RE: News aus der Forschung - 6

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STING pathway is not activated in telomerase-deficient mice with short telomeres
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p53 activation in telomerase-deficient mice with short telomeres is STING independent
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STING does not mediate aging phenotypes associated with short telomeres in mice

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STING deficiency does not rescue short telomere-mediated aging phenotypes and longevity in TERC- or TERT-telomerase deficient mice
https://www.cell.com/cell-reports/fullte...pEQemiftzamIjlw

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Our results identify TIMP2 as a modulator of age-associated microglia dysfunction. Harnessing its activity may mitigate detrimental effects of age-associated insults on microglia function.

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Youth-associated protein TIMP2 regulates microglial state and function in healthy and aged mice
https://www.nature.com/articles/s41467-0..._a1demo0jtae9sy

Gemfibrozil promotes longevity and health by restricting amino acid uptake through the Dipeptide transporter, PEPT1
https://www.nature.com/articles/s41514-026-00474-7

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Collectively, our findings identify ANGPTL8 as an endocrine regulator linking metabolic dysfunction to adipose tissue senescence and systemic aging, highlighting the ANGPTL8-AKT2-mTOR axis as a potential therapeutic target for delaying age-associated functional decline.

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An ANGPTL8-AKT2-mTOR Axis Drives Adipose Senescence and Aging-Related Functional Decline
https://pmc.ncbi.nlm.nih.gov/articles/PMC13478719/

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Our findings establish the LMNA-CK2-STING axis as a key biochemical mechanism that suppresses innate immune activation at the NE, offering a promising strategy for ameliorating aging and progeroid pathologies.

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CK2α restriction of STING accumulation underlies systemic aging
https://www.nature.com/articles/s41467-026-76351-4

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These findings demonstrate a role for CCND1/CDK6 in regulating DNA damage and inflammation in senescence and aging, highlighting it as a promising target for therapeutic repurposing.

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Inhibiting cyclin D1–CDK6 suppresses senescence-associated inflammatory gene expression and age-related functional decline
https://www.nature.com/articles/s43587-0..._a1demo0jtae9sy

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Our study provides preclinical evidence supporting dioscin as a novel intervention that ameliorates aging-associated phenotypes and highlights the pivotal role of UPRER in lifespan extension and aging suppression.

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Dioscin extends lifespan and ameliorates aging associated phenotypes in association with the endoplasmic reticulum unfolded protein response
https://pubmed.ncbi.nlm.nih.gov/42575256/

Mit Yamswurzel oder Bockshornklee (@Tizian) ist man gut dabei.

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Late-life semaglutide treatment slows ageing and extends lifespan in female mice
https://www.nature.com/articles/s41586-0...LPgRqEt5ZZ0c-EQ

Assessing mechanisms and evidence of a causal role for cellular senescence and somatic mutations in aging
https://www.aging-us.com/article/206414/...FpCwzIxIcUGLfNg

Physical Exercise in Immunotherapy
https://link.springer.com/article/10.1186/s40798-026-01101-1

Nature Biotechnology | Insilico’s AI-Driven IPF Candidate Rentosertib Shows Potential for Biological Age Reversal, as Assessed by Six Proteomic Aging Clocks
https://insilico.com/news/rnt0709261-ren...ic-aging-clocks

TNIK-Hemmung hatten wir ja schon des Öfteren hier im Forum besprochen.

Zitat

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Physiological aging results in widespread changes in RNA processing, degradation, modifications, and translation in the nervous system.

Corresponding changes in RNA-binding protein regulatory networks and aberrant ribonucleoprotein granule dynamics contribute to RNA dysregulation.

Age-related RNA dysregulation may predispose neurons to declining function and neurodegeneration.

Understanding how aging reshapes RNA regulatory networks will reveal new therapeutic opportunities for neurodegenerative disease

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RNA dysregulation as a determinant of aging and neurodegenerative vulnerability
https://www.cell.com/trends/cell-biology...R_5ki_WF2cSCyrw

Core regulatory pathways of natural products in anti-aging: Research progress at molecular, cellular, and systemic levels
https://www.sciencedirect.com/science/ar...095177926002509

Transmembrane Protein PTCHD4 Is a Novel Regulator of Cellular Senescence and Age-Related Pathologies
https://onlinelibrary.wiley.com/doi/10.1111/acel.70711

Lebenserwartung: Schlafdauer ist nach Rauchen der wichtigste Faktor

Zu wenig Schlaf verkürzt das Leben. Eine US-Studie zeigt: Die Schlafdauer ist nach dem Rauchen der stärkste verhaltensbedingte Prädiktor für Lebenserwartung.

https://www.telepolis.de/article/Lebense...r-11461647.html

Your Cells Learned Who to Be Before You Were Born. Ageing Is Them Slowly Forgetting
https://www.rapamycin.news/t/your-cells-...orgetting/26866

Direct Pharmacological Activation of AMPK Extends Lifespan in Yeast, Worms and Flies
https://onlinelibrary.wiley.com/doi/full...f6mIkZ1rBkDQ5XA

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Understanding how each path connects to the others and how these connections are regulated offers promising strategies to restore proteome integrity and extend a healthy lifespan.

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Proteostasis and ageing dissidence
https://royalsocietypublishing.org/rstb/..._Rc9eQ-i5xVF6VA

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Collectively, this study identifies a novel peptide therapeutic candidate for aging-related infertility, showing that elamipretide restores the quality of aged oocytes for fertility by coordinately boosting nuclear and cytoplasmic maturation via activation of the VEGF signaling pathway.

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Elamipretide Rejuvenates Oocyte Quality and Restores Female Fertility During Reproductive Aging
https://onlinelibrary.wiley.com/doi/full...jdXpvy80nhSmckQ

Elamipretide = SS-31

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The present study demonstrates the ability of P2X7R antagonists to suppress the neuroinflammatory response from primed human monocyte-derived microglia and human brain slices to offer direct translational data that central P2X7R antagonism might limit pathology-driven pro-inflammatory responses in the brain. This is predicted to improve the clinical outcomes for patients with traumatic brain injury and other neuroinflammatory pathologies.

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P2X7 receptor-mediated IL-1β release by human brain tissue: the impact of CNS-penetrant potential therapeutics
https://academic.oup.com/brain/advance-a...QxszA2hPIqwR-Sw

Zitat von Speedy im Beitrag #143

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Zitat

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The present study demonstrates the ability of P2X7R antagonists to suppress the neuroinflammatory response from primed human monocyte-derived microglia and human brain slices to offer direct translational data that central P2X7R antagonism might limit pathology-driven pro-inflammatory responses in the brain. This is predicted to improve the clinical outcomes for patients with traumatic brain injury and other neuroinflammatory pathologies.

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P2X7 receptor-mediated IL-1β release by human brain tissue: the impact of CNS-penetrant potential therapeutics
https://academic.oup.com/brain/advance-a...QxszA2hPIqwR-Sw

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Der Farbstoff Brilliant Blue G wäre hier eine Möglichkeit aber wie sicher das ganze ist zum Beispiel bzgl. möglicher toxischer Effekte weiß ich jetzt auch nicht genau.

Catalpol extends lifespan through sod-3-mediated mitophagy in Caenorhabditis elegans
https://pubmed.ncbi.nlm.nih.gov/42753447/

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In C. elegans, Plb1 knockdown reverses lipid elongation and extends lifespan in a lipid-length-dependent manner.

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Longer lipids mark aging and constrain lifespan
https://www.nature.com/articles/s43587-026-01223-x

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Our results indicate that cinnarizine and meclizine have no effect on C. elegans lifespan at lower doses, and that both compounds exert a toxic effect at higher doses, significantly shortening lifespan.

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Caenorhabditis Intervention Testing Program: the putative mTOR inhibitors Cinnarizine and Meclizine do not extend lifespan in C. elegans
https://pubmed.ncbi.nlm.nih.gov/42807283...W_SKnzoBaw9azwg

#149
@Prometheus
Amentoflavon wäre ein potenter natürlicher PDE4 - Inhibitor.