Hírek

Immorta Bio’s nine-amino-acid peptide aims at zombie cells

Immorta Bio says its AI-designed SenoMune-0257 prompts T cells to clear senescent cells, and plans first human evaluation before year-end. The molecule at the center of Immorta Bio’s latest announcement is just nine amino acids long, which is tiny by drug standards. On 12 October, the Miami company said it has completed planned preclinical studies […] The post Immorta Bio’s nine-amino-acid peptide aims at zombie cells appeared first on Longevity.Technology.

Mitochondrien: Wenn die Kraftwerke der Zellen stottern

Eine neue Theorie verbindet zahlreiche Volkskrankheiten über den Energiestoffwechsel.

Increased LINE-1 expression is associated with neuronal gene network downregulation in the aged mouse prefrontal cortex

BackgroundAging is associated with epigenetic alterations, neuroinflammation, and progressive decline of neuronal function. Derepression of the retrotransposon LINE-1 (L1) has been implicated in aging and age-related diseases. However, the regional expression of L1 and its relationships with DNA methylation, genomic L1 copy number, and aging-related transcriptional changes in the normal aging brain remain incompletely understood.MethodsWe examined L1 expression in the prefrontal cortex (PFC), hippocampus, and nucleus accumbens of young (17-week-old, n = 10) and aged (101-week-old, n = 7) male C57BL/6J mice. L1 expression, DNA methylation, and genomic copy number were quantified by RT-qPCR, pyrosequencing, and genomic qPCR, respectively. Transcriptomic alterations in the PFC were analyzed by RNA-seq, followed by weighted gene co-expression network analysis (WGCNA).ResultsL1 expression was

Reprogramming the gut–brain axis in neurodegeneration: comparative microbiome, metabolite, immunometabolic, polyphenol, probiotic, and epigenetic mechanisms in Alzheimer’s and Parkinson’s diseases

The gut–brain axis has emerged as a central mechanistic framework linking dietary bioactives, microbial ecology, and neurodegenerative disease progression. Similar microbiome-related mechanisms have also been implicated in colorectal cancer, suggesting potential shared links between microbial dysbiosis, inflammation, and disease progression. This study synthesizes preclinical evidence examining how polyphenols, polyphenol-derived compounds, and advanced delivery systems, including nanoparticles and synbiotics, modulate Alzheimer’s disease (AD) and Parkinson’s disease (PD) through microbiome-dependent mechanisms. Evidence from transgenic mice, toxin-induced rodent models, and Drosophila systems was compared across microbiome alterations, microbial metabolites, signaling pathways, epigenetic regulation, and functional outcomes. Across AD and PD models, dietary bioactives consistently promo

Topical Urolithin A to Improve Aged Skin Function

Mitochondria are the power plants of the cell, creating the chemical energy store molecule adenosine triphosphate used to power cellular processes. Mitochondrial function declines with age, and the research community is engaged in a variety of approaches that might at least modestly reduce this loss. The supplement urolithin A is known to improve mitochondrial function, though, and as is the case for other approaches, how exactly urolithin A accomplishes this outcome is not fully understood. Most of the ways to modestly improve mitochondrial function, ranging from exercise and calorie restriction through to NAD+ upregulation via vitamin B3 derivatives and MitoQ, may primarily function through improvements to autophagy targeted at mitochondria, improving overall mitochondrial function via improved clearance of damaged and dysfunctional mitochondria. This is by […]

Millions take fish oil for brain health. A two-year study found no benefit

A surprising two-year clinical trial found that fish oil supplements successfully delivered omega-3s to the brain but failed to improve memory or protect against Alzheimer's-related brain shrinkage. Researchers suspect that getting these nutrients through a healthy diet may offer benefits that supplements alone cannot provide.

Eos puts new gerotherapeutic to the test in aging mice

Berlin keynote details Eos SENOLYTIX’s pre-clinical results with mitochondrial-targeted geropeptide on healthspan and lifespan. A 167-week-old mouse makes an unlikely but persuasive ambassador for geroscience, particularly when he appears to be moving around with considerably more energy than animals more than a year his junior. For Eos SENOLYTIX, the animal known as Speedy represents something […] The post Eos puts new gerotherapeutic to the test in aging mice appeared first on Longevity.Technology.

Eos SENOLYTIX invites the public to keep pace with Speedy

As its CEO takes the stage in Berlin, the company opens a window on its longest-lived treated mice – and the data behind them. Most laboratory mice live and die in obscurity. Speedy has a webpage. From today, Eos SENOLYTIX is posting a 30-second clip of the 167-week-old mouse each morning, taken from his previous […] The post Eos SENOLYTIX invites the public to keep pace with Speedy appeared first on Longevity.Technology.

Too much RNA can starve cells of energy, scientists discover

Scientists have uncovered an unexpected danger lurking inside cells: too much RNA can damage the structures responsible for producing energy. A new study found that excess RNA, including the normally essential messenger RNA (mRNA), can directly disrupt mitochondria without relying on the immune system. The discovery could help explain how viral infections and certain aging-related diseases damage cells.

The Polycentric Aging Framework Positions Epigenetic Change as the Dominant Mechanism of Aging

The presently available data and understanding of aging might be thought of as a jigsaw with more missing pieces than there are pieces in hand. There is a great deal of latitude to assemble what is known into a wide variety of views of the whole without being strongly contradicted in any of them. Thus theories of aging proliferate; it is always easier to theorize about existing puzzle pieces than to run a research program that will meaningfully add to the collection of puzzle pieces. Here, researchers present a framework for the relationship of the mechanisms of aging that places epigenetic change as the dominant (but not only) important process that drives loss of function, disease, and mortality. Age-related dysfunction is unlikely to arise from […]

FDA clears Phase 2 trial for United Therapeutics’ COPD lung disease treatment

The U.S. Food and Drug Administration has cleared an investigational new drug application, allowing United Therapeutics to proceed with the SUMMIT phase 2 clinical trial of treprostinil SMI in pulmonary hypertension associated with chronic obstructive pulmonary disease. The randomized, double blind, 16 week study will evaluate safety and tolerability in approximately 40 patients; secondary endpoints […] The post FDA clears Phase 2 trial for United Therapeutics’ COPD lung disease treatment appeared first on Longevity.Technology.

Small-fiber degeneration, sensory dysfunction, and nociception comorbidity in central neurodegenerative disease

Progressive neurodegenerative disease typically calls for clinical effort to improve cognitive and motor deficits. It is also focused on improving patients' quality of life. However, across these dementias and other diseases, the underlying causes and potential mechanisms remain unclear. Most experimental and clinical research focuses on the central nervous system, examining pathogenic proteins such as tau and amyloid beta, as well as the potential cascade following mitochondrial damage and neuroinflammation. Although peripheral involvement, including gut microbiome influences and other visceral organs, is well-documented, the peripheral nervous system remains an understudied component of these progressive diseases. As peripheral terminals of primary afferent neurons are exposed to inflammatory or toxic mediators, these neurons respond to these threats via neuron-specific phenotypic chan

Cellular Senescence in Liver Aging

Senescent cells accumulate with age, perhaps primarily because the aged immune system becomes less able to efficiently destroy senescent cells as it does in youth. When a cell becomes senescent it ceases to replicate, grows in size, and secretes a potent mix of pro-inflammatory, pro-growth signals that contribute to the chronic inflammation of aging and are disruptive to tissue structure and function. Here, researchers investigate some of the specific outcomes of an increased burden of cellular senescence in the aged liver. The liver is organized into tightly regulated zones with distinct metabolic functions but zonation erodes with age. Cellular senescence contributes to aging and liver diseases, however, its impact on aging biology is ill-defined. As part of The Cellular Senescence Network Consortium, we used multiple […]

Scientists find a way to fight Alzheimer’s brain damage without removing toxic tau

Scientists have found a promising way to protect the brain from Alzheimer’s-related damage by blocking immune cells that contribute to the destruction of neurons. In mice, the treatment preserved roughly 40% more tissue in memory centers and improved memory, even without removing harmful tau protein buildup.

Decline in mitochondrial health and lysosomal acidification in human neurons during normal aging

IntroductionIn humans, aging is associated with an increased risk of developing neurodegenerative diseases such as Parkinson’s disease (PD) and Alzheimer’s disease (AD). In neurons, the effect of aging on intrinsic molecular processes, and how they tie to age-related neurodegeneration remains unclear. Animal studies have shown that mitochondrial function decline, autophagy impairment and defective elimination of damaged mitochondria by mitophagy are all central features of neuronal aging. However, very few studies have investigated such events in human neurons, due to a lack of models showing aging features. Therefore, there is a crucial need for a better understanding of the effect of aging on neuronal health.MethodsHere, we use direct neuronal reprogramming, which maintains signatures of cellular aging, to study the effect of aging on mitochondrial health and mitophagy in human neurons

An RNA Regulator Mitigates Senescence in Blood Vessels

Researchers publishing in Aging Cell have found that the regulatory protein MTR4 fights DNA damage in the blood vessel lining but decreases with aging. Vulnerable by […]

Life Biosciences Reports Initial Results from the First Reprogramming Trial

Partial epigenetic reprogramming involves exposing cells to some or all of the Yamanaka factors for a long enough period of time to reset epigenetic decorations on nuclear DNA and its supporting structures to a youthful state, but not so long as to risk dedifferentiation, and thus loss of cell state and formation of induced pluripotent stem cells that can give rise to teratomas. It is a fine balance, and different cell types need different exposure times. Thus the first practical applications of reprogramming therapy under development are limited to one cell type, or small regions of tissue where greater control over delivery can be exerted. The limited options for delivery of gene therapies further restrict the options on which tissues can be targeted. Life Biosciences […]

"Mind-blowing" Alzheimer’s breakthrough: Two hours of sleep restored without clearing brain plaques

Scientists have uncovered an unexpected culprit behind sleep loss in Alzheimer’s disease: overactive immune cells in the brain. By temporarily removing these cells, researchers restored more than two hours of sleep per day in mice, revealing a promising new target for treatment.

Physical exercise: a multi-target strategy for the prevention and treatment of Alzheimer’s disease

Alzheimer’s disease (AD) is a devastating age-related neurodegenerative disease characterized by irreversible cognitive dysfunction and neuronal loss. The complex pathogenesis of AD involves core proteinopathies of amyloid-β (Aβ) and tau, chronic neuroinflammation, and extensive cerebral metabolic disorders, which collectively drive progressive neuronal damage and disease deterioration. Currently, effective disease-modifying drugs for AD are still lacking, and physical exercise has been recognized as a safe and effective non-pharmacological intervention to prevent and alleviate AD pathological progression. Specifically, exercise inhibits abnormal Aβ deposition and tau hyperphosphorylation, suppresses microglial overactivation and sustained neuroinflammatory responses, and remodels cerebral metabolic homeostasis by improving glucose utilization, balancing lactate metabolism, restoring mit

Fight Aging! Newsletter, October 19th 2026

Fight Aging! publishes news and commentary relevant to the goal of ending all age-related disease, to be achieved by bringing the mechanisms of aging under the control of modern medicine. This weekly newsletter is sent to thousands of interested subscribers. To subscribe to the newsletter, please visit: https://www.fightaging.org/newsletter/. To unsubscribe, send email or reply to this email at newsletter@fightaging.org with "unsubscribe" in the subject or body. Longevity Industry Consulting Services Reason, the founder of Fight Aging! and Repair Biotechnologies, offers strategic consulting services to investors, entrepreneurs, and others interested in the longevity industry and its complexities. To find out more: https://www.fightaging.org/services/ Contents Age-Related Decline in Chaperone-Mediated Autophagy Impairs Clearance of Senescence Cells A Review of Differences Identified in Gu

Scientists discover that male and female skin play by different rules

Scientists have uncovered a surprising difference in how male and female skin repairs and renews itself. By tracking individual skin stem cells in living mice for five months, researchers discovered that female cells work together in a highly coordinated way, while male cells operate more independently. This synchronization, driven by sex hormones, helps explain why wounds heal faster in female mice, especially during the first few days.

Blocking STING Helps Preserve Bone in Aging Mice

A new study links STING-mediated signals from marrow fat cells to inflammation and declining NAD⁺ levels in bone-forming cells. Interrupting this pathway helped preserve aging bone [1]. […]

Inmune Bio, Quantum Computing partner on Alzheimer’s research

Inmune Bio and Quantum Computing Inc. have formed a collaboration to apply quantum computing, artificial intelligence and data analytics to identify new potential applications for XPro. The work will combine Inmune Bio’s clinical datasets from preclinical research through four clinical trials with QCi’s Dirac-3S quantum optimization machine to search for diseases and biomarkers driven by […] The post Inmune Bio, Quantum Computing partner on Alzheimer’s research appeared first on Longevity.Technology.

Immune Aging as a Shared Cause of Osteoporosis and Osteoarthritis

The aging of the immune system arises from the underlying causes of aging, but in and of itself causes significant further pathology. Here, for example, researchers discuss immune aging as a shared underlying cause of degenerative conditions of bone and joint tissues, and how this relates to the more traditional view of the cause of these conditions. In general, aging is not a neat straight line of cause and consequence, but rather a network of interacting processes of damage and dysfunction. In many cases the consequence can accelerate the cause. Consider senescent cells, for example, implicated in degenerative bone and joint conditions: the accumulation of senescent cells contributes to immune aging, which is a matter of both cellular senescence in immune cell populations and inflammatory […]

Epigenetic Aging is Accelerated in Large Dogs versus Small Dogs

Smaller dog breeds live for longer than larger dog breeds, which perhaps allows some insight into mechanisms of aging. Researchers here find that age-related change in the epigenetic regulation of nuclear DNA structure and gene expression proceeds more rapidly in larger dogs, particularly in regions containing transposable elements. Transposable elements are the remnants of ancient viral infections, capable of copying themselves across the genome when active, a form of damage that can break gene sequences. The virus-like particles created by expression of transposable elements provoke inflammatory responses, and thus loss of transposable element suppression contributes the disruptive chronic inflammation of aging. This study adds to the existing body of evidence suggesting that transposable element activation resulting from epigenetic change provides a meaningful contribution to mammalia

Intracellular C3 modulates senolytic responsiveness in senescent cells and aged tissues via AKT/S6K pro-survival signaling

XPRIZE hands $1m to a mitochondrial drug team

Mighty Therapeutics and the University of Washington will use pilot data on elamipretide to design a larger trial in older adults. Part of a ten-part series profiling each of the $101 million XPRIZE Healthspan competition’s Milestone 2 Awardees. Across the series, Longevity.Technology examines the science behind each team’s approach, the trial data supporting it and what stands between […] The post XPRIZE hands $1m to a mitochondrial drug team appeared first on Longevity.Technology.

A Review of Animal Study Evidence for Mesenchymal Stem Cell Therapy to Treat Neurodegeneration

Researchers here assess the present animal study evidence for first generation stem cell therapies to produce benefits in the most common neurodegenerative conditions, and also the consequences of stroke. The results are promising. While these therapies have been fairly widely deployed in patients via medical tourism, that data will never be available for analysis in any useful way. A few formal clinical trials have taken place, with unfortunately mixed results, which suggests that the details of manufacturing process, source of cells, and other logistical factors are important to outcomes. In general, these stem cell therapies appear to reliably modulate chronic inflammation, but all other desired outcomes are quite unreliable where they have been assessed rigorously in human patients. This is one of the reasons why […]

Suppression of Transposable Element Activity as an Approach to Therapy

Transposable elements are DNA sequences that can copy themselves. The remnants of ancient viral infections, they encode viral-like particles that act to insert DNA into the genome. Transposable elements are suppressed in youth, but with age the epigenetic control over DNA structure and gene expression is altered, and one of the consequences is that transposable elements are exposed to translation machinery and begin to copy themselves. This produces a form of DNA damage where that haphazard insertion of new sequences breaks existing genes, but perhaps more importantly generates an inflammatory response to the viral-like particles that innate immune sensors recognize as foreign. Some fraction of the harmful chronic inflammation results from transposable element activity, and thus suppression may form a useful basis for therapy. The […]

Serum neuron-derived extracellular vesicle mitochondrial DNA as a potential biomarker for mild cognitive impairment due to AD

BackgroundMild cognitive impairment (MCI) represents the initial clinical manifestation, eventually evolving into the distinctive features of Alzheimer’s disease (AD), making its early identification crucial. Notably, mitochondrial dysfunction is an early characteristic of AD. Neuron-derived extracellular vesicles (NDEVs) can cross the blood-brain barrier, and their mitochondrial DNA (mtDNA) can reflect intracerebral lesions, showing considerable potential. In this study, we investigated the alterations in mtDNA within serum NDEVs and evaluated their potential as early diagnostic biomarkers for MCI due to AD.MethodsA total of 42 MCI patients, 49 AD patients, and 57 age-matched cognitively unimpaired (CU) controls were enrolled. Serum NDEVs were enriched and characterized, and their mtDNA levels were quantified by qPCR. ROC curve was used to analyze diagnostic performance, and the integra

Dental Pulp Stem Cell Secretome as a Treatment to Improve Outcomes Following Stroke

Since stem cell therapies produce beneficial effects via a short burst of signaling from the transplanted cells rather than via any long-lasting survival and engraftment of those cells, researchers are attempting to build therapies that deliver the signals instead of the cells. Manufacture involves culturing stem cells and harvesting the culture medium in order to obtain the molecules or extracellular vesicles secreted by the stem cells, and then introducing that material into patients. The signaling produced by different stem cell populations will likely prove to be more versus less useful in different contexts, and so some experimentation is needed. Here, researchers show that the secreted signals generated by dental pulp stem cells help to improve the outcome following stroke in mice. Ischemic stroke induces oxidative […]

miR-128-3p Inhibition Improves Muscle Mass and Function in Aged Mice

That the calorie restriction imposed by GLP-1 receptor agonists induces loss of muscle mass has proved a boon for research into ways to address the loss of muscle mass that occurs with age, contributing to frailty. Suddenly a relatively large amount of funding and industry attention is available for programs that might result in a drug to prevent muscle loss in GLP-1 receptor agonist patients, and most of those options can at least in principle be used to treat age-related muscle loss. Here, researchers demonstrate a novel approach to inducing muscle growth in aged mice, by inhibiting a relevant microRNA; the technology is developed by Elenae Therapeutics which, as is usual, targets more severe and less common indications at the outset, such as improving outcomes […]

Sex and stage-defined exploratory inflammatory and amyloid-associated readout patterns in female APP/PS1 mice exposed to TAK-242

TLR4-related inflammatory signaling has been implicated in Alzheimer’s disease-related immune responses, and TAK-242 has been used as an experimental tool in studies examining this signaling context. This exploratory study characterized inflammatory cytokine and amyloid-associated histological readout patterns associated with TAK-242 exposure in female early-stage APP/PS1 mice. Female APP/PS1 mice were assigned to saline, lipopolysaccharide, or TAK-242 exposure conditions for 6 weeks, with age-matched non-transgenic mice serving as reference controls (n = 8/group). Brain TNF-α, IL-1β, and IL-6 levels were measured by ELISA, and 6E10-positive staining area was quantified by immunohistochemistry. Directional differences in cytokine levels and 6E10-positive staining area were observed between APP/PS1 mice exposed to TAK-242 and untreated APP/PS1 mice. However, because a vehicle-matched APP/

Senescent-like activated naive B cells contribute to progression to clinical rheumatoid arthritis

Rubedo reports younger skin age in Phase 1b trial

GPX4-targeting therapy reduces epigenetic age markers and circulating inflammation, raising questions about effects beyond treated skin. Rubedo Life Sciences has reported a statistically significant reduction in measured skin epigenetic age following treatment with its investigational senotherapeutic RLS-1496, adding a new dimension to the company’s growing body of early clinical evidence for targeting cellular senescence. The […] The post Rubedo reports younger skin age in Phase 1b trial appeared first on Longevity.Technology.

Phase 1b data show Rubedo Life Sciences reduces skin epigenetic age

Rubedo Life Sciences released Phase 1b clinical findings for RLS-1496 in patients with atopic dermatitis. The company claims four weeks of topical treatment produced a statistically significant mean reduction of 2.1 years in measured skin epigenetic age across 11 paired photoaged skin samples (p=0.032), with a best responder showing an 11.7-year reduction at Day 63. […] The post Phase 1b data show Rubedo Life Sciences reduces skin epigenetic age appeared first on Longevity.Technology.

Immorta Bio develops AI-designed senolytic immunotherapy

Immorta Bio completed planned preclinical studies for SenoMune-0257, an AI-designed nine-amino-acid peptide immunotherapy intended to restore immune recognition and elimination of senescent cells, and is preparing to advance the candidate into clinical development in 2026. Preclinical laboratory studies showed SenoMune-0257 stimulates cytotoxic T cells that selectively eliminate senescent cells while sparing healthy cells under the […] The post Immorta Bio develops AI-designed senolytic immunotherapy appeared first on Longevity.Technology.

A History of Research into Cellular Senescence

Cells become senescent in response to various forms of damage and stress, including the stress induced by reaching the Hayflick limit on replication. This was first described in the context of replicative senescence in cell cultures, and from there cellular senescence became a topic of interest in cancer research. In more recent years, the accumulation of senescent cells in aged tissues was demonstrated to be an important contribution to degenerative aging, and a small industry of biotech companies has emerged to develop a variety of therapies to either selectively destroy or modulate the behavior of senescent cells. The history of cellular senescence is, in many ways, a history of expanding biological complexity. What began as an observation of finite proliferative capacity in cultured cells has […]

Scientists uncover a hidden map of the brain with 539 distinct regions

Scientists have uncovered a hidden layer of organization in the brain by creating the first detailed 3D map of its lipids, the fatty molecules essential for brain structure and communication. By analyzing millions of measurements from mouse brains, researchers identified 539 distinct chemical zones, revealing patterns and boundaries that traditional brain maps have missed. Surprisingly, even white matter, once thought to be relatively uniform, contains a complex patchwork of chemically distinct regions.

An Anti-Senescence Gene May Fight Spinal Disc Deterioration

In Aging Cell, a team of researchers has described how a little-known gene, ZNF865, has a significant influence on back pain through the regulation of cellular senescence. Lower back pain and senescence […]