Abstract: In this work, we analyze the reasons for the absence of immortality from the perspective of “genetic information metabolism.” All living organisms synthesize and release genes, including novel and previously unknown genes, into the external environment through the process of genetic information metabolism. As a result, new genes become available for inclusion in the unified complex of genetic information represented by all living and non-living carriers, which has been termed the “Pangenome,” ensuring the maintenance of life on Earth under changing biotic and abiotic conditions. Part of the newly created genetic information remains inaccessible to spreading to other members of the Pangenome during the lifetime of an organism and can only be released after its death. We hypothesize, to our knowledge for the first time, that the absence of immortality is associated with the necessity of releasing novel genes for spread within the Pangenome, which can happen efficiently only after an organism’s death. We define the spread of genes and their integration into the genomes of other organisms as “gene reincarnation.” Within the Pangenome, genes are redistributed, ensuring the further evolution of life. We formulate a new definition of death as “a stage in the metabolism of genetic information during which all genes of an organism become available for reincarnation.” This understanding for the first time views death as a crucial part of the genetic cycle of life. Based on above novel concepts, we propose certain properties that immortal organisms should possess.

Abstract: Melanogenesis is a highly complex process regulated by multiple signaling pathways that control melanin synthesis in melanocytes and its subsequent transfer to keratinocytes. This process is further influenced by an intricate network of interactions among various skin cell populations, including inflammatory cells, which release paracrine factors in response to internal and external stimuli, such as UV radiation. The aim of this study was to evaluate effectiveness a new cosmetic formulation Skin Glow Complex designed for the topical treatment of skin dyschromia. We investigated the potential benefits of the for-mulation in two major resident skin cell types, keratinocytes and fibroblasts subjected to UV irradiation. Additionally, its effects were tested in 3D human melanocyte spheroid model, that better mimics the skin's environment. Treatment with the new formulation prevented UV-induced reactive oxygen species (ROS) formation in keratinocytes. In dermal fibroblasts, the formulation decreased the expression of matrix metalloproteinases while simultaneously promoting cell proliferation and collagen synthesis. Finally, results obtained from the melanocyte spheroid model confirmed the formulation’s ability to reduce melanin production, reinforcing its potential use in the treatment of skin dyschromia. Overall, these findings indicate that the new product represents a promising natural option to support skin repair and counteract aging and UV-induced damage.

Abstract: Background: Immunosenescence, the age-related decline in immune function, represents a critical challenge in geriatric medicine. Traditional modeling approaches fail to capture the spatial heterogeneity and compositional complexity of the aging immune system.Methods: We developed a quantum-inspired tensor product Hilbert space framework integrating 11 immune cell types across 8 tissue compartments (dimension: 88). Two cohorts—young adults (<50 years) and elderly individuals (>65 years)—were simulated using empirically derived distributions from recent immune cell census studies. State evolution was governed by a spatial Hamiltonian incorporating intratissue dynamics, cellular trafficking, and cytokine-mediated coupling.Results: The elderly cohort exhibited hallmark immunosenescence signatures: 30% reduction in naive T lymphocytes (p<0.001), 25% expansion of NK cells (p<0.001), and 33% impairment in migration capacity. Tissue-specific Shannon entropy decreased by 8-12% across major compartments (lymph nodes: -11%, bone marrow: -8%, peripheral blood: -9%), providing a quantitative metric for immune aging. Enhanced intertissue coupling (1.5-fold increase) captured inflammaging signatures. Multivariate analysis yielded a composite aging index with 89% discrimination accuracy (AUC=0.89, 95% CI: 0.83-0.94).Conclusions: Information-theoretic diversity metrics derived from spatially resolved models provide quantifiable biomarkers of immunological aging with strong clinical correlations. This framework enables personalized immune age assessment, vaccine responsiveness prediction, and rational design of immune rejuvenation strategies.

Abstract: Pelvic radiation therapy is an essential treatment for several pelvic malignancies, but can lead to radiation cystitis (RC), a severe progressive inflammatory bladder disorder lacking effective diagnosis and therapeutic options. RC evolves through acute, latent, and chronic phases, ultimately resulting in bladder fibrosis, vascular damage, and hematuria. Here, we characterize the molecular and immunological mechanisms underlying RC progression using a preclinical mouse model. Building on prior analysis of the acute and chronic phases, we examined the previously unanalyzed latent phase and integrated transcriptomic, immune cell profiling, inflammatory protein measurements, and bladder function assessments across all stages. Acute radiation injury was marked by strong activation of apoptotic pathways, whereas latent and chronic phases were dominated by inflammatory signaling with distinct cytokine and chemokine signatures. Persistent upregulation of Cdkn1a (P21) suggested sustained senescence, while reductions in IL-27 and shifts in granulocyte–lymphocyte proportions during the latent phase indicated impaired immune surveillance. At chronic stages, increased SASP-associated proteins and matrix-remodeling mediators coincided with bladder functional decline. Together, these findings support a model in which radiation-induced senescence, coupled with immune dysregulation during the latent phase, drive ongoing inflammation, tissue remodeling, and bladder dysfunction in RC.

Abstract: Nutraceuticals, bioactive compounds derived from foods, are increasingly investigated as interventions to promote healthy ageing. Multi-ingredient formulations may offer additive or synergistic benefits by targeting multiple ageing pathways while using low doses of each component for improved safety. However, their efficacy in mammals remains poorly understood. Here, we compared the effects of a continuous multi-ingredient nutraceutical intervention with two short-courses of senolytic regimen in naturally aged male C57Bl/6J mice. Importantly, these mice were overweight following a switch to soaked food at 20 months, a protocol that increased caloric intake and likely induced metabolic stress. This context frames the study as a model of ‘rescue’ from premature ageing rather than extension of maximum lifespan. Mice were assigned to either control, nutraceutical (12 pro-longevity natural compounds), or senolytic (Navitoclax plus BAM15) groups at 20 months of age. Lifespan and healthspan indicators were assessed longitudinally. Both interventions improved survival compared to controls (median lifespan +18–21%) and mitigated frailty progression, but with distinct patterns: nutraceutical benefits accumulated gradually, whereas senolytic effects were transient. Cognitive performance was preserved in nutraceutical-treated mice and improved shortly after senolytic treatment. In vitro, the nutraceutical lacked senolytic activity but exhibited senostatic effects, reducing nuclear size, ROS release, and IL-6 secretion in senescent fibroblasts. These findings suggest that multi-ingredient nutraceuticals can restore healthspan compromised by metabolic stress and deliver benefits comparable to senolytics when administered continuously, potentially through senostatic mechanisms. Combining senolytics to reduce senescent burden with long-term nutraceutical treatment may offer a safe, accessible strategy to optimise healthspan, particularly in the context of modern human ageing, which often occurs under conditions of caloric excess and metabolic syndrome.

Abstract: Due to the allergenicity of soy protein, this study aimed to develop a hypoallergenic, dysphagia-friendly matrix using pea protein. We investigated the effects of three hydrocolloid thickeners—xanthan gum (XG), guar gum (G), and carrageenan (C) at various concentrations on the beverage's rheological properties, textural characteristics, and dysphagia diet classification. The unthickened pea protein base was unstable, exhibiting rapid phase separation and low viscosity, unsuitable for dysphagia diets. The addition of XG (0.4-0.6 g), G (0.5-1.0 g), and C (0.8-1.2 g) successfully produced matrices meeting the slightly, mildly, and moderately thick levels of the Japanese Society of Dysphagia Rehabilitation (JSDR) framework. However, discrepancies were noted between instrumental viscosity and syringe flow test classifications. Rheological analysis revealed that XG samples were predominantly elastic (G' > G") in the linear visco-elastic region (LVR) and exhibited shear-thinning behavior. In contrast, G and C samples were predominantly viscous (G" > G'). Frequency sweeps characterized XG samples as weak gels, G samples as dilute polymer solutions, and C samples as gel-like structures. Texture profile analysis further showed that xanthan gum imparted the highest firmness and thickness, whereas guar gum provided the best flowability.

Abstract: While phosphatidylserine (PS) is recognized for its neuroprotective properties, the effects of PS purity on human cortical neurons remains unexplored. This study investigates three different PS purities (15 µM of 50%, 70%, and 80%) on neuronal health using human embryonic stem cell-derived cortical neurons. Our findings reveal that higher PS purity enhances the expression of key regulatory proteins SIRT1 and PGC-1α, known for their roles in neuroprotection and mitochondrial function. Specifically, 80% purity PS significantly increases SIRT1 and PGC-1α levels, suggesting that PS purity strengthens neuroprotective pathways and improves mitochondrial quality control. Through SIRT1 knockdown experiments, we demonstrate that PS-induced upregulation of PGC-1α is SIRT1-dependent, highlighting a SIRT1-PGC-1α regulatory axis that enhances mitochondrial health. In an amyloid-beta (Aβ42)-induced Alzheimer’s disease (AD) model, PS treatment, particularly at 70% and 80% purity, reduced cytotoxicity and countered the Aβ42-induced downregulation of SIRT1 and PGC-1α, indicating PS’s role in preserving neuronal viability and combating AD-like pathology. Further analyses showed that PS purity modulates mitochondrial fission and fusion gene expression, which are often dysregulated in neurodegenerative diseases, thereby restoring mitochondrial integrity and reducing oxidative stress. These results emphasize the importance of PS purity in human cortical neuron models and suggest that PS, as a nutritional supplement or a potential treatment for early Alzheimer’s patients, could be applied effectively in neurodegeneration strategies, targeting mitochondrial dysfunction.

Abstract:

The age-related chronic, low-grade inflammation known as inflammaging contributes to tissue damage and disease. In the lungs inflammaging leads to abnormal tissue remodeling, reduced function, and decreased immunity. A key factor in inflammaging is declining acetylcholine signaling, which normally suppresses inflammation and promotes tissue repair. We tested whether increasing acetylcholine responsiveness could reverse age-related lung damage. Aged mice were treated with donepezil to increase acetylcholine availability. After six months blood oxygen saturation and voluntary activity were significantly improved. Histologically, treated mice showed reversal of alveolar enlargement (a hallmark of emphysema) and complete restoration of elastic fibers. Donepezil treatment also dramatically increased bronchus-associated lymphoid tissue (iBALT) formation. iBALT is the repository of tissue resident memory lymphocytes, including memory cholinergic lymphocytes that produce acetylcholine to suppress inflammation during secondary infections. The age-related loss of iBALT contributes to the increased risks associated with respiratory infection in the elderly. This indicates age-related lung function and respiratory immune deficits can be modulated by improving acetylcholine signaling. Repurposing an approved medication provides a direct pathway to clinical application for improving respiratory health and infection resistance during aging.

Abstract: BackgroundVertebral fractures are among the most common and clinically important outcomes of osteoporosis in older adults. They significantly contribute to pain, functional limitations, and a decline in quality of life. A significant proportion of these fractures remain clinically silent or present with vague symptoms, which often delays diagnosis. As a result, imaging plays a central role in detection. Distinguishing uncomplicated osteoporotic fractures from those caused by malignancy or infection is essential, as missed or delayed recognition may lead to inappropriate management and avoidable neurological complications.AimThis review aims to outline the typical radiological patterns of vertebral fractures in the elderly and to highlight key imaging “red flag” features that raise suspicion of secondary pathology or structural instability.MethodsA narrative review of the literature was conducted, drawing on published studies that address the epidemiology, imaging appearances, and management of vertebral fractures. The discussion focuses on the role of PET/CT, computed tomography, magnetic resonance imaging, nuclear medicine, and PET/CT, with particular attention to imaging features that help distinguish benign osteoporotic fractures from pathological fractures.ResultsPlain radiographs are useful for identifying vertebral deformity but have limited value in differentiating acute from chronic fractures. Computed tomography allows a more accurate assessment of cortical disruption, fracture morphology, and retropulsed fragments. Magnetic resonance imaging remains the reference standard for characterising vertebral fractures, as marrow signal changes, soft-tissue components, and posterior element involvement reliably separate benign from malignant causes. Nuclear medicine studies assist in assessing fracture chronicity, while PET/CT helps differentiate metastatic disease from benign lesions. Imaging features that should prompt concern include paraspinal soft-tissue masses, involvement of posterior elements, multiple contiguous vertebral lesions, and a convex posterior vertebral body margin.ConclusionCareful recognition of typical imaging patterns and associated red flag signs is fundamental in differentiating benign osteoporotic vertebral fractures from secondary causes. Accurate and timely diagnosis helps in appropriate management, minimises neurological complications, and ultimately improves outcomes in elderly patients.

Abstract: Liver fibrosis, the progressive accumulation of scar tissue resulting from chronic liver disease, is increasingly recognized as a multi-system condition whose effects transcend the liver, affecting brain health. In parallel, dementia determining progressively impaired cognition severe enough to impede daily functioning, is a significant global health issue whose risk factors and pathogenic precursors are incompletely defined. Increasing evidence suggests that certain pathophysiological correlates of chronic liver disease may negatively affect neuronal health through incompletely defined pathophysiological mechanisms. With this background, we appraise our current understanding of the relationship between liver fibrosis and cognitive impairment/dementia, using a variety of different methodologies. Firstly, the pathophysiology and clinical significance of liver fibrosis are discussed. Next, we describe the various types of dementia and related risk factors. We then present research evidence supporting the association between cognitive impairment/dementia and liver fibrosis. We highlight both consistency and heterogeneity of findings, including the degree of association being affected by liver fibrosis severity. We thoroughly examine potential causal mechanisms, comprising the role of chronic systemic and neuroinflammation, insulin resistance, vascular dysfunction, and intestinal microbiota-liver-brain axis as potential connectors of liver health with cognitive impairment and dementia. We briefly analyze how sex and age may modify the above associations, how liver fibrosis and cognitive function should be diagnosed, and those potential preventive/treatment strategies based on the shared metabolic/inflammatory pathways associating liver fibrosis, cognitive impairment and dementia. Finally, major research gaps are identified, together with matching proposals for prioritizing advancements in our understanding of the increasingly identified connections between liver fibrosis and dementia/cognitive impairment.

Abstract: The order in which anti-aging interventions are administered determines their effectiveness. This paper identifies a specific twelve-week sequence—NAD+ restoration followed by rapamycin followed by senolytics—that outperforms simultaneous administration of the same compounds. The sequence succeeds because aged cells lack the energy reserves to execute multiple repair processes simultaneously. NAD+ restoration rebuilds cellular energy capacity. Rapamycin activates autophagy once energy is available. Senolytics eliminate senescent cells once the tissue can process the resulting debris. Each phase prepares the cellular environment for the next. Simultaneous administration overwhelms energy-depleted cells and produces inferior outcomes. This finding reframes combination longevity therapy: intervention sequence matters as much as intervention selection.

Abstract: The pursuit of extending human healthspan and lifespan has become a central focus in modern biomedical research. Aging is a complex, multifactorial process influenced by genetics, epigenetics, environmental factors, and stochastic molecular events. Traditional approaches, relying on observational studies or single-omic analyses, have provided limited mechanistic insights into the determinants of longevity. Recent advances in multi-omics, genome editing, and artificial intelligence (AI) now offer a transformative framework for predictive and personalized longevity research. In particular, the integration of AI-driven computational modeling, CRISPR-based genome engineering, and comprehensive multi-omic datasets holds the promise of elucidating key molecular drivers of aging and informing targeted interventions.

Abstract: Microglia are a key brain cell population pivotal for homeostasis, and in brain aging and neurodegeneration they exhibit both adaptive phagocytic and maladaptive proinflammatory responses. To understand this dynamics, I independently analyzed five human datasets, totaling 83,190 microglial nuclei and covering Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, frontotemporal lobar degeneration, and aging, as well as one Macaca fascicularis hippocampal aging dataset with 39,589 nuclei. Homeostatic microglia subpopulations in humans exhibited marked heterogeneity in GRID2 and CCDC26 expression. The expansion of GPNMB/IQGAP2-expressing clusters of phagocytic microglia was found to be the most conservative and reproducible response of microglia across pan-neurodegenerative conditions and aging, and the gene PTPRG from this signature was reproducibly evelated in pseudobulk; notably, the entire GPNMB⁺ signature is highly restricted to perivascular macrophages in macaques. Microglia subpopulations expressing ribosomal genes at high levels, along with FTL/H1, C1QA/B/C, TPT1, PLEKHA7, etc., although sometimes considered pathogenic, tended to be youth/health-enriched, and their coexpression modules were strongly increased in young and healthy samples. I also observed ST18⁺ and NRG3⁺ subpopulations, which reproduced across all human datasets and in monkeys, although their nature is not yet completely understood: some marker genes arise from myelin phagocytosis (e.g., ST18), while others may reflect intrinsic microglial expression (e.g., PCDH9). Gene coexpression network analysis revealed SORL1, MAML3, ELMO1, MEF2A/C, ADAM28, ABCC4, and several other genes as key putative regulators of evolutionarily conserved homeostatic modules, while identifying TANC2, NHSL1, FMN1, ETV6, and particularly DPYD as potential central players in activation-related networks. Transcriptional factor analysis revealed FOXP1 as a positive regulator of activation-related genes (e.g., DPYD and LRRK2), highlighted the role of TCF4/12 in activation (via TMEM163 and LRRK2), showed MITF and POU3F1 as regulators of numerous genes within the GPNMB-IQGAP2 signature, and identified FOXP2, FOXN3, FLI1, and KLF12 as key homeostatic regulators, alongside the well-studied MEF2A/C. Although many of these results are highly preliminary, this may shed light on microglial physiology in health and disease.

Abstract: We recently published that phycocyanin, a phycobiliprotein which accounts for up to 20% of Arthrospira platensis dry weight, has a powerful anti-aging effect, greatly extending the chronological life span (CLS) of yeast cells grown in synthetic-defined medium, both under caloric restriction (CR) conditions (0.2% glucose) or under non-CR conditions (2% glucose). In this study, to explore the molecular mechanisms underlying the effects of phycocyanin, we investigated its impact on key signalling pathways involved in aging. Specifically, we performed CLS experiments using ras2Δ and snf1Δ yeast mutants. The Snf1 pathway is known to promote longevity (anti-aging), whereas the Ras2/PKA pathway accelerates aging (pro-aging). We show that, while in the snf1 mutant the anti-aging effect of phycocyanin was still evident, in the ras2Δ mutant phycocyanin did not appear to exert any anti-aging activity, suggesting that the Ras2/PKA pathway may be essential for mediating the anti-aging effect of phycocyanin. To evaluate the activity of phycocyanin under different nutritional conditions, we performed the CLS experiment in a YPDA rich medium. We show that in this medium phycocyanin accelerated the chronological aging of yeast cells, greatly decreasing the CLS, both when glucose was present at low (0.2%) or at high (2%) concentration. Our data suggest that Saccharomyces cerevisiae could serve as a model not only to investigate the anti-aging properties and targets of phycocyanin, but also its potential side effects, possibly present in higher eukaryotes under certain conditions.

Abstract: Recent advances in large language models (LLMs) have unlocked new possibilities for scientific discovery, yet most remain limited to text summarization or hallucination-prone dialogue. Here, we present LongevityLLM—a function-driven AI agent engineered to execute real, reproducible analyses in structural bioinformatics, comparative genomics, and aging biology. Unlike conventional chatbots, LongevityLLM maps natural language queries to deterministic bioinformatics pipelines, producing structured outputs (FASTA, PDB, XLSX, phylogenetic trees, aging clock reports) while grounding all responses in empirical data. The system retrieves and summarizes scientific information from peer-reviewed literature (via Europe PMC) and biological databases (e.g., UniProt). It integrates five major epigenetic clocks—Horvath, Hannum, PhenoAge, Brunet, and Wyss-Coray—as well as AlphaFold2-based structural mutation impact prediction, cross-species ortholog retrieval with phylogenetic analysis, and curated mammalian life-history traits from the AnAge database and incorporates a time-calibrated mammalian phylogeny and the AROCM (Average Rate of Change in Methylation) metric—a cross-species epigenetic biomarker of aging derived from conserved CpG sites. Built on open-source tools and designed for full auditability, LongevityLLM enables researchers to explore questions such as “How is IFI27 implicated across different aging clock models?” or “What is the structural effect of the IL17A-E100K mutation?” through a single natural language query, without compromising scientific rigor. We release LongevityLLM as an open framework to accelerate hypothesis generation, education, and collaborative geroscience.

Abstract: Aging is not an immutable fate but a malleable biological process driven by interconnected molecular, cellular, and systemic failures. While modern medicine excels at managing acute conditions, it largely fails to address the root cause of most chronic diseases – aging itself. In this review, I synthesize current evidence that aging arises from the interplay of stochastic damage and evolutionarily shaped regulatory programs (exemplified by conserved parameters such as AROCM) and manifests through the hallmarks of aging, including genomic instability, proteostatic collapse, mitochondrial dysfunction, cellular senescence, and inflammaging, ultimately driving chronic disease across organ systems. I argue that defeating aging requires a strategic shift from symptom palliation to restoration of youthful function, achieved through three synergistic pillars: (1) elimination of damage (e.g., senolytics, monoclonal antibodies against pathogenic immune clones or DAMPs), (2) reactivation of endogenous repair mechanisms (e.g., caloric restriction, metformin, GLP-1 agonists, transient OSK expression), and (3) cell, tissue, and organ replacement (e.g., stem cell–derived islets, FOXO3-enhanced MSCs). I highlight evolutionary insights from long-lived species, the centrality of chronic inflammation and fibrosis in age-related disease, and the transformative role of AI: from multi-omic aging clocks to agentic systems for target discovery and personalized longevity medicine. The tools to initiate this paradigm shift are already emerging; what is needed now is scientific rigor, interdisciplinary integration, and a collective commitment to treating aging as the fundamental driver of human morbidity and mortality.

Abstract: Cognitive disorders present significant medical and social challenges nowadays, due to their high prevalence, progressive course and a lack of effective methods for treatment of neurodegenerative diseases and comorbid pathologies. An important path for solving this problem is the search for reliable biomarkers that allow for early and differential diagnosis, especially in view of the similarity between clinical manifestations of different forms of dementia. This study provides an overview of the most relevant signaling molecules for diagnosing cognitive disorders. It presents data on the effectiveness of using comprehensive panels of molecular biomarkers in clinical practice, including β-amyloid, CD34, claudin, DRP1, endothelin-1, NF-kB, PINK1, RAGE, S100, α-synuclein, and tau protein, in patients with Alzheimer's disease (AD) and vascular dementia (VD). The study results demonstrate a high diagnostic relevance of the combined use of signaling molecules as a biomarker panel for screening and differentiating neurodegenerative diseases.

Abstract: Cellular senescence is driven by DNA damage, telomere attrition, and metabolic/mitochondrial stress, culminating in a state of durable proliferative arrest accompanied by a senescence-associated secretory phenotype (SASP) that amplifies inflammation and paracrine remodeling across tissues, thereby accelerating functional decline and age-related pathologies. This review examines the molecular mechanisms and in vivo activities of procyanidin C1 (PCC1), a natural dualmode senotherapeutic. Its dual behavior is characterized by an early or lowdose phase in which PCC1 attenuates selected NFκB–driven SASP components while stabilizing redox and bioenergetic homeostasis; under high senescent burden or tumor-associated stress, elevated doses of PCC1 enable the selective reduction of refractory senescent cells and mitigation of pro-tumorigenic SASP outputs, concomitant with modulation of immune infiltration and metabolic reprogramming. PCC1 further exhibits pronounced anti-inflammatory and anti-tumor potential by reshaping inflammatory and chemotactic gradients within the tumor microenvironment. Reflecting broad multi-organ geroprotective activity, PCC1 can exert antioxidative, mitochondrial-supportive, and anti-fibrotic modulation in cardiovascular/metabolic tissues, skin, liver, kidney, and neural niches. Compared with BCL-2 inhibitors or multi-kinase senolytics, PCC1 shows lower cytotoxicity toward normal proliferating cells and fewer indications of platelet or hematopoietic suppression, with its staged regulatory profile and natural scaffold suggesting a wider therapeutic window. Future priorities include quantifying dose–timing transition thresholds, establishing integrated biomarker panels, and optimizing delivery strategies to define its translational potential in precision, phase-adapted senescence and tumor microenvironment interventions.

Abstract: What is the ultimate goal of biogerontology (the study of the biology of aging)? Ask a biogerontologist and a common answer these days is that it is to extend healthspan rather than lifespan. But is this really a coherent aim for the field? Here we argue that it is not.

Abstract: Research into longevity and aging involves comparing the size of cohorts at certain points on survival curves. However, this analysis is oversimplified because it provides limited information about the sample structure and the distribution of lifespan as a trait within the studied population. Here, we introduce a method for estimating lifespan across the entire data range using distribution analysis. More specifically, we propose dividing the lifespan series into intervals, obtaining the frequencies of phenotypes by lifespan within the sample, followed by distribution analysis using the normality crite-rion. Additionally, to visualize the differences, we propose describing the resulting distributions formally using the normal distribution function and the β-function. We demonstrate that the proposed methodology enables to extract additional information from survival data, providing new insights into the processes that occur in populations in response to genetic interventions and shedding light on their impact on ontogenesis. The proposed approach adds a new layer of information to studies of longevity and aging and expands the toolkit of methods used to analyze survival data.