RE: News aus der Forschung - 3

Extracellular vesicles from human urine-derived stem cells delay aging through the transfer of PLAU and TIMP1

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This study demonstrates that extracellular vesicles from human urine-derived stem cells (USC-EVs) efficiently inhibit cellular senescence in vitro and in vivo. The intravenous injection of USC-EVs improves cognitive function, increases physical fitness and bone quality, and alleviates aging-related structural changes in different organs of senescence-accelerated mice and natural aging mice.

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https://www.sciencedirect.com/science/ar...211383523004768

Somatic mutations in human ageing: New insights from DNA sequencing and inherited mutations

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• Because of the relatively modest burden of age-related somatic mutations identified so far and their stochastic nature, it is difficult to envision how somatic mutation accumulation alone can explain most ageing phenotypes that develop gradually.
• With a few exceptions like cancer, results from recent DNA sequencing studies do not add weight to the idea that somatic mutations with age drive ageing phenotypes.
• Studies in patients with a higher somatic mutation burden and no signs of premature ageing further question the role of somatic mutations in ageing.

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https://www.sciencedirect.com/science/ar...568163724000862

‘We want to give everyone a new thymus to reboot their immune system’

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The company leading the government-funded thymus rejuvenation project is Thymmune Therapeutics, which is developing thymic cell therapies to restore immune function in aging and disease. Backed by renowned Harvard geneticist George Church, the Cambridge, MA-based startup is on a mission to use stem cells to build an “off-the-shelf” thymus that could one day be offered to everyone. To learn more, we caught up with Thymmune’s founder and CEO, Dr Stan Wang.

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https://longevity.technology/news/we-wan...-immune-system/

cGAS-STING is responsible for aging of telomerase deficient zebrafish
https://www.biorxiv.org/content/10.1101/...v4E36L7kYPaAbxE

Chip im Gehirn - Erster Neuralink-Patient spielt Schach mit Hilfe seiner Gedanken

"Der erste Patient, dem das Start-up-Unternehmen Neuralink von Tesla-Chef Elon Musk einen Computerchip ins Gehirn implantiert hat, macht offenbar Fortschritte bei der Steuerung einer Computermaus mit seinen Gedanken. Der 29-jährige Patient, der nach einem Tauchunfall unterhalb der Schulter gelähmt ist, war am Mittwoch in einem Livestream auf Musks Social-Media-Plattform X beim Online-Schach am Laptop zu sehen und bewegte dabei mit seinen Gedanken den Mauszeiger."

https://www.welt.de/vermischtes/article2...r-Gedanken.html

Predicting Chronological Age via the Skin Volatile Profile

https://www.ncbi.nlm.nih.gov/pmc/article...1460/#sec4title


Man kann auch jünger riechen!
Und meide Aldehyd C9!

#54
Früher roch ich noch gut und habe den Parfüm - Baukasten leider nicht von den Eltern bekommen. Jetzt rieche ich im besten Fall blumig, so soll ja auch "heilig" riechen aber wahrscheinlich trifft die Note "erloschene Kerze" meinen Ist-Wert am ehesten.

stark wachsartig mit blumigen Akzenten

verleihen einen Duft, der dem verbrannten Wachs einer erloschenen Kerze ähnelt

PS: Eine biologischer Anzeiger für C-9, wären die Culex mosquitoes. Da müsste nach meiner graphischen Auswertungen die jungen weiße CO2-neutrale Frauen die am wenigsten gestochen werden.
https://pubmed.ncbi.nlm.nih.gov/19858490/

Zitat von Prometheus im Beitrag #36

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Zitat von Speedy im Beitrag #35

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Hätte hier eigentlich oral eingenommenes Natriumacetat überhaupt eine Chance zum Wirkungsort zu gelangen?

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@Speedy

Ich hatte diese Erkenntnis damals leider nicht weiter verfolgt.

https://www.pharmawiki.ch/wiki/index.php?wiki=Natriumacetat

Welche Gründe würden denn dagegen sprechen, dass Natriumacetat von den Zellen aufgenommen wird?

EDIT:
Vermutlich ist das Hauptproblem, bei einer Einnahme von Dosierungen, die die intrazelluläre Konzentration wirklich steigern können, bereits gravierende Nebenwirkungen auftreten könnten:
https://www.nature.com/articles/srep46210

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Time is ticking faster for long genes in aging
https://www.cell.com/trends/genetics/ful...5vsGKJ3M482QSOw

Depleting myeloid-biased haematopoietic stem cells rejuvenates aged immunity
https://www.nature.com/articles/s41586-0...Tr15eBafVshWl1o

Zitat von Prometheus im Beitrag #59

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Zitat von Speedy im Beitrag #58

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Depleting myeloid-biased haematopoietic stem cells rejuvenates aged immunity
https://www.nature.com/articles/s41586-0...Tr15eBafVshWl1o

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Das halte ich für einen sehr wichtigen Ansatz!

Diese Myeloid-Stammzellen können im Laufe der Zeit das Knochenmark förmlich überwuchern. Leider habe ich keinen Volltext-Zugriff. Gab es evtl ein Preprint? So wie ich das sehe, wurden noch keine Experimente hinsichtlich der Lebensspanne der Mäuse mit bzw ohne Intervention durchgeführt. Mit welchem Antikörper wurden die My-HSC depletiert?

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Zu beachten hierbei in Krebszellen zum Beispiel ist eher eine ACSS2 Downregulation erwünscht.

ACSS2 upregulation enhances neuronal resilience to aging and tau-associated neurodegeneration
https://www.biorxiv.org/content/10.1101/...nqUegahesaNNJAM

Natural molecule boosts NAD+ levels, improving muscle function during aging

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Trigonelline, which can be found in coffee, declines during sarcopenia – but increasing its levels can improve physical performance.

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https://longevity.technology/news/natura...n-during-aging/

Lifelong persistence of nuclear RNAs in the mouse brain

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RNA is generally considered a short-lived mediator of genetic information. Zocher et al. discovered that certain nuclear RNAs produced during postnatal development can persist for years in a subset of cells in the mammalian brain (see the Perspective by Lawrence and Hall). The authors also showed that some of these long-lived RNAs play a crucial role in maintaining genome integrity and cellular plasticity. Because adult mammals have limited capacity to replace neurons, the longevity of these RNAs could be critical for lifelong function of the brain but might also contribute to its age-dependent decline. —Stella M. Hurtley

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https://www.science.org/doi/10.1126/science.adf3481

Impact of aldehydes on DNA damage and aging

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“DNA damage is linked with aging phenotypes,” said Oka. “However, for the first time, we propose a relationship between aldehyde-derived DNA damage and premature aging.”

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https://www.nagoya-u.ac.jp/researchinfo/...0240411-01.html

Did dinosaurs impact how today’s mammals age?

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The longevity bottleneck hypothesis is significant since it explains several aging traits such as tooth erosion, the absence of very slow demographic aging and reproductive senescence. However, further studies are required to confirm whether other defence, repair, or regeneration systems were lost or inactivated in mammals due to other predation or ecological constraints.

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https://longevity.technology/news/did-di...ys-mammals-age/

Identification of prospective aging drug targets via Mendelian randomization analysis
https://onlinelibrary.wiley.com/doi/full...idphR5oFIHpjxys

Immenser Anstieg von Krebsfällen bei unter 50-Jährigen: Neue Ursache möglicherweise gefunden

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Ursache für mehr frühe Krebserkrankungen? Forschende nehmen biologisches Alter ins Visier

Ein neuer möglicher Risikofaktor für Krebserkrankungen in jüngeren Altersgruppen wurde jetzt von einem US-Forscherteam entdeckt. Die Wissenschaftler stellten fest, dass das biologische Alter einer Person eng mit dem Krebsrisiko verbunden ist. Da Alter generell als Risikofaktor für diverse Krebsarten gilt, spielt auch das biologische Alter eine ähnliche Rolle.

Schnelleres Altern: Blut-basierte Marker als Anhaltspunkt

Albumin: Nimmt mit dem Alter ab und wird von der Leber gebildet

Kreatinin: Niedrigere Werte stehen mit höherer Lebenserwartung in Verbindung

Glukose: Bleibt mit höherem Alter nach dem Essen länger erhöht

C-reaktives Protein: Hohe Werte entsprechen einer schnelleren Alterung

Lymphozyten-Anteil: Konzentration nimmt mit Alter eher ab

Mittleres Zellvolumen: Nimmt mit dem Alter zu

Breite der Erythrozyten-Verteilung: Nimmt mit dem Alter eher zu

Alkalische Phosphatase: Nimmt mit dem Alter eher zu

Anzahl der weißen Blutkörperchen: Befindet sich die Anzahl im oberen Bereich des Normalbereichs, kann das mit einem höheren Alterungsgrad in Verbindung stehen

In dieser Studie wurde das chronologische Alter der Teilnehmenden mit ihrem biologischen Alter verglichen, was ein beschleunigtes Altern aufzeigen konnte. Insbesondere Personen, die nach 1965 geboren wurden, weisen eine um 17 Prozent höhere Tendenz zu beschleunigtem Altern auf als jene, die zwischen 1950 und 1954 geboren wurden.

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https://www.msn.com/de-de/gesundheit/oth...d0b77a4030&ei=9

#66
Ich habe jugendliche Werte, mein biologisches Alter scheint also noch ziemlich jung zu sein. Allerdings nehme ich auch außer L Thyroxin keine zusätzlichen Medikamente, nur NEMs. Würde ich Statine, Blutdrucksenker und sonstiges nehmen, hätte ich mit Sicherheit auch ein höheres biologisches Alter.

Low-Molecular Weight Compounds that Extend the Chronological Lifespan of Yeasts, Saccharomyces cerevisiae, and Schizosaccharomyces pombe
https://onlinelibrary.wiley.com/doi/10.1002/adbi.202400138

The Gehan test identifies life-extending compounds overlooked by the log-rank test in the NIA Interventions Testing Program: Metformin, Enalapril, caffeic acid phenethyl ester, green tea extract, and 17-dimethylaminoethylamino-17-demethoxygeldanamycin hydrochloride
https://link.springer.com/article/10.1007/s11357-024-01161-9

Mitochondrial Transplantation’s Role in Rodent Skeletal Muscle Bioenergetics: Recharging the Engine of Aging

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Methods: Fifteen female mice (24 months old) were randomized into two groups (placebo or mitochondrial transplantation). Isolated mitochondria from a donor mouse of the same sex and age were transplanted into the hindlimb muscles of recipient mice (quadriceps femoris, tibialis anterior, and gastrocnemius complex). Results: The results indicated significant increases (ranging between ~36% and ~65%) in basal cytochrome c oxidase and citrate synthase activity as well as ATP levels in mice receiving mitochondrial transplantation relative to the placebo. Moreover, there were significant increases (approx. two-fold) in protein expression of mitochondrial markers in both glycolytic and oxidative muscles. These enhancements in the muscle translated to significant improvements in exercise tolerance. Conclusions: This study provides initial evidence showing how mitochondrial transplantation can promote skeletal muscle bioenergetics in an aging rodent model.

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https://www.mdpi.com/2218-273X/14/4/493

Effect of long-term caloric restriction on telomere length in healthy adults: CALERIE™ 2 trial analysis

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No differences were observed when considering TL change across the study duration from baseline to 24-months, leaving it unclear whether CR-related effects reflect long-term detriments to telomere fidelity, a hormesis-like adaptation to decreased energy availability, or measurement error and insufficient statistical power.

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https://onlinelibrary.wiley.com/doi/10.1111/acel.14149

Exploring juventology: unlocking the secrets of youthspan and longevity programs

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This review discusses the idea of juventology, a novel field proposing the existence of longevity programs that can maintain organisms in a highly functional state for extended periods of time. Drawing upon research on Saccharomyces cerevisiae and other model organisms, the review explores the distinctiveness of juventology from traditional aging-centered views. The focus on the “age of youth” challenges conventional thinking and opens new avenues for understanding and extending the period of peak functionality in organisms. Thus, a “juventology”-based strategy can complement the traditional gerontology approach by focusing not on aging but on the longevity program affecting the life history period in which mortality is very low and organisms remain youthful, healthy, and fully functional.

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https://www.frontiersin.org/articles/10....24.1379289/full

Kommentar: Genau so sollte man das Thema angehen, finde ich.


Epigenetic age oscillates during the day

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Thirteen clocks exhibited significant oscillations with the youngest and oldest age estimates around midnight and noon, respectively. In addition, daily oscillations were consistent with the changes of epigenetic age across different times of day observed in an independant populational dataset. While these oscillations can in part be attributed to variations in white blood cell type composition, cell count correction methods might not fully resolve the issue. Furthermore, some epigenetic clocks exhibited 24-h periodicity even in the purified fraction of neutrophils pointing at plausible contributions of intracellular epigenomic oscillations. Evidence for circadian variation in epigenetic clocks emphasizes the importance of the time-of-day for obtaining accurate estimates of epigenetic age.

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https://onlinelibrary.wiley.com/doi/10.1111/acel.14170

Kommentar: Könnte dies bedeuten, dass man bei einem Test des epigenetischen Alters je nach Tageszeit ein anderes Ergebnis erhält?

Pyrviniumembonat wurde eingesetzt hier.

Nuclear speckle rejuvenation alleviates proteinopathies at the expense of YAP1
https://www.biorxiv.org/content/10.1101/2024.04.18.590103v1

Blood biomarker profiles and exceptional longevity: comparison of centenarians and non-centenarians in a 35-year follow-up of the Swedish AMORIS cohort

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Higher levels of total cholesterol and iron and lower levels of glucose, creatinine, uric acid, aspartate aminotransferase, gamma-glutamyl transferase, alkaline phosphatase, lactate dehydrogenase, and total iron-binding capacity were associated with reaching 100 years. Centenarians overall displayed rather homogenous biomarker profiles. Already from age 65 and onwards, centenarians displayed more favorable biomarker values in commonly available biomarkers than individuals dying before age 100. The differences in biomarker values between centenarians and non-centenarians more than one decade prior death suggest that genetic and/or possibly modifiable lifestyle factors reflected in these biomarker levels may play an important role for exceptional longevity.

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10828184/

Study finds RNA modification is responsible for disruption of mitochondrial protein synthesis in Alzheimer's disease

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"But there are also proteins that are synthesized by the mitochondria themselves. One of these is ND5, a subunit of complex I of the respiratory chain," explained Professor Kristina Friedland. A substance called NADH gives electrons to complex I, which transfers these to ubiquinone, resulting in ubiquinol.

During this process, four proteins are pumped from the matrix into the intermembrane space. ND5 plays an important role in this connection, and any mutations of the mitochondrial encoded gene of this subunit can result in serious mitochondrial disorders, such as Leigh syndrome.

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https://medicalxpress.com/news/2024-04-r...ochondrial.html

Rejuvenating aged stem cells: therapeutic strategies to extend health and lifespan
https://febs.onlinelibrary.wiley.com/doi...1873-3468.14865