搜索结果：Current aging science

Dry eye disease (DED) is highly prevalent in older adults and represents a growing public health burden in aging societies. Although age is a well-recognized risk factor for DED, it is still often treated as a background variable rather than an active biological driver of disease. Emerging evidence indicates that aging itself promotes progressive structural remodeling and functional decline across multiple ocular surface tissues, giving rise to a distinct, aging-driven DED phenotype. In this review, we synthesize current knowledge on how biological aging disrupts ocular surface homeostasis at tissue, cellular, and molecular levels. We describe age-associated changes in the lacrimal gland (LG), meibomian gland (MG), cornea, and conjunctiva, including secretory cell exhaustion, lipid dysregulation, epithelial barrier impairment, neural degeneration, and goblet cell (GC) loss. These structural changes are tightly linked to core aging mechanisms such as cellular senescence, oxidative stress, mitochondrial dysfunction, inflammaging, neuroendocrine imbalance, and stem/progenitor cell decline. Importantly, these processes interact as an integrated network, creating a self-reinforcing cycle of tear film instability, chronic low-grade inflammation, and impaired tissue repair that differs mechanistically from environmentally induced or autoimmune forms of DED. By reframing aging as a central pathogenic driver and considering age-related DED as a distinct subtype, this perspective highlights the need for mechanism-informed therapeutic strategies. Beyond conventional lubrication and anti-inflammatory therapy, interventions targeting oxidative stress, cellular senescence, inflammaging, neurosensory dysfunction, and hormonal alterations may offer more fundamental disease modification in elderly patients.

The purpose of this paper is to synthesize current mechanistic insights and translational progress on neurocognitive aging after critical illness and to outline a framework for developing neurotherapeutic drugs for clinical application. The method includes a narrative, focused review of clinical studies in patients' neurocognitive symptoms after critical illness, such as sepsis, trauma, and burns, reported up to December 2025. Evidence was organized across domains, including acute systemic inflammation (ASI), communication channels to the central nervous system (CNS), neuroinflammation and neural integrity, autoimmunity in critically ill patients, and potential therapeutic targets and strategies. Acute illness and inflammatory states, including sepsis, trauma, and burns, can lead to accelerated neurocognitive aging, early-onset cognitive impairment, and memory loss. In acute and critical illness, this is attributed to neuroinflammation, microvascular damage, blood-brain barrier (BBB) disruption, and microglial activation resulting from ASI and immune dysregulation. Current research suggests that it also induces cellular senescence, triggering immune dysregulation and subsequent autoimmunity and autoantibody production, contributing to the progression of neurocognitive aging amid chronic low-grade inflammation and inflammaging. These processes affect the function and integrity of the CNS, leading to neurocognitive decline. This review examined the scientific basis for the development of neurocognitive aging after acute illness and how this information may be used to develop potential targets to modulate inflammatory and immune responses and treat this debilitating condition. Such interventions may reduce the burden of senescent cells, mitigate BBB breakdown, restore immune balance, and enhance the brain's neuroplasticity and resilience.

Autism is a lifelong neurodevelopmental condition, yet aging trajectories in autistic adults remain poorly understood. We conducted a systematic review of studies examining age-related cognitive, neural, and physical health outcomes in autistic adults to clarify emerging patterns and identify priority areas for future research. A systematic search of PubMed, PsycINFO, and Web of Science identified 56 eligible studies that included autistic adults and provided either longitudinal data or explicit age-by-diagnosis comparisons. Findings were synthesized separately by domain. Current evidence does not support globally accelerated or attenuated aging in autism. Most objective cognitive measures showed comparable age-related patterns across autistic and non-autistic adults, although subjective cognitive complaints were consistently elevated. Neuroimaging findings were similarly mixed. Most studies reported no structural or functional differences, though some found evidence of vulnerability in white matter microstructure. Physical health studies more consistently identified elevated rates of neurodegenerative diseases, sensory impairments, and musculoskeletal conditions, but comparable or lower rates for cancer. Cardiovascular findings were complex, with lower hypertension rates but higher rates of severe outcomes such as heart failure and stroke, suggesting gaps in early detection and preventive care. Rather than generalized accelerated aging, findings point toward targeted vulnerabilities in autism. Subjective cognitive complaints, white matter integrity, and elevated neurodegeneration rates represent the clearest targets for future surveillance. Critically, existing research almost exclusively involves autistic adults without intellectual disability, limiting generalizability. Advancing the field requires longitudinal designs, more inclusive samples, and a shift from group-level comparisons toward understanding within-group heterogeneity and individual risk profiles.

Aging-related diseases impose an escalating burden on global healthcare, with their pathogenesis closely linked to dysregulation of molecular metabolism, characterized by the accumulation of harmful metabolites, including reactive oxygen species and glucose, alongside the depletion of essential metabolites such as nicotinamide adenine dinucleotide and glutathione. Over the past decade, artificial metabzymes-particularly nanozymes engineered to catalyze metabolic reactions-have emerged as promising candidates for restoring molecular metabolic homeostasis, offering potential therapeutic avenues for aging-related diseases. Realizing their full potential, however, requires a systematic understanding of aging-associated metabolic abnormalities as well as the chemical design and structure-activity relationships of these materials, which collectively underpin effective molecular metabolism restoration. This review summarizes the chemical design and biomedical applications of nano-engineered artificial metabzymes aimed at restoring molecular metabolism in aging-related diseases. We begin by outlining the key metabolic alterations underpinning these diseases, establishing a rationale for the design of artificial metabzymes. Next, we focus on the chemical designs and catalytic mechanisms of artificial metabzymes, emphasizing their ability to rectify these metabolic imbalances. Furthermore, we summarize recent advances in their applications across a spectrum of aging-related diseases, spanning neurodegenerative, musculoskeletal, cardiovascular, and metabolic diseases. Finally, current challenges and forward-looking perspectives of artificial metabzymes are discussed, aiming to steer future innovations in the development of next-generation artificial metabzymes.

Mitochondria have complex functional and information-processing networks that play key roles in both health regulation and disease progression. However, the multiple properties and complex thresholds of mitochondrial dysfunction and quality control make the contribution of mitochondria to bone aging elusive. These factors prevent mitochondria from being among the most important precision therapies. Currently, many strategies that target mitochondrial homeostasis have entered clinical trials. In mitochondria, mitochondrial DNA (mtDNA) and its associated proteins are potential therapeutic agents for immunometabolic diseases and tissue injury, with the aim of enhancing mitochondrial function. Here, we comprehensively review the intrinsic mechanisms of mitochondrial dysfunction and quality control leading to bone aging and summarize current strategies for the treatment of skeletal aging disorders and the clinical translation of relevant agents in terms of unraveling dysfunctional pathways and developing precision therapies. In this review, we offer a general overview of the progress of clinical application in the treatment of skeletal senescence diseases, and we also provide prospects for the challenges associated with the role of mitochondrial dysfunction in bone senescence in clinical application and future trends in this field.

Nicotinamide (NAM), the amide form of vitamin B3, has gained increasing attention in dermatology due to its potential role in both skin aging and non-melanoma skin cancer (NMSC) prevention. This review summarizes the biological rationale and current clinical evidence supporting the use of NAM and other NAD+ precursors in photoaging and cutaneous carcinogenesis. Chronic ultraviolet exposure induces DNA damage, oxidative stress, inflammation, immune dysregulation, and extracellular matrix remodeling, linking photoaged skin to increased susceptibility to actinic keratoses (AKs), squamous cell carcinoma (SCCs), and basal cell carcinoma (BCCs). Through the NAD+ salvage pathway, NAM contributes to the maintenance of intracellular NAD+ pools, thereby influencing energy metabolism, DNA repair, mitochondrial function, redox homeostasis, and the activity of NAD+-dependent enzymes. Preclinical studies indicate that NAM enhances DNA repair, reduces oxidative stress and inflammatory signaling, supports autophagy and mitophagy, and improves epidermal barrier function and extracellular matrix integrity. Clinically, the strongest evidence for anti-aging effects concerns topical NAM, which consistently improves wrinkles, texture irregularities, pigmentation, and barrier function. Oral NAM has demonstrated chemopreventive activity in high-risk patients with previous NMSC, particularly by reducing the incidence of new SCCs and AKs during active treatment. However, despite a strong mechanistic rationale, current evidence remains heterogeneous, and additional long-term, skin-focused clinical trials are needed to better define efficacy, safety, optimal dosing strategies, and patient selection.

Tremendous electrolyte additives have demonstrated effectiveness in the zinc-ion batteries, however still face the serious issue of trade-off between Zn utilization, areal capacity and anti-calendar aging those are important for practical application. Here, the 3-Cyclohexylamine-2-hydroxypropionic acid (CAPSO) is proposed to address this issue considering its "anchoring-desolvating-shielding" spatially configurated interface layer on the Zn electrode surface. In this interface layer, the sulfonic acid group enables CAPSO molecular strongly anchored on the Zn electrode surface, the amino and hydroxyl groups simultaneously facilitate desolvation and ionic transport, and the hydrophobic carbon ring as the shielding layer to create a local H2O-poor environment. Under these synergistic effects, the Zn electrode demonstrates high stability, high areal capacity, high Zn utilization and anti-calendar aging performance. The symmetric cells show a long lifespan of 700 h at high current density of 20 mA cm-2, 200 h under high areal capacity of 40 mAh cm-2, 150 h at a high Zn utilization of 75% under 5 mA cm-2/5 mAh cm-2, and excellent anti-aging performance of 3000 h at 1 mA cm-2/1 mAh cm-2 with 24 h rest for each cycle; The full cell retains 73.73% of capacity over 200 cycles under low N/P = 2.5.

Researchers now see aging as a process shaped by the interactions among metabolism, epigenetics, and hormones. Recent studies suggest that gut microbes play an important role in this system by making metabolites that can affect gene expression and chromatin structure. Still, it is not fully clear how gut microbes and the body influence each other as we age, since both are constantly changing. This review brings together current research on how metabolites from gut microbes-such as short-chain fatty acids, bile acids, tryptophan derivatives, and polyamines-affect the body's epigenetic machinery through processes such as DNA methylation, histone modifications, and chromatin remodeling. We examine evidence from cell studies, animal experiments, and human research to assess the strength of the links and distinguish direct effects on chromatin from indirect metabolic or gene-expression changes. We focus especially on endocrine and reproductive organs, such as the hypothalamus, pancreas, liver, fat tissue, and cells that support the gonads, where signals from gut microbes overlap with hormonal control and metabolism. In these tissues, microbial metabolites influence key pathways related to inflammation, mitochondria, and nutrient sensing, but there is still little direct evidence in humans. The review also points out differences between lab models and what is observed in patients, highlighting the need for further work to apply these findings in real-world settings. Interactions between gut microbes and epigenetics form a two-way link between metabolism, immunity, and aging of the endocrine system. While more evidence shows that microbial metabolites can shape gene activity and epigenetic patterns, most of what we know comes from animal studies rather than direct tests in people. Moving forward, researchers will need to use broad, long-term studies that combine different types of data to figure out cause and effect and which tissues are involved. Understanding this system better could help create new biomarkers and treatments to influence aging by targeting the microbiome and its effects on epigenetics.

Aging-related cognitive decline is frequently concomitant with systemic metabolic dysregulation. However, the mechanisms linking age-related cognitive decline to systemic metabolic dysregulation remain poorly defined. We collected magnetic resonance imaging (MRI), electroencephalogram (EEG), and serum markers from 193 individuals (135 young adults [94 males] and 58 older adults [29 males]) in a multimodal dataset. Glymphatic system (GS) metrics were assessed indirectly using diffusion tensor image analysis along the perivascular space (DTI-ALPS) index and blood-oxygen-level-dependent cerebrospinal fluid (BOLD-CSF) coupling. EEG data were used to evaluate 40-Hz neural oscillatory dynamics. Partial correlation analyses and moderation analyses were performed to identify relationships among age, GS metrics, serum markers, cognitive performance, and 40-Hz oscillatory dynamics. The MRI metrics of GS activity declined with age in healthy adults. The power of 40-Hz neural oscillations across the whole brain showed a negative correlation with global BOLD-CSF coupling, similar correlations were also observed between regional 40-Hz power and corresponding regional BOLD-CSF coupling in the anterior, middle, and posterior regions of the brain. The MRI metrics of GS activity significantly associated with several serum markers and moderated the relationship between serum markers and cognitive performance. The results established an integrated neurophysiological framework of aging, metabolic dysregulation, gamma oscillation deficits, GS metrics decline, and cognitive decline. These findings emphasize the critical importance of maintaining normal GS function and preserving 40-Hz oscillatory activity in the current landscape of therapeutics targeting age-related cognitive deterioration.

Taurine is a non-proteinogenic β-amino acid that plays fundamental roles in cellular homeostasis. Although it is the most abundant free amino acid in many tissues, the full spectrum of its molecular functions has only recently begun to be elucidated. Taurine supplementation has shown promising outcomes in human studies, with emerging relevance in precision nutrition and the prevention of metabolic and age-related diseases. In this review, we summarize the current knowledge on taurine's molecular mechanisms, including its roles in antioxidant defense, anti-inflammatory signaling, calcium regulation, mitochondrial function, and lipid metabolism. We integrate mechanistic insights with evidence from clinical and nutritional studies examining taurine supplementation in the contexts of oxidative stress, inflammation, metabolic syndrome, and physical performance. Increasing data suggest that taurine can modulate key pathways linked to metabolism, inflammation, and healthy aging. Physiological synthesis and dietary intake appear sufficient to maintain basal health; however, human trials indicate that supplementation of 1-6 g day-1 may further promote metabolic resilience and mitochondrial function without adverse effects. Collectively, these findings position taurine as a promising dietary compound at the interface of metabolism, inflammation, and aging, highlighting its potential as a modulator of healthspan within precision nutrition strategies.

Ribes nigrum L. (Blackcurrant) is a widely cultivated shrub that originated in the temperate and cold regions of the Northern Hemisphere. It has been used for its medicinal properties throughout history and is rich in various bioactive compounds, including polysaccharides. Published studies have shown that R. nigrum polysaccharides (RNPs) are key macromolecules with multiple health-promoting effects, such as antioxidant, anti-diabetic, immunomodulatory, anti-inflammatory, anti-tumor, anti-aging, anti-gout, etc. Although extensive research has been conducted on the extraction and purification methods, structural characteristics, and pharmacological activities of RNPs in the fruits, seeds, and other parts of the plant, knowledge regarding their structure-activity relationships, safety features, and pharmacokinetic behaviors is still limited. This is mainly due to the complex and variable structure of natural polysaccharides, which makes it difficult to precisely characterize them. This review systematically summarizes the latest progress in the extraction, purification, structural characterization, biological activities, and potential applications of RNPs, and discusses the current challenges and future prospects of using them as therapeutic drugs and functional food components. It also points out that future research should combine multiple analytical techniques (such as atomic force microscopy) to address the limitations of current studies.

In 2024, the National Academies of Sciences, Engineering, and Medicine (NASEM) published a report entitled Advancing Research on Chronic Conditions in Women. A major purpose of this report was to summarize the current state of research into a series of 21 chronic conditions that affect women differently or that are more common in women. The American Society for Bone and Mineral Research (ASBMR) established a working group to evaluate the NASEM report's implications for women's MSK health. This perspective summarizes key research gaps identified in the NASEM report, including the lack of sex-specific data, underrepresentation of women in clinical studies, and minimal integration of MSK health with other chronic conditions. The NASEM report underscores the need for more comprehensive study designs that consider hormonal, genetic, and social determinants of health across the lifespan. In addition to osteoporosis, in this perspective, the ASBMR working group highlights emerging but poorly understood evidence of detrimental effects on musculoskeletal biology in non-MSK, chronic diseases that were identified in the NASEM report to disproportionately affect women. To advance the field, we advocate for better diagnostics, increased investment, and stronger representation of women in research studies. Addressing these gaps is critical for improving prevention, care, and outcomes for chronic conditions that uniquely or disproportionately affect women. Chronic health conditions affect women more than men, but past research has often overlooked this fact. In 2024, a national report highlighted how chronic conditions like osteoporosis, back pain and arthritis in women are underfunded and poorly understood. In response, a group from the American Society for Bone and Mineral Research reviewed the report to focus specifically on women’s musculoskeletal health. The report found that women are often not included in clinical studies, and that links between musculoskeletal health and many chronic conditions that impact women’s daily lives, including endometriosis and depression, have not been adequately investigated. In addition, reproductive transitions, such as menopause, are often associated with musculoskeletal symptoms and conditions in addition to osteoporosis, that are poorly understood. Musculoskeletal conditions often start early and last a lifetime, affecting mobility, pain levels, and quality of life. Yet, tools to diagnose, treat, and prevent these chronic conditions are limited. We believe research must do a better job reflecting women’s unique biology and life experiences. This includes ensuring that study participants are representative of the population, identifying better ways to track health over time, and improving access to care. As mobility is central to overall health and disease prevention, we believe that investing in women’s health research—especially in musculoskeletal health—can lead to earlier diagnosis, more effective treatments, cost savings and better lives for millions of women.

Aging is increasingly viewed as an organism-wide process marked by systemic decline and multimorbidity. This Review frames immunosenescence as a context-dependent mediator, amplifier, or consequence of multi-organ dysfunction, integrating niche-centered mechanisms, bidirectional immune-organ interactions, innate-adaptive remodeling, immune-tissue axes, and multidimensional biomarkers. We also highlight current limitations, including context heterogeneity and unresolved causality, and discuss senolytic, senomorphic, and other therapeutic strategies with potential relevance and limitations for healthspan extension.

Screening for cervical cancer using the Papanicolaou (Pap) smear has reduced morbidity and mortality associated with cervical cancer. However, anatomical and hormonal changes with age make diagnosis more complex in elderly women. This narrative review used a structured literature search of databases including PubMed, Scopus, Google Scholar, and ScienceDirect from 2010 to 2024. It included studies related to the impact of age on cervical cytology and HPV prevalence, the importance of cervical sampling adequacy, the diagnostic difficulties encountered in postmenopausal women, and the use of adjunctive cervical screening methods such as liquid-based cytology (LBC), high-risk HPV (HR-HPV) DNA testing, and topical estrogen therapy. Clinical practice guidelines from various organizations, including ACS, USPSTF, and WHO, were also reviewed. Studies have shown that menopause-related estrogen deficiency causes atrophy, reduced cellularity, and transformation zone (TZ) recession, resulting in a high number of unsatisfactory smears and false-positive interpretations that may mask HSIL. Although HPV prevalence decreases with age, persistent and re-emerging high-risk HPV types among older women are strongly associated with CIN2+. Both HR-HPV testing and LBC have demonstrated higher sensitivity for detecting cervical lesions in postmenopausal women compared with conventional cytology. Evidence also indicates that short-term topical estrogen therapy facilitates transformation zone visualization and improves sample adequacy. Gaps in screening persist among women aged 65 and older. To optimize cervical cancer prevention in this aging demographic, it is important to develop individualized cervical screening strategies that take into consideration hormone status, high-risk HPV persistence, and improved diagnostic techniques to strengthen the protection of elderly women who remain at risk.

Transposable elements (TEs), particularly retrotransposons that dominate mammalian genomes, are pervasive components of mammalian genomes whose activation is constrained by multilayered repression systems. In germ cells, this repression architecture is particularly elaborate, integrating chromatin-based silencing, DNA methylation, and small RNA-guided pathways to safeguard genome integrity during epigenetic reprogramming. These mechanisms are coordinated yet mechanistically specialized, targeting distinct phases of the transposon life cycle and different TE families across developmental stages. Yet the distinctive chromatin landscape of germ cells also creates windows of developmental permissiveness during which TE transcription can occur. Beyond the germline, TE expression can emerge in defined stages of early embryogenesis, extraembryonic development, neural differentiation, and aging, with consequences ranging from chromatin remodeling and regulatory co-option to inflammatory signaling and genome instability. Together, these observations raise a central question: how do different mammalian lineages balance epigenetic plasticity with genome defense? Here, we synthesize current understanding of the molecular logic of TE repression, emphasizing the germline, and integrate evidence across development and aging. We highlight shared principles-such as epigenetic permissiveness and RNA-guided targeting-while underscoring a key difference in regulatory outcome: somatic contexts may tolerate, co-opt, or pathologically amplify TE activity, whereas the germline converts transient activation into heritable, sequence-specific silencing. Transposable elements are repeated DNA sequences that can move or copy themselves within the genome. Because of this ability, they can damage DNA and disrupt normal cell function. For many years, they were mainly viewed as harmful “genetic parasites.” However, recent studies have shown that they can also contribute to normal biological processes, including early development and gene regulation. This review discusses how mammals control transposable elements, with a particular focus on reproductive cells that give rise to sperm and eggs. These cells undergo major changes in their DNA packaging and gene regulation during development. Such changes can temporarily weaken the systems that normally keep transposable elements silent, creating periods when these elements become more active. To prevent harmful effects, reproductive cells use several layers of protection, including chemical modifications of DNA and RNA-based defense systems. We also compare transposable element activity in reproductive cells with other biological settings, including early embryos, the placenta, the nervous system, and aging tissues. In some situations, transposable element activity may contribute to normal development or gene control. In others, excessive activation is linked to infertility, inflammation, aging, and disease. Together, these findings show that mammals must carefully balance two competing needs: allowing enough flexibility in the genome for development and adaptation, while still protecting the genome from harmful transposable element activity. Understanding this balance may improve our knowledge of fertility, aging, and human disease.

Compassion-based interventions, like Mindfulness-Based Compassionate Living (MBCL), are increasingly recognized as treatments for depression. This study explores the impact of MBCL on self-schemas. As part of an RCT on MBCL for depression, self-description interviews of approximately 3 min in duration were conducted with 24 patients before and after MBCL and were analyzed using mixed methods. Qualitative analysis used both a deductive approach (based on the Five Factor Model) to identify themes and an inductive approach to explore subthemes within those themes. Additionally, Linguistic Inquiry and Word Count (LIWC) software analyzed words in psychologically relevant categories. Deductive analysis revealed a shift from neuroticism to emotional stability and a decrease in agreeableness. Inductive analysis highlighted a transition from self-criticism to self-compassion, and a shift from prioritizing others 'needs at the expense of self-care to a more balanced approach. LIWC analysis indicated that post-MBCL, patients used more words overall (W = 2.8; p = 0.006), but fewer positive emotion words (W = -3.1; p = 0.002) and fewer words related to cognitive processes (W = -2.6; p = 0.009). MBCL appears to be associated with changes in self-schemas and interpersonal dynamics, providing insights for future (linguistic) studies on the mechanisms of MBCL. These findings should be carefully interpreted considering the methodological limitations of the current investigation, including differing pre- and post-interview prompts and a sample of treatment completers.

Musculoskeletal and back health of school aged children is a global health problem, with evidence that the prevalence of these problems is increasing. Many modern school systems require children to assume sedentary positions for extended periods of time, and the increasing use of classroom-based technology adds to the number of hours seated. With the incidence of musculoskeletal pain reported not only in adult populations but increasingly in young people, an understanding of spinal health and posture may be essential for students. The main objective for conducting this review was to conduct a best evidence systematic review. This means we only included the highest quality papers on the effectiveness of school-based education programs on back health for improving knowledge of back health, ergonomics and postural behaviour in school children aged 4-18 years. We searched the following 21 electronic databases from inception till the 20th January 2023: AMED (EBSCOhost), APA PsycINFO (EBSCOhost), Best Evidence Medical Education (BEME) (EBSCOhost), British Education Index (EBSCOhost), CINAHL (EBSCOhost), Cochrane Central Register of Controlled Trials (Wiley), EMBASE (Ovid), ERIC (EBSCOhost), EThOS (British Library), Europe PMC (Europepmc.org), GoogleScholar. Health Technology Assessment (HTA) (INAHTA), Health Management Information Consortium (HMIC) (Ovid), MEDLINE (EBSCOhost), PEDro (pedro.org.au), ProQuest Dissertations & Theses (Proquest), ProQuest Nursing and Allied Health Database (ProQuest), SCOPUS (Elsevier), SportDISCUS (EBSCOhost), Web of Science (Arts and Humanities Citation Index, Science Citation Index Expanded, Social Sciences Citation Index, Emerging Sources Citation Index, Conference Proceedings Citation Index - Science, Conference Proceedings Citation Index - Social Sciences and Humanities; Clarivate), ZEToC (British Library). Selection Criteria. The population eligible for the review included all children and young people between 4 and 18 years of age, attending school. Exclusion criteria: Children under 4 years of age and adults over 18 years of age; chronic disease or conditions or co-morbidities. Studies needed to meet the following criteria to be included: any formal educational school-based programme that included back health, ergonomics and postural behaviour that was designed to support the educational performance of students' knowledge of posture and ergonomics within an educational establishment. We excluded physical activity or exercise only interventions. Included studies were required to have a control group that represented either business-as-usual (no intervention), or a wait-list design. We included studies that examined back care knowledge, knowledge of back care ergonomics, back care behaviours and knowledge of back posture. This was a Best Evidence Systematic Review and only research papers scoring a "good" or "excellent "on the Downs and Black (1998) risk-of-bias form were included. The following research designs were included: randomised controlled trials (RCTs), cluster randomised controlled trials (CRCT) and quasi-randomised controlled trials (QRCTs). We included prospective non-randomised studies (NRSs) with a control group because it was anticipated that very few RCTs would be found. Controlled before-after studies (CBAs), interrupted time series (ITS) studies as well as controlled studies that were non-randomised and included a pre- and post-test were also eligible for inclusion. Titles and abstracts were screened in duplicate. Full texts of studies with seemingly relevant abstracts were retrieved and assessed for eligibility using the pre-specified inclusion criteria. Full texts were also screened in duplicate. Studies were classified as either included or excluded. Two authors independently extracted data from relevant studies. 1,327 potentially relevant papers were found through the searches of the academic databases, while no studies were identified through searches of grey literature and reference lists. After removing 1,256 articles which did not meet the inclusion criteria, 71 studies remained for screening. 37 articles were excluded based on screening the titles and abstracts. This left 34 articles for further examination of full texts. After the full texts had been read, these 34 studies continued to the quality assessment/risk of bias stage using the Downs and Black ROB form. Only two papers scored 20 or over (i.e. good or excellent) and were included in this systematic review. As the outcomes of the two studies differed, it was not possible to conduct a meta-analysis. Therefore, a narrative synthesis was conducted. Each of these studies showed statistically significant improvements on knowledge and behaviour, in the short term (3-8 months) though these need to be interpreted in light of concerns regarding risk of bias. Despite the comprehensive search of electronic databases, grey literature, hand searching, journals and reference lists of included studies, we only found two 'good' quality studies (scoring 20-25). No studies achieved an "excellent" score, that provided "excellent" evidence, on the effectiveness of school-based education programs on back health for improving knowledge of back health, ergonomics and postural behaviour in school children aged 4-18 years. This highlights the urgent need for high-quality studies to be conducted to assess the effects of these programmes due to the importance of ergonomics and posture in the activities of daily living of school children. Declarative title Educating School children on their Back Health can improve their Knowledge of Back Health, Posture and Ergonomics (functional design) The review in brief: A review of 1,327 studies identified only two robust enough for analysis. While these studies reported improvements in students’ knowledge and behaviour, potential selection and confounding biases limit the findings. Consequently, there is insufficient high-quality evidence to confirm the efficacy of school-based back health programs for children aged 4–18. Further rigorous research is essential to determine if these interventions effectively improve long-term ergonomics and postural habits. What is this review about? Proper posture training helps the body move efficiently, reducing strain on bones, joints, and soft tissues. Poor posture can cause muscle soreness, headaches, poor circulation, stress, and sleep disturbances. To avoid these issues, the work or school environment should be adapted to the user’s needs, a principle known as ergonomics. Ergonomics boosts productivity and comfort by reducing discomfort. Understanding ergonomics helps students prevent injuries in schools by adjusting tools like desks, chairs, and computer screens, emphasising correct posture to reduce repetitive strain and musculoskeletal issues. Poor ergonomic practices and resulting postures are recognised causes of musculoskeletal aches and pains (Sellschop et al., 2018). Ergonomic assessment in schoolchildren is important, as their activities and postures may contribute to the high prevalence of pain among young people, potentially leading to chronic issues later in life (Pavithra & Anand, 2013; Weiguang et al., 2011). The high rates of back pain in children and adolescents, as well as its predictive value for adult spinal pain, have prompted calls for spinal health interventions in schools . Habits formed during school years can influence the likelihood of developing back problems in adulthood. Back pain in adolescence is a risk factor for pain in later years (Harreby et al., 1996), with risk increasing alongside the frequency of adolescent pain (Lise, Charlotte, & Kyvik Kirsten, 2006; Lise, Charlotte, Ohm, et al., 2006). A systematic review and meta-analysis by Salsali et al. (2023) found a weak correlation between physical activity and posture, suggesting multiple factors influence posture. The study emphasises the need for caution when interpreting meta-analyses due to heterogeneity and publication bias. This Campbell best evidence systematic review assesses the effectiveness of school-based education programmes on back health for improving knowledge, ergonomics, and postural behaviour in school children aged 4–18 years. Despite extensive searching, only two methodologically robust studies met the criteria for inclusion. What are the main findings of this review? Out of 34 studies reviewed (1961–2013), only two were robust enough for inclusion. Due to outcome variations, a narrative synthesis replaced a meta-analysis. Although both studies reported significant gains in knowledge and behaviour, a high risk of bias requires cautious interpretation. Ultimately, the scarcity of high-quality research means there is no strong evidence that school-based programs effectively improve ergonomics or postural behaviour in children aged 4–18. The current evidence base remains insufficient to support broad implementation. What do the findings of this review mean? Despite extensive searches across academic databases, grey literature, and reference lists, only two studies scored ‘good’ (20+ on the Downs and Black scale), and none reached ‘excellent’ (25-28). This highlights the urgent need for high-quality research on school-based back health programmes, as ergonomics and posture are crucial for school children’s well-being and preventing back pain in adulthood. How up to date is this review? The review authors searched for studies published up to 20th January 2023.

BackgroundCognitive remediation (CR) combined with transcranial direct current stimulation (tDCS) has been shown to slow cognitive decline in older adults with mild cognitive impairment (MCI) or remitted major depressive disorder (rMDD). Dysregulated angiogenesis is implicated in early neurodegeneration and may influence response to these interventions.ObjectiveTo determine whether baseline plasma angiogenesis markers moderate short-term and long-term cognitive response to CR&#x2009;+&#x2009;tDCS in older adults at risk for dementia.MethodsNineteen angiogenesis-related plasma biomarkers were measured at baseline in participants from the PACt-MD randomized controlled trial. Participants received active or sham CR plus active or sham tDCS for 8 weeks, followed by semi-annual booster sessions and online CR between visits. Cognitive assessments occurred at baseline, 8 weeks, and yearly. Elastic net regression identified relevant markers and baseline variables associated with the 8-week cognitive change. For selected markers, treatment*marker interactions were tested using multivariable linear regression adjusted for relevant demographic, clinical, and genetic covariates. Significant interactions were further examined using likelihood ratio tests in linear mixed-effects models across follow-up.ResultsIn 271 participants, angiopoietin-2, endocan, and VCAM-1 were identified as relevant markers. Out of these three markers, only angiopoietin-2 interacted with treatment (&#x3b2;(SE)&#x2009;=&#x2009;0.17(0.08), p&#x2009;=&#x2009;0.04, padj&#x2009;=&#x2009;0.11, f2&#x2009;=&#x2009;0.02), with lower levels associated with greater 8-week cognitive improvement in the active treatment group, controlling for covariates. This moderating effect persisted during follow-up (&#x3c7;2LRT(3)&#x2009;=&#x2009;24.9, p&#x2009;<&#x2009;0.001).ConclusionsLower baseline angiopoietin-2 may identify older adults with MCI or rMDD that are more likely to benefit from CR&#x2009;+&#x2009;tDCS.ClinicalTrials.gov; https://clinicaltrials.gov/study/NCT02386670; NCT02386670.

Pediatric solid organ and hematopoietic stem cell transplant recipients paradoxically experience accelerated immune aging despite chronological youth, establishing a paradigm with profound implications for cancer risk and long-term outcomes. This comprehensive review synthesizes current evidence demonstrating how transplantation-related factors, anti-thymocyte globulin-mediated T cell depletion, cytomegalovirus reactivation, chronic immunosuppression, and thymic dysfunction, induce premature immunosenescent phenotypes. These processes converge to generate T cell populations exhibiting CD28 loss, killer cell lectin-like receptor G1 positivity, telomere attrition, and functional exhaustion characteristic of elderly individuals. Concurrently, inflammaging pathways and senescence-associated secretory phenotypes establish pro-tumorigenic microenvironments. Consequently, pediatric recipients demonstrate 4- to 20-fold elevated cancer incidence, with standardized incidence ratios for post-transplant lymphoproliferative disease exceeding 200 in some cohorts. Beyond hematological malignancies, significant increases in solid tumors suggest fundamental immunosurveillance failure. Emerging biomarkers including flow cytometric senescence panels, telomere length measurement, and epigenetic clocks enable personalized risk stratification. Therapeutic horizons encompass senolytic agents, checkpoint inhibitor modulation, thymic regeneration strategies, and metabolic interventions targeting aging pathways. This paradigm shift necessitates reconceptualizing pediatric transplantation through the aging lens, integrating precision medicine approaches that balance graft survival, immune competence preservation, and cancer prevention in this vulnerable population.