deceleration and Reversal Gene Patterns in Dauer Diapause. We can learn from nature how aging of a whole organism with completely differentiated tissues can be slowed and how that organism can be completely rejuvenated.
onlinelibrary.wiley.com/doi/10.1111/...

🚨🚨Job! 🚨🚨Permanent (75% time) job! We are a pretty awesome research group & seek a manager who deals with everything: personnel tasks, organizing retreats, preparing code for teaching / data structures for research... Fluency in German & English essential. stellenboerse.uni-mainz.de#/jgu/job/51527

Super grateful that our scETM work (from my summer internship with Dr. Yue Li, in collab. with Huiyu Cai and @tangjian.bsky.social) was recognized with an honourable mention at SIB PhD Paper Award competition. Many thanks to the jury and congrats to @meyerdh.bsky.social and Can Chen! #bc2basel

A fantastic few days of ageing talks, great people, and excellent food!

Massive thanks to (Hanna!) @kokkonut.bsky.social, Margaux Bieuville, Victor Ronget, and the fantastic people at The Gutenberg Workshops in the Life Sciences

Ribonucleotide incorporation into mitochondrial DNA drives inflammation - Nature Imbalanced nucleotide metabolism leads to age- and mtDNA-dependent inflammatory responses and senescence-associated secretory phenotype in senescence.

Ribonucleotide incorporation into mitochondrial DNA drives inflammation

www.nature.com/articles/s41...

Congratulations to the Langer lab @mpiage.bsky.social, Amir, and the rest of the team!

This review of our @crc1678.bsky.social member @bjornschumacher.bsky.social and @meyerdh.bsky.social is greatly summarizing fundamentals of the molecular biology of aging. What causes aging? Read the answer!

Aging by the clock and yet without a program - Nature Aging Meyer and colleagues refute the idea that, as aging can be tracked precisely by clocks, it must be driven by a biological program. They propose that imperfect maintenance and repair processes resultin...

🔥🔥🔥Out now: our Perspectives article in @nataging.nature.com outlining how aging is driven by molecular damage leading to increasing molecular noise whose quantification could track aging with the precision of a clock @meyerdh.bsky.social @alexeimaklakov.bsky.social
www.nature.com/articles/s43...

We argue that selection shadow - gradual decline in the force of selection after the onset of reproduction - is sufficient/parsimonious to explain why damage accumulates with age. 'Aging clocks' measure damage accumulation, they neither require nor support any kind of 'program'-based explanation.