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The accumulation of senescent cells drives inflammaging and increases morbidity of chronic inflammatory lung diseases. Immune responses are built upon dynamic changes in cell metabolism that supply energy and substrates for cell proliferation, differentiation, and activation. Metabolic changes imposed by environmental stress and inflammation on immune cells and tissue microenvironment are thus chiefly involved in the pathophysiology of allergic and other immune‐driven diseases. Altered cell metabolism is also a hallmark of cell senescence, a condition characterized by loss of proliferative activity in cells that remain metabolically active. Accelerated senescence can be triggered by acute or chronic stress and inflammatory responses. In contrast, replicative senescence occurs as part of the physiological aging process and has protective roles in cancer surveillance and wound healing. Importantly, cell senescence can also change or hamper response to diverse therapeutic treatments. Understanding the metabolic pathways of senescence in immune and structural cells is therefore critical to detect, prevent, or revert detrimental aspects of senescence‐related immunopathology, by developing specific diagnostics and targeted therapies. In this paper, we review the main changes and metabolic alterations occurring in senescent immune cells (macrophages, B cells, T cells). Subsequently, we present the metabolic footprints described in translational studies in patients with chronic asthma and chronic obstructive pulmonary disease (COPD), and review the ongoing preclinical studies and clinical trials of therapeutic approaches aiming at targeting metabolic pathways to antagonize pathological senescence. Because this is a recently emerging field in allergy and clinical immunology, a better understanding of the metabolic profile of the complex landscape of cell senescence is needed. The progress achieved so far is already providing opportunities for new therapies, as well as for strategies aimed at disease prevention and supporting healthy aging. [ABSTRACT FROM AUTHOR]

The composite interlamination is the key part of load transfer and plays a decisive role in the overall mechanical performance of composite structures. The interlaminar property is predominantly influenced by the matrix resin which is easily affected by the hygrothermal environment. This paper delved into the effect of hygrothermal aging duration on the interlayer debonding behavior of unidirectional (UD) laminates. The pre‐cracked specimens were treated by hygrothermal aging with a period of 0, 15, 30, 60, 90, and 120 days. The double cantilever beam (DCB) tests were employed to evaluate the interlaminar property. The effect of hygrothermal aging on load–displacement responses, R‐curves, crack growth speed, and fracture surface topography was analyzed. The results revealed that the load‐bearing capacity of aged specimens presented a reduction of 18.6%–29.0% compared with unaged ones. The interlaminar fracture toughness of specimens subjected to 15 days of treatment decreased significantly compared with that of unaged specimens due to the increase of water absorption caused by hygrothermal aging. With the increase in hygrothermal aging time, the interlaminar fracture toughness peaked at 60 days because of the post‐curing effect, followed by a declining trend influenced by the dominant hygrothermal aging effect. The fiber bridging of aged samples was increasingly obvious, became the most prominent at 60 days, and then gradually reduced. The fiber bridging diminished the crack propagation speed, hindered interlaminar debonding, and contributed to the interlaminar toughening. Highlights: The samples underwent hygrothermal aging for 0, 15, 30, 60, 90, and 120 days.Load ability of aged samples was at least 18.6% lower than that of unaged ones.R‐curves rose before the crack length of 79 mm and then tended to stabilize.Fracture toughness first decreased, then increased and reduced with aging time.Fiber bridging could hinder crack growth and improve the interlayer property. [ABSTRACT FROM AUTHOR]

The glymphatic system is cerebrospinal fluid–brain tissue fluid exchange flow mediated by aquaporin‐4 (AQP4) on the end feet of astrocytes for a system, which is capable of rapidly removing brain metabolites and thus maintaining brain homeostasis, and is known as the central immune system. Dysfunction of the glymphatic system causes accumulation of misfolded and highly phosphorylated proteins (amyloid‐β and Tau proteins), which destabilizes the proteins, and the body's neuroinflammatory factors are altered causing aging of the immune system and leading to neurodegenerative diseases. Damage to the glymphatic system and aging share common manifestations, as well as unstudied biological mechanisms that are also linked, such as mitochondria, oxidative stress, chronic inflammation, and sleep. In this paper, we first summarize the structure, function, and research methods of the glymphatic system and the relationship between the glymphatic system and the peripheral immune system, and second, sort out and summarize the factors of the glymphatic system in removing metabolites and resolving aging‐related diseases and factors affecting aging, to explore its related biological mechanisms, and moreover, to provide a new way of thinking for treating or intervening aging‐related diseases. [ABSTRACT FROM AUTHOR]

The central nervous system (CNS) is widely recognized as the only organ system without lymphatic capillaries to promote the removal of interstitial metabolic by‐products. Thus, the newly identified glymphatic system which provides a pseudolymphatic activity in the nervous system has been focus of latest research in neurosciences. Also, findings reported that, sleep stimulates the elimination actions of glymphatic system and is linked to normal brain homeostatis. The CNS is cleared of potentially hazardous compounds via the glymphatic system, particularly during sleep. Any age‐related alterations in brain functioning and pathophysiology of various neurodegenerative illnesses indicates the disturbance of the brain's glymphatic system. In this context, β‐amyloid as well as tau leaves the CNS through the glymphatic system, it's functioning and CSF discharge markedly altered in elderly brains as per many findings. Thus, glymphatic failure may have a potential mechanism which may be therapeutically targetable in several neurodegenerative and age‐associated cognitive diseases. Therefore, there is an urge to focus for more research into the connection among glymphatic system and several potential brain related diseases. Here, in our current review paper, we reviewed current research on the glymphatic system's involvement in a number of prevalent neurodegenerative and neuropsychiatric diseases and, we also discussed several therapeutic approaches, diet and life style modifications which might be used to acquire a more thorough performance and purpose of the glymphatic system to decipher novel prospects for clinical applicability for the management of these diseases. Key points: Age‐associated dementia is growing rapidly leading to various neurological diseases and is currently one of the prime reasons for diseases and related morbidity which impacts a wide range of populations.Recently discovered glymphatic system, through which CNS is cleared of potentially harmful substances and plays a significant role in modulating various neurodegenerative and neuropsychiatric illnesses.To avert these diseases various natural interventions like traditional herbal medicine, non‐invasive neurological stimulation, regular sleep cycle and dietary additives may ameliorate disease pathogenesis by improving glymphatic activity are recently identified.Furthermore, investigations are going on the role of nutrigenomics and micronutrients in boosting the activity of glymphatic clearance in various neurological diseases. [ABSTRACT FROM AUTHOR]

Findings from the Study of Muscle, Mobility and Aging (SOMMA) in this issue of Aging Cell show that several biological pathways in skeletal muscle cells play an important role in determining mobility in older adults. These are based on assays in skeletal muscle biopsies obtained from participants, aged 70 years and older in SOMMA tested for association with assessments related to mobility, including muscle mass, strength, power, cardiopulmonary fitness, and 400 m walking speed. The papers show that, using mass spectrometry, oxidative modifications of proteins essential to myocellular function are associated with poorer mobility. Using RNA‐seq to quantify gene expression, lower levels of expression of antioxidant enzymes located in mitochondria, autophagy, patterns of expression of genes involved in autophagy, and higher levels of RNA transcripts that increase with denervation were associated with poorer performance on tests of mobility. These results extend previous research from the Baltimore Longitudinal Study of Aging and recent studies from SOMMA showing the importance of mitochondrial energetics in mobility. Together, these findings are painting a picture of how fundamental cellular processes influence the loss of mobility with aging. They may also be a window on aging in other cells, tissues, and systems. The data collected in SOMMA are publicly available and SOMMA welcomes collaborations with scientists who are interested in research about human aging. [ABSTRACT FROM AUTHOR]

The development of advanced practice nursing has evolved globally over the past decades and has become an important component in the contemporary healthcare system. The term 'advanced practice nurse' is used to refer to nurses practising at a higher level than traditional nurses and is defined as a registered nurse who has acquired the expert knowledge base, complex decision‐making skills and clinical competencies for expanded practice. In 2003, Singapore embarked on the development of advanced practice nurses as an initiative to improve the nursing professional image, retain excellent clinical nurses and fill the gaps in the provision of healthcare services for the ageing population. This paper documents Singapore's journey of advanced practice nursing development and shares our unique learning experience in the aspects of education, certification, registration and scope of practice. [ABSTRACT FROM AUTHOR]

As people age, there is a natural decline in cognitive functioning and brain structure. However, the relationship between brain function and cognition in older adults is neither straightforward nor uniform. Instead, it is complex, influenced by multiple factors, and can vary considerably from one person to another. Reserve, compensation, and maintenance mechanisms may help explain why some older adults can maintain high levels of performance while others struggle. These mechanisms are often studied concerning memory and executive functions that are particularly sensitive to the effects of aging. However, language abilities can also be affected by age, with changes in production fluency. The impact of brain changes on language abilities needs to be further investigated to understand the dynamics and patterns of aging, especially successful aging. We previously modeled several compensatory profiles of language production and lexical access/retrieval in aging within the Lexical Access and Retrieval in Aging (LARA) model. In the present paper, we propose an extended version of the LARA model, called LARA‐Connectivity (LARA‐C), incorporating recent evidence on brain connectivity. Finally, we discuss factors that may influence the strategies implemented with aging. The LARA‐C model can serve as a framework to understand individual performance and open avenues for possible personalized interventions. [ABSTRACT FROM AUTHOR]

Current research on human aging has largely been guided by the milestone paper "hallmarks of aging," which were first proposed in the seminal 2013 paper by Lopez‐Otin et al. Most studies have focused on one aging hallmark at a time, asking whether the underlying molecular perturbations are sufficient to drive the aging process and its associated phenotypes. More recently, researchers have begun to investigate whether aging phenotypes are driven by concurrent perturbations in molecular pathways linked to not one but to multiple hallmarks of aging and whether they present different patterns in organs and systems over time. Indeed, preliminary results suggest that more complex interactions between aging hallmarks must be considered and addressed, if we are to develop interventions that successfully promote healthy aging and/or delay aging‐associated dysfunction and diseases. Here, we summarize some of the latest work and views on the interplay between hallmarks of aging, with a specific focus on mitochondrial dysfunction. Indeed, this represents a significant example of the complex crosstalk between hallmarks of aging and of the effects that an intervention targeted to a specific hallmark may have on the others. A better knowledge of these interconnections, of their cause‐effect relationships, of their spatial and temporal sequence, will be very beneficial for the whole aging research field and for the identification of effective interventions in promoting healthy old age. [ABSTRACT FROM AUTHOR]

Background: Vocabulary scores increase until approximately age 65 years and then remain stable or decrease slightly, unlike scores on tests of other cognitive abilities that decline significantly with age. Aims: To review the findings on ageing‐related changes in vocabulary, and to discuss four methodological issues: research design; test type; measurement; and vocabulary ability as a proxy for general intelligence. Main Contribution: A discussion of cross‐sectional and longitudinal research designs shows that cohort membership accounts for some but not all ageing‐related changes in vocabulary, and that drop‐out and test–retest effects do not alter conclusions regarding these changes. Test type affects age trends in vocabulary, and if researchers use only one test, they should choose a multiple‐choice synonym test. While some authors suggest that vocabulary tests do not measure the same underlying ability in younger and older adults, more research of this suggestion is needed. A brief examination of the use of vocabulary ability as a proxy for general intelligence in healthy ageing and for premorbid abilities in dementia indicates that such practice is often questionable. Conclusions: Vocabulary knowledge increases through the mid‐60s regardless of measurement method. However, there is little information on how word knowledge serves other verbal skills in old age, how and when adults learn new words, or how much exposure is necessary for meanings to remain in storage for a lifetime. Research of these issues may require new methodologies, as well as novel theoretical accounts of ageing‐related effects on vocabulary. WHAT THIS PAPER ADDS: What is already known on this subject: Unlike many cognitive abilities that decline with ageing, vocabulary knowledge continues to increase until approximately age 65, and then remains stable or decreases slightly. These findings have been replicated in different research designs and across languages. What this paper adds to existing knowledge: The article presents a summary of findings on changes in vocabulary across adulthood, and a discussion of four key methodological issues: research design, test type, measurement, and the use of vocabulary ability as a proxy for general intelligence. What are the potential or actual clinical implications of this work?: To better understand changes in vocabulary knowledge across adulthood, clinicians must be aware of methodological considerations that affect the field. Such considerations have direct clinical implications regarding the choice of vocabulary tests and their use as a proxy for other abilities in both healthy older adults and in individuals with dementia. [ABSTRACT FROM AUTHOR]

Background Purpose Methods Results Conclusions Cushing's Disease (CD) is a rare clinical syndrome characterized by excessive secretion of adrenocorticotrophic hormone, leading to significant functional and structural brain alterations as observed in Magnetic Resonance Imaging (MRI). While traditional statistical analysis has been widely employed to investigate these MRI changes in CD, it has lacked the ability to predict individual‐level outcomes.To address this problem, this paper has proposed an interpretable machine learning (ML) framework, including model‐level assessment, feature‐level assessment, and biology‐level assessment to ensure a comprehensive analysis based on structural MRI of CD.The ML framework has effectively identified the changes in brain regions in the stage of model‐level assessment, verified the effectiveness of these altered brain regions to predict CD from normal controls in the stage of feature‐level assessment, and carried out a correlation analysis between altered brain regions and clinical symptoms in the stage of biology‐level assessment.The experimental results of this study have demonstrated that the Insula, Fusiform gyrus, Superior frontal gyrus, Precuneus, and the opercular portion of the Inferior frontal gyrus of CD showed significant alterations in brain regions. Furthermore, our study has revealed significant correlations between clinical symptoms and the frontotemporal lobes, insulin, and olfactory cortex, which also have been confirmed by previous studies.The ML framework proposed in this study exhibits exceptional potential in uncovering the intricate pathophysiological mechanisms underlying CD, with potential applicability in diagnosing other diseases. [ABSTRACT FROM AUTHOR]

Living organisms experience a range of stresses. To cope effectively with these stresses, eukaryotic cells have evolved a sophisticated mechanism involving the formation of stress granules (SGs), which play a crucial role in protecting various types of RNA species under stress, such as mRNAs and long non‐coding RNAs (lncRNAs). SGs are non‐membranous cytoplasmic ribonucleoprotein (RNP) granules, and the RNAs they contain are translationally stalled. Importantly, SGs have been thought to contribute to the pathophysiology of neurodegenerative diseases, including Alzheimer's disease (AD). SGs also contain multiple RNA‐binding proteins (RBPs), several of which have been implicated in AD progression. SGs are transient structures that dissipate after stress relief. However, the chronic stresses associated with aging lead to the persistent formation of SGs and subsequently to solid‐like pathological SGs, which could impair cellular RNA metabolism and also act as a nidus for the aberrant aggregation of AD‐associated proteins. In this paper, we provide a comprehensive summary of the physical basis of SG‐enriched RNAs and SG‐resident RBPs. We then review the characteristics of AD‐associated gene transcripts and their similarity to the SG‐enriched RNAs. Furthermore, we summarize and discuss the functional implications of SGs in neuronal RNA metabolism and the aberrant aggregation of AD‐associated proteins mediated by SG‐resident RBPs in the context of AD pathogenesis. Geriatr Gerontol Int 2024; 24: 7–14. [ABSTRACT FROM AUTHOR]

Background and aim: The aim of the present article was to elaborate on a research approach and method called 'lifeworld hermeneutics'. Significant to lifeworld hermeneutics is that interpretation is the main methodological instrument for explaining and understanding existential research questions and lived experiences. From a caring science perspective, this often refers to research that aims to gain a deeper understanding of existential phenomena and issues, such as existential meaning of health, well‐being, homelessness, lostness, suffering and ageing, as well as what it means to experience unhealthiness and illness, the need for care, and caring that responds to such needs. Design: Theoretical paper. Result: The article briefly covers ontology and epistemology that clarifies the meaning and importance of a lifeworld hermeneutic attitude. This is followed by suggestions for how to perform a lifeworld hermeneutic study, expressed in relation to methodological principles for the interpretation, validation and structuring of interpretations. Thereafter, follow reflections on how to use theoretical or philosophical support to develop and deepen existential interpretations. The findings of lifeworld hermeneutic research consist of existential interpretations where the researcher, with an open and pliable attitude towards the phenomenon and the aim of the study, clarifies, explains and suggests new ways of understanding participants' lived experiences; the researcher should maintain such an attitude towards their understanding of the phenomenon as well. Conclusion: The lifeworld hermeneutical approach and method described in this article makes it possible to further deepen the understanding and knowledge about existential issues that is relevant for caring and caring science. [ABSTRACT FROM AUTHOR]

There is strong evidence that most individuals in the elderly population are characterized by inflamm‐aging which refers to a subtle increase in the systemic pro‐inflammatory environment and impaired innate immune activation. Although a variety of distinct factors are associated with the progression of inflamm‐aging, emerging research is demonstrating a dynamic relationship between the processes of cellular senescence and inflamm‐aging. Cellular senescence is a recognized factor governing organismal aging, and through a characteristic secretome, accumulating senescent cells can induce and augment a pro‐inflammatory tissue environment that provides a rationale for immune system‐independent activation of inflamm‐aging and associated diseases. There is also accumulating evidence that inflamm‐aging or its components can directly accelerate the development of senescent cells and ultimately senescent cell burden in tissues in a likely vicious inflammatory loop. The present review is intended to describe the emerging senescence‐based molecular etiology of inflamm‐aging as well as the dynamic reciprocal interactions between inflamm‐aging and cellular senescence. Therapeutic interventions concurrently targeting cellular senescence and inflamm‐aging are discussed and limitations as well as research opportunities have been deliberated. An effort has been made to provide a rationale for integrating inflamm‐aging with cellular senescence both as an underlying cause and therapeutic target for further studies. Significance statement: The present work is aimed at understanding the interactions between cellular senescence and inflamm‐aging that together predispose the elderly to recurring infections and inflammatory disorders. The rationale for viewing these two processes together with their interdependent pathophysiology has been presented. This paper intends to apprise the scientific community of this developing interconnection and underlying disease pathology that may ultimately help identify novel molecular markers and therapeutic targets of inflammatory disorders during aging. [ABSTRACT FROM AUTHOR]

Family quality of life (FQOL) is a multidimensional social construct that can be used to enhance a family's well‐being by providing a framework to plan interventions and evaluate outcomes. Although researchers and policymakers see value in the FQOL domains and dimensions, families and practitioners are often skeptical of lengthy evaluations and aggregate scores. Furthermore, many practitioners find that family caregivers who require support and services overwhelmingly focus on the family member needing the most care. In doing so, they perceive their situations in a "spaghetti‐like" way. This strong focus on one aspect of the situation, or one "spaghetti" strand, can result in conversations about planning and implementing interventions becoming cyclical, like a messy tangle of strands. The FQOL lens can be used in intervention planning to transform overlapping spaghetti‐like thoughts into a waffle‐like system of interconnected and compartmentalized thoughts. The purpose of this paper was to describe the individual‐level application of the FQOL theory to plan and evaluate the benefits of a peer‐mediated family empowerment project for aging caregivers of adults with intellectual/ developmental disabilities in Michigan, USA. The study provides examples of how individual‐level FQOL evaluation at pretest informed the development of individualized action plans that focused on the strengths, desires, and challenges of 100 aging families in this statewide project. [ABSTRACT FROM AUTHOR]

Oxidative stress is an important mechanism of aging, and in turn, aging can also aggravate oxidative stress, which leads to a vicious cycle. In the process of the brain converting light into visual signals, the eye is stimulated by harmful blue‐light radiation directly. Thus, the eye is especially vulnerable to oxidative stress and becomes one of the organs most seriously involved during the aging process. Cataracts, age‐related macular degeneration (AMD), glaucoma, diabetic retinopathy (DR), and dry eye are inextricably linked to the aging process and oxidative stress. Chlorogenic acid (CGA) has been demonstrated to have antioxidant and anti‐inflammatory activities, and its validity has been established experimentally in numerous fields, including cardiovascular disease, metabolic disorders, cancers, and other chronic diseases. There has previously been evidence of CGA's therapeutic effect in the field of ophthalmopathy. Considering that many ophthalmic drugs lead to systemic side effects, CGA may act as a natural exogenous antioxidant for patients to take regularly, controlling their condition while minimizing side effects. In this paper, in vitro and in vivo studies of CGA in the treatment of age‐related eye diseases are reviewed, and the prospects of CGA's antioxidant application for the eye are discussed. The aim of this review is to summarize the relevant knowledge and provide theoretical support for future research. [ABSTRACT FROM AUTHOR]

Background: The global population is ageing rapidly and there is a need for strategies to promote health and wellbeing among older adults. Nutrition knowledge is a key predictor of dietary intake; therefore, effective educational programmes are urgently required to rectify poor dietary patterns. Digital health technologies provide a viable option for delivering nutrition education that is cost‐effective and widely accessible. However, few technologies have been developed to meet the unique needs and preferences of older adults. Objective: The aim of this study was to explore technology use among older adults and qualitatively determine the content needs and design preferences for an online nutrition education resource tailored to older adult consumers in Australia. Methods: Twenty adult participants aged 55 years and older (95% female) participated in one of four 2‐h participatory design workshops. In each workshop, prompted discussion questions were used to explore participants' technology use and preferences and to explore content needs and design preferences for an online nutrition education resource specific to older adults. Results: All participants were regularly using a range of different devices (e.g., smartphones, tablets and computers) and reported being comfortable doing so. Participants wanted a website that provided general nutrition information, practical advice and recipes. To enhance engagement, they sought a personalised resource that could be adjusted to suit their needs, included up‐to‐date information and allowed for easy sharing with others by exporting information as a PDF. Conclusions: Participatory design methods generate new knowledge for designing and tailoring digital health technologies to be appropriate and useful for the target audience. Specifically, older adults seek an online resource that has large and simple fonts with clear categories, providing them with practical advice and general nutrition information that can be personalised to suit their own needs and health concerns, with the option to export and print information into a paper‐based format. Patient or Public Contribution: Older adults actively participated in the development and evaluation process to generate ideas about potential features, functionalities, uses and practicalities of an online nutrition education resource. [ABSTRACT FROM AUTHOR]