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Q4 2023
ISSN 2817-8831
Candidate Preprints
Q4 2023
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Fundamental equations linking methylation dynamics to maximum lifespan in mammals

Fundamental equations linking methylation dynamics to maximum lifespan in mammals

Steve Horvath, Joshua Zhang, Amin Haghani, Ake T. Lu, Zhe Fei

Methylation change rates in chromatin state and lifespan show an inverse relationship in a study of 125 mammalian species.

Q4 2023
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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

Jun Yang, H. Karimi Kinyamu, James M. Ward, Erica Scappini, Trevor K. Archer

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

Q4 2023
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Epistemic uncertainty challenges aging clock reliability in predicting rejuvenation effects

Epistemic uncertainty challenges aging clock reliability in predicting rejuvenation effects

Dmitrii Kriukov, Ekaterina Kuzmina, Evgeniy Efimov, Dmitry V. Dylov, Ekaterina E. Khrameeva

A critique of the epigenetic aging clocks for their high uncertainty in rejuvenation predictions during cellular reprogramming, due to misrepresentation in training data and inconsistent outcomes. It suggests incorporating uncertainty estimates into aging clock models for more accurate assessments.

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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