RE: News aus der Forschung - 5

Pig-organ transplants: what three human recipients have taught scientists
https://www.nature.com/articles/d41586-024-01453-2

The Vicious Cycle of Protein Clumping in Alzheimer’s Disease and Normal Aging
https://www.buckinstitute.org/news/the-v...d-normal-aging/

Chromosome Ends in Double Jeopardy

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Researchers have finally uncovered the other half of the end-replication problem at the lagging strand.

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https://www.the-scientist.com/chromosome...-jeopardy-71852

Lifespan effects in male UM-HET3 mice treated with sodium thiosulfate, 16-hydroxyestriol, and late-start canagliflozin
https://link.springer.com/article/10.100...KXFBVI0007sWecs


Ketogenic diet induces p53-dependent cellular senescence in multiple organs
https://www.science.org/doi/10.1126/sciadv.ado1463

"Chance as a (non)explanation: a cross-cultural examination of folk understanding of chance and coincidence" by Ze Hong
> https://osf.io/preprints/psyarxiv/ezxqp

Zufall und Zufallsvorstellung.
Ich habe es nur überflogen. Dennoch ist es interessant. Unsere Vorstellung vom Zufall ist nicht selbstverständlich. Eigentlich ist die Vorstellung sogar hoch komplex und kann als eine Art "philosophischer Fortschritt" interpretiert werden.

Was denkt ihr?

Was Gott zusammengeführt hat, soll der Mensch nicht trennen.
6 Dimension Richtungsstrom?
🤔

A Brain Anti-Senescence Transcriptional Program Triggered by Hypothalamic-Derived Exosomal microRNAs

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In contrast to the hypothesis that aging results from cell-autonomous deterioration processes, the programmed longevity theory proposes that aging arises from a partial inactivation of a “longevity program” aimed at maintaining youthfulness in organisms. Supporting this hypothesis, age-related changes in organisms can be reversed by factors circulating in young blood. Concordantly, the endocrine secretion of exosomal microRNAs (miRNAs) by hypothalamic neural stem cells (htNSCs) regulates the aging rate by enhancing physiological fitness in young animals. However, the specific molecular mechanisms through which hypothalamic-derived miRNAs exert their anti-aging effects remain unexplored. Using experimentally validated miRNA–target gene interactions and single-cell transcriptomic data of brain cells during aging and heterochronic parabiosis, we identify the main pathways controlled by these miRNAs and the cell-type-specific gene networks that are altered due to age-related loss of htNSCs and the subsequent decline in specific miRNA levels in the cerebrospinal fluid (CSF). Our bioinformatics analysis suggests that these miRNAs modulate pathways associated with senescence and cellular stress response, targeting crucial genes such as Cdkn2a, Rps27, and Txnip. The oligodendrocyte lineage appears to be the most responsive to age-dependent loss of exosomal miRNA, leading to significant derepression of several miRNA target genes. Furthermore, heterochronic parabiosis can reverse age-related upregulation of specific miRNA-targeted genes, predominantly in brain endothelial cells, including senescence promoting genes such as Cdkn1a and Btg2. Our findings support the presence of an anti-senescence mechanism triggered by the endocrine secretion of htNSC-derived exosomal miRNAs, which is associated with a youthful transcriptional signature.

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https://www.mdpi.com/1422-0067/25/10/5467

Timing of TORC1 inhibition dictates Pol III involvement in Caenorhabditis elegans longevity
https://pubmed.ncbi.nlm.nih.gov/38740431/

Lack of T04C9.1, the Homologue of Mammalian APPL2, Leads to Premature Ageing and Shortens Lifespan in Caenorhabditis elegans

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Ageing has been identified as an independent risk factor for various diseases; however, the physiological basis and molecular changes related to ageing are still largely unknown. Here, we show that the level of APPL2, an adaptor protein, is significantly reduced in the major organs of aged mice. Knocking down APPL2 causes premature ageing of human umbilical vein endothelial cells (HUVECs). We find that a lack of T04C9.1, the homologue of mammalian APPL2, leads to premature ageing, slow movements, lipid deposition, decreased resistance to stresses, and shortened lifespan in Caenorhabditis elegans (C. elegans), which are associated with decreased autophagy. Activating autophagy by rapamycin or inhibition of let-363 suppresses the age-related alternations, impaired motility, and shortened lifespan of C. elegans, which are reversed by knocking down autophagy-related genes. Our work provides evidence that APPL2 and its C. elegans homologue T04C9.1 decrease with age and reveals that a lack of T04C9.1 bridges autophagy decline and ageing in C. elegans.

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https://www.mdpi.com/2073-4425/15/6/659

Zitat von Easyflip im Beitrag #77

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Longevity Week Berlin

https://www.lifespan.io/news/longevity-w...held-in-berlin/

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Molecular mechanisms of aging and anti-aging strategies
https://biosignaling.biomedcentral.com/a...964-024-01663-1

Accumulation of senescent cells in the adrenal gland induces hypersecretion of corticosterone via IL1β secretion
https://onlinelibrary.wiley.com/doi/full/10.1111/acel.14206

Hydroxycitrate delays early mortality in mice and promotes muscle regeneration while inducing a rich hepatic energetic status
https://onlinelibrary.wiley.com/doi/full...mEbH12Iy9rnoxcC

Molecules Derived from Sea Sponge Show Promising Effects in Mitochondrial Function and Cancer

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Mycothiazole and its synthetic derivative target the mitochondria’s electron transport chain and show targeted toxicity against human cancer cells as well as anti-aging properties in worms.

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https://gero.usc.edu/2024/05/30/sea-spon...g-mycothiazole/

Centromeres Mutate More Rapidly Than Expected

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After sequencing centromeres in humans and other primates, researchers found that they vary greatly across species and potentially contribute to aging and disease.

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https://www.the-scientist.com/centromere...-expected-71876

Impact of urolithin A supplementation, a mitophagy activator on mitochondrial health of immune cells (MitoIMMUNE): A randomized, double-blind, placebo-controlled trial in healthy adults.
https://ascopubs.org/doi/abs/10.1200/JCO...16_suppl.e14562

Elastin Biosciences Announces Positive Preclinical In Vivo Data Demonstrating Elastin Preservation and Restoration in Models of Abdominal Aortic Aneurysm and Williams Syndrome
https://www.prnewswire.com/news-releases...ncRIvisvPdlUssv

https://nachrichten.idw-online.de/2024/0...in?groupcolor=3
Netzhaut weist auf Schweregrad der Schizophrenie hin
https://en.m.wikipedia.org/wiki/Optical_coherence_tomography
Würde ich glatt kaufen, wenn es unter Tausend kostet.

Genetics of aging uncovered with rare disease discovery

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New research uncovering the DNA-damaging mechanism by which a mutated gene causes a rare, fatal disease may have repercussions for the treatment of many other diseases linked to aging, including heart disease, autoimmune disorders, and cancer.

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https://newatlas.com/medical/rare-diseas...echanism-aging/

Epigenetic predictors of species maximum life span and other life-history traits in mammals

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By analyzing 15,000 samples from 348 mammalian species, we derive DNA methylation (DNAm) predictors of maximum life span (R = 0.89), gestation time (R = 0.96), and age at sexual maturity (R = 0.85). Our maximum life-span predictor indicates a potential innate longevity advantage for females over males in 17 mammalian species including humans. The DNAm maximum life-span predictions are not affected by caloric restriction or partial reprogramming. Genetic disruptions in the somatotropic axis such as growth hormone receptors have an impact on DNAm maximum life span only in select tissues. Cancer mortality rates show no correlation with our epigenetic estimates of life-history traits. The DNAm maximum life-span predictor does not detect variation in life span between individuals of the same species, such as between the breeds of dogs. Maximum life span is determined in part by an epigenetic signature that is an intrinsic species property and is distinct from the signatures that relate to individual mortality risk.

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https://www.science.org/doi/10.1126/sciadv.adm7273

Integrative epigenetics and transcriptomics identify aging genes in human blood

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Recent epigenome-wide studies have identified a large number of genomic regions that consistently exhibit changes in their methylation status with aging across diverse populations, but the functional consequences of these changes are largely unknown. On the other hand, transcriptomic changes are more easily interpreted than epigenetic alterations, but previously identified age-related gene expression changes have shown limited replicability across populations. Here, we develop an approach that leverages high-resolution multi-omic data for an integrative analysis of epigenetic and transcriptomic age-related changes and identify genomic regions associated with both epigenetic and transcriptomic age-dependent changes in blood. Our results show that these “multi-omic aging genes” in blood are enriched for adaptive immune functions, replicate more robustly across diverse populations and are more strongly associated with aging-related outcomes compared to the genes identified using epigenetic or transcriptomic data alone. These multi-omic aging genes may serve as targets for epigenetic editing to facilitate cellular rejuvenation.

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https://www.biorxiv.org/content/10.1101/...0.596713v1.full

A mild increase in nutrient signaling to mTORC1 in mice leads to parenchymal damage, myeloid inflammation and shortened lifespan
https://www.nature.com/articles/s43587-0...xLYVLFJDjh2wJ_j

Blut-Biomarker-Profile und außergewöhnliche Langlebigkeit: Vergleich von Hundertjährigen und Nicht-Hundertjährigen in einem 35-Jahres-Follow-up der schwedischen AMORIS-Kohorte

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Unsere Arbeit ist bisher die größte Studie, die Biomarkerprofile vergleicht, die in ähnlichem Alter früher im Leben bei außergewöhnlich langlebigen Personen und ihren kurzlebigeren Altersgenossen gemessen wurden. Wir verglichen die Biomarkerprofile von werdenden Hundertjährigen und ihren kurzlebigeren Altersgenossen, untersuchten den Zusammenhang zwischen einer Reihe häufig gemessener Biomarker und den Chancen, Hundertjährige zu werden, und untersuchten, wie homogen die Biomarkerprofile in der Hundertjährigen Bevölkerung in früheren Jahren waren. Wir fanden heraus, dass alle eingeschlossenen Biomarker mit Ausnahme von ALAT und Albumin für die Wahrscheinlichkeit, das 100. Lebensjahr zu erreichen, prädiktiv waren. Darüber hinaus hatten Hundertjährige mehr als ein Jahrzehnt vor ihrem 100. Geburtstag günstigere Biomarkerwerte als ihre gleichaltrigen Altersgenossen und waren in Bezug auf ihre Biomarkerprofile ziemlich homogen. Dennoch wurden zwei unterschiedliche Profile identifiziert. Das Profil der "höheren Ernährung" ähnelte eher dem Profil der Nicht-Hundertjährigen, während die "niedrigere, aber ausreichende Ernährung" durch günstigere Biomarkerwerte gekennzeichnet war. Die Unterschiede waren jedoch gering und wurden hauptsächlich für TC, Albumin und TIBC gefunden

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https://link.springer.com/article/10.1007/s11357-023-00936-w

Estrogen Metabolite Robustly Increases Lifespan in Male Mice
https://www.lifespan.io/news/estrogen-me...Uvs9MTsdtP4Q1f3

Why do women outlive men? Cells that develop into sperm and eggs could give the answer

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Scientists in Japan have shown for the first time in vertebrates that cells that develop into eggs in females and sperm in males drive sex differences in lifespan, and that removing the cells leads to animals with the same life expectancy.

The experiments were performed on small, turquoise killifish, a freshwater species that reaches sexual maturity in a fortnight and lives for a matter of months, but the researchers suspect a similar biological mechanism could influence the lifespan gap in humans and other species too.

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https://www.theguardian.com/science/arti...give-the-answer

Interessant auch der Absatz über Vitamin D und dass es bei den männlichen Fischen zu einer Lebensverlängerung von 21% führte (bei den weiblichen nur 7%).

Is Use of Psychedelic Drugs a Risk or Protective Factor for Late-Life Cognitive Decline?

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We included 2,503 individuals (Mage = 64 ± 11). After controlling for covariates, the finding revealed that psychedelic usage was independently associated with more favorable changes in executive function (β = .102, SE = 0.047, p = .031) and less depressive symptoms (β = −.090, SE = 0.021, p < .001). The same effect was not found for episodic memory (β = .039, SE = 0.066, p = .553).

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https://journals.sagepub.com/doi/10.1177/23337214241250108

Ketogenic diet’s role in boosting healthspan and memory in mice

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Longevity.Technology: While exploring how the high fat, low carbohydrate diet boosts memory in older mice, the researchers identified a new molecular signaling pathway that improves synapse function and helps explain the diet’s benefit on brain health and aging. Published in Cell Reports Medicine, the findings provide new directions for targeting the memory effects on a molecular level, without requiring a ketogenic diet or even the byproducts of it.
(...)
“BHB is almost certainly not the only molecule in play, but we think this is an important part of understanding how the ketogenic diet and ketone bodies work,” said Newman “This is the first study to really connect deep molecular mechanisms of ketone bodies all the way through to improving the aging brain.”

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https://longevity.technology/news/ketoge...memory-in-mice/

Lifestyle changes stabilize cognition in Alzheimer’s patients

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The study, which was published in the journal Alzheimer’s Research and Therapy, demonstrated that patients who implemented lifestyle changes, such as consuming whole foods, engaging in regular moderate exercise and performing stress management techniques, saw their dementia symptoms stabilize. In contrast, the control patients, who did not alter their habits, experienced continued worsening in thinking and memory [1].

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https://longevity.technology/news/lifest...imers-patients/

Suppressed basal mitophagy drives cellular aging phenotypes that can be reversed by a p62-targeting small molecule
https://www.cell.com/developmental-cell/...1bW15MTZieXRlcw

TERT activation targets DNA methylation and multiple aging hallmarks
https://www.cell.com/cell/abstract/S0092...Fshowall%3Dtrue