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Top Voted Preprints
Q4 2023
ISSN 2817-8831
Candidate Preprints
Q4 2023
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Nature of epigenetic aging from a single-cell perspective

Nature of epigenetic aging from a single-cell perspective

Andrei E. Tarkhov, Thomas Lindstrom-Vautrin, Sirui Zhang, Kejun Ying, Mahdi Moqri, Bohan Zhang, Alexander Tyshkovskiy, Orr Levy, Vadim N. Gladyshev

Epigenetic aging involves both co-regulated and stochastic DNA methylation changes, comparing tissue and single-cell data with development stages and RNA analysis. A new algorithm identifies CpG clusters, offering insights into aging interventions.

Q4 2023
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Circulating senescent myeloid cells drive blood brain barrier breakdown and neurodegeneration

Circulating senescent myeloid cells drive blood brain barrier breakdown and neurodegeneration

C. Matthias Wilk, Flurin Cathomas, Orsolya Török, Jessica Le Berichel, Matthew D. Park, George R. Heaton, Pauline Hamon, Leanna Troncoso, Brooks P. Scull, Diana Dangoor, Aymeric Silvin, Ryan Fleischmann, Meriem Belabed, Howard Lin, Elias Merad Taouli, Steffen Boettcher, Markus G. Manz, Julia K. Kofler, Zhenyu Yue, Sergio A. Lira, Florent Ginhoux, John F. Crary, Kenneth L. McClain, Jennifer L. Picarsic, Scott J. Russo, Carl E. Allen, Miriam Merad

Neurodegenerative diseases linked to Langerhans cell histiocytosis (LCH-ND) are caused by mutated myeloid cells compromising the blood-brain barrier, leading to inflammation and neuronal damage in the brain. Targeting MAPK activity and cell senescence reduces these effects and improves neurological outcomes.

Q4 2023
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The germline regulates longevity and somatic repair in a sex-specific manner

The germline regulates longevity and somatic repair in a sex-specific manner

Eitan Moses, Tehila Atlan, Xue Sun, Roman Franek, Atif Siddiqui, Georgi K. Marinov, Sagiv Shifman, David M. Zucker, Adi Oron-Gottesman, William J. Greenleaf, Ehud Cohen, Oren Ram, Itamar Harel

Germline manipulation in turquoise killifish shows sex-specific aging effects: depletion boosts female repair and male lifespan, indicating metabolic rejuvenation and pro-longevity genes, challenging classical evolutionary tradeoffs.

Q4 2023
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A Fully-Automated Senescence Test (FAST) for the high-throughput quantification of senescence-associated markers

A Fully-Automated Senescence Test (FAST) for the high-throughput quantification of senescence-associated markers

Francesco Neri, Selma N. Takajjart, Chad A. Lerner, Pierre-Yves Desprez, Birgit Schilling, Judith Campisi, Akos A. Gerencser

The Fully-Automated Senescence Test (FAST) is an automated, image-based method for quantifying senescence in cultured cells by assessing key markers. It standardizes senescence measurement, supports various cell types and microscopes, and aids in evaluating compounds affecting senescence.

Q4 2023
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Chronically disrupted sleep induces senescence in the visceral adipose tissue of C57BL/6 mice

Chronically disrupted sleep induces senescence in the visceral adipose tissue of C57BL/6 mice

Disrupted sleep is linked to accelerated aging, demonstrating that lack of sleep causes cellular senescence in mice's adipose tissue, leading to oxidative stress and DNA damage. Poor sleep quality may accelerate aging and increase the risk of age-related diseases by promoting senescence in adipose tissue.

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Unlocking cellular plasticity: Enhancing human iPSC reprogramming through bromodomain inhibition and extracellular matrix gene expression regulation

Unlocking cellular plasticity: Enhancing human iPSC reprogramming through bromodomain inhibition and extracellular matrix gene expression regulation

PFI-3 enhances iPSC reprogramming by inducing MET in fibroblasts, upregulating E-cadherin, and reducing ECM gene expression, including collagen.

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Circulating senescent myeloid cells drive blood brain barrier breakdown and neurodegeneration

Circulating senescent myeloid cells drive blood brain barrier breakdown and neurodegeneration

Neurodegenerative diseases linked to Langerhans cell histiocytosis (LCH-ND) are caused by mutated myeloid cells compromising the blood-brain barrier, leading to inflammation and neuronal damage in the brain. Targeting MAPK activity and cell senescence reduces these effects and improves neurological outcomes.

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The impact of short-lived controls on the interpretation of lifespan experiments and progress in geroscience

The impact of short-lived controls on the interpretation of lifespan experiments and progress in geroscience

Reanalysis of lifespan studies shows that short-lived controls overstate longevity interventions' efficacy. The study suggests a mouse longevity intervention should only be considered with high confidence when control lifespans are close to 900 days or if the final lifespan of the treated group is considerably above 900 days.

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