The evolutionary biology of aging is fundamental to understanding the mechanisms of aging and how to develop anti-aging treatments. Thus far most evolutionary theory concerns the genetics of aging with limited physiological integration. Here we present an intuitive evolutionary framework built on how physiology is regulated and how this regulation itself is then predicted to age. Life has evolved to secure reproduction and avoid system failure in early life, and it is the physiological regulation that evolves in response to those early life selection pressures that leads to the emergence of aging. Importantly, asymmetrical regulation of physiology will evolve as the Darwinian fitness costs of loss of regulation will not be symmetrical. When asymmetrical regulatory systems break during aging, they cause physiological function to drift towards the physiological range where costs of dysregulation are lowest, rendering aging directional. Our model explains many puzzling aspects of the biology of aging. These include why aging appears (but is not) programmed, why aging is gradual yet heterogeneous, why cellular and hormonal signaling are closely related to aging, the compensation law of
Based on the study of cellular aging using the single-cell model organism of budding yeast and corroborated by other studies, we propose the Emergent Aging Model (EAM). EAM hypothesizes that aging is an emergent property of complex biological systems, exemplified by biological networks such as gene networks. An emergent property refers to traits that a system has at the system level but which its low-level components do not. EAM is based on a quantitative definition of aging using the mortality rate. A biological entity with a constant mortality rate is considered non-aging which is equivalent to a first-order chemical reaction. Aging can be quantitatively defined as an increasing mortality rate over time, corresponding to an organism's increasing chance of dying over time. EAM posits that biological aging can arise at the system level of an organism, even if the system is composed of only non-aging components. EAM is consistent with the observation that aging is largely stochastic, influenced by numerous genes and epigenetic factors, with no single gene or factor known as the bona fide cause of aging. A parsimonious version of EAM can predict the Gompertz model of biological aging
Addressing the unavoidable bias inherent in supervised aging clocks, we introduce Sundial, a novel framework that models molecular dynamics through a diffusion field, capturing both the population-level aging process and the individual-level relative aging order. Sundial enables unbiasedestimation of biological age and the forecast of aging roadmap. Fasteraging individuals from Sundial exhibit a higher disease risk compared to those identified from supervised aging clocks. This framework opens new avenues for exploring key topics, including age- and sex-specific aging dynamics and faster yet healthy aging paths.
Simulating prospective magnetic resonance imaging (MRI) scans from a given individual brain image is challenging, as it requires accounting for canonical changes in aging and/or disease progression while also considering the individual brain's current status and unique characteristics. While current deep generative models can produce high-resolution anatomically accurate templates for population-wide studies, their ability to predict future aging trajectories for individuals remains limited, particularly in capturing subject-specific neuroanatomical variations over time. In this study, we introduce Individualized Brain Synthesis (InBrainSyn), a framework for synthesizing high-resolution subject-specific longitudinal MRI scans that simulate neurodegeneration in both Alzheimer's disease (AD) and normal aging. InBrainSyn uses a parallel transport algorithm to adapt the population-level aging trajectories learned by a generative deep template network, enabling individualized aging synthesis. As InBrainSyn uses diffeomorphic transformations to simulate aging, the synthesized images are topologically consistent with the original anatomy by design. We evaluated InBrainSyn both quantitativ
We investigate the effects of aging in the noisy voter model considering that the probability to change states decays algebraically with age $τ$, defined as the time elapsed since adopting the current state. We study the complete aging scenario, which incorporates aging to both mechanisms of interaction: herding and idiosyncratic behavior, and compare it with the partial aging case, where aging affects only the herding mechanism. Analytical mean-field equations are derived, finding excellent agreement with agent-based simulations on a complete graph. We observe that complete aging enhances consensus formation, shifting the critical point to higher values compared to the partial aging case. However, when the aging probability decays asymptotically to zero for large $τ$, a steady state is not always attained for complete aging.
We introduce the Aging Multiverse, a framework for generating multiple plausible facial aging trajectories from a single image, each conditioned on external factors such as environment, health, and lifestyle. Unlike prior methods that model aging as a single deterministic path, our approach creates an aging tree that visualizes diverse futures. To enable this, we propose a training-free diffusion-based method that balances identity preservation, age accuracy, and condition control. Our key contributions include attention mixing to modulate editing strength and a Simulated Aging Regularization strategy to stabilize edits. Extensive experiments and user studies demonstrate state-of-the-art performance across identity preservation, aging realism, and conditional alignment, outperforming existing editing and age-progression models, which often fail to account for one or more of the editing criteria. By transforming aging into a multi-dimensional, controllable, and interpretable process, our approach opens up new creative and practical avenues in digital storytelling, health education, and personalized visualization.
Aging, understood as the tendency to remain in a given state the longer the persistence time in that state, plays a crucial role in the dynamics of complex systems. In this paper, we explore the influence of aging on coevolution models, that is, models in which the dynamics of the states of the nodes in a complex network is coupled to the dynamics of the structure of the network. In particular we consider the coevolving voter model, and we introduce two versions of this model that include aging effects: the Link Aging Model (LAM) and the Node Aging Model (NAM). In the LAM, aging is associated with the persistence time of a link in the evolving network, while in the NAM, aging is associated with the persistence time of a node in a given state. We show that aging significantly affects the absorbing phase transition of the coevolution voter model, shifting the transition point in opposite directions for the LAM and NAM. We also show that the generic absorbing phase transition can disappear due to aging effects.
We propose a new theory for aging based on dynamical systems and provide a data-driven computational method to quantify the changes at the cellular level. We use ergodic theory to decompose the dynamics of changes during aging and show that aging is fundamentally a dissipative process within biological systems, akin to dynamical systems where dissipation occurs due to non-conservative forces. To quantify the dissipation dynamics, we employ a transformer-based machine learning algorithm to analyze gene expression data, incorporating age as a token to assess how age-related dissipation is reflected in the embedding space. By evaluating the dynamics of gene and age embeddings, we provide a cellular aging map (CAM) and identify patterns indicative of divergence in gene embedding space, nonlinear transitions, and entropy variations during aging for various tissues and cell types. Our results provide a novel perspective on aging as a dissipative process and introduce a computational framework that enables measuring age-related changes with molecular resolution.
Face aging is an ill-posed problem because multiple plausible aging patterns may correspond to a given input. Most existing methods often produce one deterministic estimation. This paper proposes a novel CLIP-driven Pluralistic Aging Diffusion Autoencoder (PADA) to enhance the diversity of aging patterns. First, we employ diffusion models to generate diverse low-level aging details via a sequential denoising reverse process. Second, we present Probabilistic Aging Embedding (PAE) to capture diverse high-level aging patterns, which represents age information as probabilistic distributions in the common CLIP latent space. A text-guided KL-divergence loss is designed to guide this learning. Our method can achieve pluralistic face aging conditioned on open-world aging texts and arbitrary unseen face images. Qualitative and quantitative experiments demonstrate that our method can generate more diverse and high-quality plausible aging results.
Automatically generated software, especially code produced by Large Language Models (LLMs), is increasingly adopted to accelerate development and reduce manual effort. However, little is known about the long-term reliability of such systems under sustained execution. In this paper, we experimentally investigate the phenomenon of software aging in applications generated by LLM-based tools. Using the Bolt platform and standardized prompts from Baxbench, we generated four service-oriented applications and subjected them to 50-hour load tests. Resource usage, response time, and throughput were continuously monitored to detect degradation patterns. The results reveal significant evidence of software aging, including progressive memory growth, increased response time, and performance instability across all applications. Statistical analyzes confirm these trends and highlight variability in the severity of aging according to the type of application. Our findings show the need to consider aging in automatically generated software and provide a foundation for future studies on mitigation strategies and long-term reliability evaluation.
Widespread interest in non-destructive biomarkers of aging has led to a curse of plenty: a multitude of biological ages that each proffers a 'true' health-adjusted age of an individual. While each measure provides salient information on the aging process, they are each univariate, in contrast to the "hallmark" and "pillar" theories of aging which are explicitly multidimensional, multicausal and multiscale. Fortunately, multiple biological ages can be systematically combined into a multidimensional network representation. The interaction network between these biological ages permits analysis of the multidimensional effects of aging, as well as quantification of causal influences during both natural aging and, potentially, after anti-aging intervention. The behaviour of the system as a whole can then be explored using dynamical network stability analysis which identifies new, efficient biomarkers that quantify long term resilience scores on the timescale between measurements (years). We demonstrate this approach using a set of 8 biological ages from the longitudinal Swedish Adoption/Twin Study of Aging (SATSA). After extracting an interaction network between these biological ages, we
File systems must allocate space for files without knowing what will be added or removed in the future. Over the life of a file system, this may cause suboptimal file placement decisions that eventually lead to slower performance, or aging. Conventional wisdom suggests that file system aging is a solved problem in the common case; heuristics to avoid aging, such as colocating related files and data blocks, are effective until a storage device fills up, at which point space pressure exacerbates fragmentation-based aging. However, this article describes both realistic and synthetic workloads that can cause these heuristics to fail, inducing large performance declines due to aging, even when the storage device is nearly empty. We argue that these slowdowns are caused by poor layout. We demonstrate a correlation between the read performance of a directory scan and the locality within a file system's access patterns, using a dynamic layout score. We complement these results with microbenchmarks that show that space pressure can cause a substantial amount of inter-file and intra-file fragmentation. However, our results suggest that the effect of free-space fragmentation on read performan
This chapter demonstrates how computational social science (CSS) tools are extending and expanding research on aging. The depth and context from traditionally qualitative methods such as participant observation, in-depth interviews, and historical documents are increasingly employed alongside scalable data management, computational text analysis, and open-science practices. Machine learning (ML) and natural language processing (NLP), provide resources to aggregate and systematically index large volumes of qualitative data, identify patterns, and maintain clear links to in-depth accounts. Drawing on case studies of projects that examine later life--including examples with original data from the DISCERN study (a team-based ethnography of life with dementia) and secondary analyses of the American Voices Project (nationally representative interview)--the chapter highlights both uses and challenges of bringing CSS tools into more meaningful dialogue with qualitative aging research. The chapter argues such work has potential for (1) streamlining and augmenting existing workflows, (2) scaling up samples and projects, and (3) generating multi-method approaches to address important question
Age progression is defined as aesthetically re-rendering the aging face at any future age for an individual face. In this work, we aim to automatically render aging faces in a personalized way. Basically, for each age group, we learn an aging dictionary to reveal its aging characteristics (e.g., wrinkles), where the dictionary bases corresponding to the same index yet from two neighboring aging dictionaries form a particular aging pattern cross these two age groups, and a linear combination of all these patterns expresses a particular personalized aging process. Moreover, two factors are taken into consideration in the dictionary learning process. First, beyond the aging dictionaries, each person may have extra personalized facial characteristics, e.g. mole, which are invariant in the aging process. Second, it is challenging or even impossible to collect faces of all age groups for a particular person, yet much easier and more practical to get face pairs from neighboring age groups. To this end, we propose a novel Bi-level Dictionary Learning based Personalized Age Progression (BDL-PAP) method. Here, bi-level dictionary learning is formulated to learn the aging dictionaries based o
We explore the aging transition in a network of globally coupled Stuart-Landau oscillators under a discrete time-dependent coupling. In this coupling, the connections among the oscillators are turned ON and OFF in a systematic manner, having either a symmetric or an asymmetric time interval. We discover that depending upon the time period and duty cycle of the ON-OFF intervals, the aging region shrinks drastically in the parameter space, therefore promoting restoration of oscillatory dynamics from the aging. In the case of symmetric discrete coupling (where the ON-OFF intervals are equal), the aging zone decreases significantly with the resumption of dynamism with an increasing time period of the ON-OFF intervals. On the other hand, in the case of asymmetric coupling (where the ON-OFF intervals are not equal), we find that the ratio of the ON and OFF intervals controls the aging dynamics: the aging state is revoked more effectively if the interval of the OFF state is greater than the ON state. Finally, we study the transition in aging using a discrete pulse coupling: we note that the pulse interval plays a crucial role in determining the aging region. For all the cases of discrete
It is now increasingly realized that the underlying mechanism which governs aging (ageing) is a complex interplay of genetic regulation and damage-accumulation. "Aging as a result of accumulation of 'faults' on cellular and molecular levels", has been proposed in the damage (fault)-accumulation theory. However, this theory fails to explain some aging phenotypes such as fibrosis and premature aging, since terms such as 'damage' and 'fault' are not specified. Therefore we introduce some crucial modifications of this theory and arrive at a novel theory: aging of the body is the result of accumulation of Misrepair of tissue. It emphasizes: a) it is Misrepair, not the original damage, that accumulates and leads to aging; and b) aging can occur at different levels, however aging of the body takes place necessarily on the tissue level, but not requiring the aging of cells/molecules. The Misrepair-accumulation theory introduced in the present paper unifies the understanding of the roles of environmental damage, repair, gene regulation, and multicellular structure in the aging process. This theory gives explanations for the aging phenotypes, premature aging, the difference of longevity in d
We simultaneously measure the static friction and the real area of contact between two solid bodies. Under static conditions both quantities increase logarithmically in time, a phenomenon coined aging. Indeed, frictional strength is traditionally considered equivalent to the real area of contact. Here we show that this equivalence breaks down when a static shear load is applied during aging. The addition of such a shear load accelerates frictional aging while the aging rate of the real area of contact is unaffected. Moreover, a negative static shear - pulling instead of pushing - slows frictional aging, but similarly does not affect the aging of contacts. The origin of this shear effect on aging is geometrical. When shear load is increased, minute relative tilts between the two blocks prematurely erase interfacial memory prior to sliding, negating the effect of aging. Modifying the loading point of the interface eliminates these tilts and as a result frictional aging rate becomes insensitive to shear. We also identify a secondary memory-erasure effect that remains even when all tilts are eliminated and show that this effect can be leveraged to accelerate aging by cycling between tw
A long term operation of Multi-Strip Multi-Gap Resistive Plate Chambers (MSMGRPC) with gas mixtures based on C2H2F4 and SF6 leads to aging effects, observed as depositions on the surface of the resistive electrodes. Moreover, enhanced depositions and higher noise rates were evidenced around the nylon spacers used for defining the gas gaps between the resistive electrodes. The aging effects are reflected in an increase of the dark current and dark counting rate, with negative impact on the long term performance of the chamber and data volume in a free running readout mode operation. MSMGRPC prototypes designed with a direct gas flow through the gas gaps and minimization of the number of spacers in the active area were developed as mitigation solution. Prototypes with this new design and different granularities were assembled using fishing line as spacers and investigated for aging effects. Although a significant reduction in the dark current and dark counting rate was evidenced, dark counting rate localized around the fishing line spacers remains. In this paper, a new generation of direct flow chambers based on discrete spacers is presented. The results of their aging investigations
While General Fractional Calculus has successfully expanded the scope of memory operators beyond power-laws, standard formulations remain predominantly restricted to the half-line via Riemann-Liouville or Caputo definitions. This constraint artificially truncates the system's history, limiting the thermodynamic consistency required for modeling processes on unbounded domains. To overcome these barriers, we construct the \textbf{Weighted Weyl-Sonine Framework}, a generalized formalism that extends non-local theory to the entire real line without history truncation. Unlike recent algebraic approaches based on conjugation for finite intervals, we develop a rigorous harmonic analysis framework. Our central contribution is the \textbf{Generalized Spectral Mapping Theorem}, which establishes the Weighted Fourier Transform as a unitary diagonalization map for these operators. This result allows us to rigorously classify and solve distinct physical regimes under a single algebraic structure. We explicitly derive exact solutions for \textit{diffusive relaxation} (governed by Complete Bernstein Functions), \textit{inertial wave propagation} (exhibiting oscillatory dynamics), and \textit{reta
Facial aging is a complex process, highly dependent on multiple factors like gender, ethnicity, lifestyle, etc., making it extremely challenging to learn a global aging prior to predict aging for any individual accurately. Existing techniques often produce realistic and plausible aging results, but the re-aged images often do not resemble the person's appearance at the target age and thus need personalization. In many practical applications of virtual aging, e.g. VFX in movies and TV shows, access to a personal photo collection of the user depicting aging in a small time interval (20$\sim$40 years) is often available. However, naive attempts to personalize global aging techniques on personal photo collections often fail. Thus, we propose MyTimeMachine (MyTM), which combines a global aging prior with a personal photo collection (using as few as 50 images) to learn a personalized age transformation. We introduce a novel Adapter Network that combines personalized aging features with global aging features and generates a re-aged image with StyleGAN2. We also introduce three loss functions to personalize the Adapter Network with personalized aging loss, extrapolation regularization, and