Progression Of Aging Research Articles

Association of biomarkers and Barthel Index with occurrence of age-related adverse health outcomes in individuals with diabetes.

The clinical significance of age-related biomarkers in patients with diabetes has not been fully elucidated. In this study, we aimed to establish models to predict the progression of aging in patients with diabetes using biomarkers. This single-center, retrospective cohort study included 115 Japanese patients with diabetes aged ≥60 years. Age-related adverse health outcomes were defined as emergency hospitalization, any increase in the level of nursing care certification, admission to a nursing home or death. The associations of age-related biomarker levels (adiponectin, growth differentiation factor 15 [GDF15], C-X-C motif chemokine ligand 9 and apelin) and clinical indicators with age-related adverse health outcomes were evaluated. Factors that predominantly influenced the occurrence of age-related adverse health outcomes were explored using the Cox proportional hazards model. The mean age of the 115 participants was 73 years, 50.6% were men, the mean body mass index and hemoglobin A1c level were 25.3 kg/m2 and 9.79%, respectively. There were 26 age-related adverse health outcomes during the study period (median 1.93, range 0-4.65 years). In a model combining clinical indicators and biomarkers, including the Barthel Index, GDF15 and adiponectin, the occurrence of age-related adverse health outcomes was found to be significantly associated with GDF15 and Barthel Index. The group with both GDF15 and adiponectin levels higher than the median proved to be significantly higher than the group with both lower. The measurement of GDF15 and adiponectin levels and the Barthel Index might be useful for predicting age-related adverse health outcomes in patients with diabetes.

Obesity and 1-year all-cause survival of adult intensive care patients with heart failure: data from the MIMIC-IV.

BackgroundHeart failure is a disease that threatens global public safety. In recent years, the obesity paradox has been studied in cardiovascular disease and other fields. With the progress of aging, metabolic changes and regulation of fat function, it also provides many bridges for the dialogue between disease and molecular metabolism. The purpose of this study is to investigate the effect of obesity on the outcome of adult intensive care patients with heart failure combined with age factors.MethodData were derived from the fourth-generation Medical Information Marketplace for Intensive Care (MIMIC-IV version2.1) using structured query language on the Navicat (12.0.11) platform. People were divided into two groups based on the body mass index (BMI), one group with BMI ≥ 30 kg/m² and another group with BMI < 30 kg/m². Afterwards, the patients were divided into two subgroups based on their ages. One group included patients aged<60, and the other included patients aged ≥ 60. The extracted information includes demographic characteristics, laboratory findings, comorbidities, scores. Main results included in-hospital mortality, ICU mortality, and 1-year mortality. Secondary outcomes included hospital interval and ICU interval, use of renal replacement therapy, and rates of noninvasive and invasive ventilation support.ResultIn this cohort study, 3390 people were in the BMI<30 group, 2301 people were in the BMI ≥ 30 group, 960 people were in the age<60 group, and 4731 people were in the age ≥ 60 group, including 3557 patients after propensity score matching in high age group. Among patients aged ≥ 60, BMI ≥ 30 group vs. BMI<30 group showed significantly lower in-hospital mortality (13% vs. 16%) and one-year mortality (41% vs. 55%), respectively. Neither primary nor secondary outcomes were significantly described in the competition among patients aged under 60. Restricted cubic spline reveals a J-shaped nonlinear association between BMI and clinical endpoints within the entire cohort. Kaplan-Meier curves revealed a survival advantage in BMI ≥ 30 group (p < 0.001). Following age stratification, a beneficial effect of BMI categories on one-year mortality risk was observed in heart failure patients aged ≥ 60 (Univariable HR, 0.71, 95% CI, 0.65–0.78, p < 0.001; Multivariable HR, 0.74, 95% CI, 0.67–0.81, p < 0.001), but not in those under 60 years old.OutcomeIn ICU patients with heart failure, obesity offers a survival benefit to those aged ≥ 60. No obesity paradox was observed in patients younger than 60 years old. The obesity paradox applies to patients aged ≥ 60 with heart failure.

Pathological and functional significance of aging mouse kidneys: clinical implications to reduce the risk of hyper- or hypokalemia in the elderly.

Elderly patients are prone to develop hyper- or hypokalemia, since they are susceptible to drugs or diets that affect the urinary or fecal potassium (K+) excretion. In aging mouse kidneys, in addition to glomerulosclerosis, proximal tubular atrophy, and atherosclerosis in renal arterioles, there was diffuse tubulointerstitial fibrosis with a number of inflammatory leukocytes infiltrating into the cortical interstitium. Since these pathological features greatly influence renal K+ handling, slowing the progression of kidney aging would fundamentally reduce the risk of developing hyper- or hypokalemia. Immunohistochemistry demonstrated the overexpression of K+ channels (Kv1.3) in leukocytes within the cortical interstitium, which was strongly associated with "chronic inflammation" in aging kidneys and the subsequent progression of renal fibrosis. In our basic studies, antihypertensive drugs (benidipine, nifedipine, verapamil, diltiazem) and anticholesterol drugs (lovastatin, simvastatin, pravastatin) strongly suppressed the leukocyte Kv1.3 channels and thus exerted anti-inflammatory effects. Given such pharmacological properties of these drugs, they may also be useful in slowing the progression of tubulointerstitial fibrosis in aging kidneys and reducing the risk of hyper- or hypokalemia in elderly patients.

Aqueous Extract of Wolfberry Alleviates Aging-Related Skeletal Muscle Dysfunction by Modulating PRRs Signaling Pathways and Enhancing DNA Repair.

Aging can lead to a series of degenerative changes in skeletal muscle, which would negatively impact physical activity and the quality of life of the elderly. Wolfberry contains numerous bioactive substances. It's vital to further explore the mechanisms underlying its healthy effects on skeletal muscle function during aging progress. This study discusses the benefits and mechanisms of aqueous extract of wolfberry (AEW) to protect skeletal muscle from aging-related persistent DNA damage based on its anti-inflammatory activity. It is found that AEW improves muscle mass, strength, and endurance, modulates the expression of Atrogin-1, MyH, and MuRF-1, and decreases oxidative stress and inflammation levels in aging mice, which is consistent with the in vitro results. Mechanistically, AEW inhibits the pattern recognition receptors (PRRs) pathway induced by inflammatory gene activation, suggesting its potential in response to DNA damage. AEW is also observed to mitigate chromatin decompaction. Network pharmacology is conducted to analyze the potential targets of AEW in promoting DNA repair. In conclusion, the study shows the anti-aging effects of AEW on skeletal muscle by promoting DNA repair and reducing the transcriptional activity of inflammatory factors. AEW intake may become a potential strategy for strengthening skeletal muscle function in the elderly.

Effects of chronic treatment with metformin on brain glucose hypometabolism and central insulin actions in transgenic mice with tauopathy

Brain glucose hypometabolism and insulin alterations are common features of many neurological diseases. Herein we sought to corroborate the brain glucose hypometabolism that develops with ageing in 12-months old Tau-VLW transgenic mice, a model of tauopathy, as well as to determine whether this model showed signs of altered peripheral glucose metabolism. Our results demonstrated that 12-old months Tau mice exhibited brain glucose hypometabolism as well as basal hyperglycemia, impaired glucose tolerance, hyperinsulinemia, and signs of insulin resistance. Then, we further studied the effect of chronic metformin treatment (9 months) in Tau-VLW mice from 9 to 18 months of age. Longitudinal PET neuroimaging studies revealed that chronic metformin altered the temporal profile in the progression of brain glucose hypometabolism associated with ageing. Besides, metformin altered the content and/or phosphorylation of key components of the insulin signal transduction pathway in the frontal cortex leading to significant changes in the content of the active forms. Thus, metformin increased the expression of pAKT-Y474 while reducing pmTOR-S2448 and pGSK3β. These changes might be related, at least partially, to a slow progression of ageing, neurological damage, and cognitive decline. Metformin also improved the peripheral glucose tolerance and the ability of the Tau-VLW mice to maintain their body weight through ageing. Altogether our study shows that the tau-VLW mice could be a useful model to study the potential interrelationship between tauopathy and central and peripheral glucose metabolism alterations. More importantly our results suggest that chronic metformin treatment may have direct beneficial central effects by post-transcriptional modulation of key components of the insulin signal transduction pathway.

The Relationship between the Composition of Intestinal Flora and Dementia

With the aging process of society, the incidence of dementia is increasing year by year and has become a common disease among the elderly which is prognosed to affect approximately 131 million individuals by 2050. The gut microbiome, as a diverse community of microorganisms, plays a crucial role in maintaining health and well-being. Recent research suggests that the gut microbiome significantly influences the development and progression of Alzheimer’s Disease (AD) and other neurodegenerative dementias in the elderly. Interventions targeting the gut microbiome through diet, probiotics, and lifestyle changes may offer promising avenues for preventing these conditions. Aging is associated with specific changes in the gut microbiome composition, including the loss of certain beneficial bacteria at the expense of other potentially pathological microorganisms like Akkermansia and Butyricimonas, which may lead to dysbiosis, which was implicated in various aging-related diseases, including AD. Despite advancements in identifying pathobionts associated with unhealthy aging and disease progression, more research is needed to delineate changes attributable to aging from those due to independent disease processes, nevertheless, some studies suggest that modulating the gut microbiome through diet and probiotic supplementation may have potential in improving health status and reducing rate of neurodegeneration. Especially maintaining a healthy, diverse gut flora through diet and lifestyle may be an important factor in preventing dementia and delaying the progression of aging. Further research is needed to fully elucidate the causal mechanisms linking the gut and brain in neurodegenerative diseases. Therefore, this paper aims to present the latest knowledge on gut microbiota changes and their contribution to dementia, proposing strategies for prevention and delaying neurodegenerative processes.

Real-time detection of aging status of methylammonium lead iodide perovskite thin films by using terahertz time-domain spectroscopy

The inadequate stability of organic–inorganic hybrid perovskites remains a significant barrier to their widespread commercial application in optoelectronic devices. Aging phenomena profoundly affect the optoelectronic performance of perovskite-based devices. In addition to enhancing perovskite stability, the real-time detection of aging status, aimed at monitoring the aging progression, holds paramount importance for both fundamental research and the commercialization of organic–inorganic hybrid perovskites. In this study, the aging status of perovskite was real-time investigated by using terahertz time-domain spectroscopy. Our analysis consistently revealed a gradual decline in the intensity of the absorption peak at 0.968 THz with increasing perovskite aging. Furthermore, a systematic discussion was conducted on the variations in intensity and position of the terahertz absorption peaks as the perovskite aged. These findings facilitate the real-time assessment of perovskite aging, providing a promising method to expedite the commercialization of perovskite-based optoelectronic devices.Graphical

NFκB dynamics-dependent epigenetic changes modulate inflammatory gene expression and induce cellular senescence.

Upregulation of nuclear factor κB (NFκB) signaling is a hallmark of aging and a major cause of age-related chronic inflammation. However, its effect on cellular senescence remains unclear. Here, we show that alteration of NFκB nuclear dynamics from oscillatory to sustained by depleting a negative feedback regulator of NFκB pathway, NFκB inhibitor alpha (IκBα), in the presence of tumor necrosis factor α (TNFα) promotes cellular senescence. Sustained NFκB activity enhanced inflammatory gene expression through increased NFκB-DNA binding and slowed the cell cycle. IκBα protein was decreased under replicative or oxidative stress in vitro. Furthermore, a decrease in IκBα protein and an increase in DNA-NFκB binding at the transcription start sites of age-associated genes in aged mouse hearts suggested that nuclear NFκB dynamics may play a critical role in the progression of aging. Our study suggests that nuclear NFκB dynamics-dependent epigenetic changes regulated over time in a living system, possibly through a decrease in IκBα, enhance the expression of inflammatory genes to advance the cells to a senescent state.

Targeting Microglia in Alzheimer's Disease: Pathogenesis and Potential Therapeutic Strategies.

Microglia, as resident macrophages in the central nervous system, play a multifunctional role in the pathogenesis of Alzheimer's disease (AD). Their clustering around amyloid-β (Aβ) deposits is a core pathological feature of AD. Recent advances in single-cell RNA sequencing (scRNA-seq) and single-nucleus RNA sequencing (snRNA-seq) have revealed dynamic changes in microglial phenotypes over time and across different brain regions during aging and AD progression. As AD advances, microglia primarily exhibit impaired phagocytosis of Aβ and tau, along with the release of pro-inflammatory cytokines that damage synapses and neurons. Targeting microglia has emerged as a potential therapeutic approach for AD. Treatment strategies involving microglia can be broadly categorized into two aspects: (1) enhancing microglial function: This involves augmenting their phagocytic ability against Aβ and cellular debris and (2) mitigating neuroinflammation: Strategies include inhibiting TNF-α signaling to reduce the neuroinflammatory response triggered by microglia. Clinical trials exploring microglia-related approaches for AD treatment have garnered attention. Additionally, natural products show promise in enhancing beneficial effects and suppressing inflammatory responses. Clarifying microglial dynamics, understanding their roles, and exploring novel therapeutic approaches will advance our fight against AD.

MTORC2: A neglected player in aging regulation.

Mammalian target of rapamycin (mTOR) is a serine/threonine kinase that plays a pivotal role in various biological processes, through integrating external and internal signals, facilitating gene transcription and protein translation, as well as by regulating mitochondria and autophagy functions. mTOR kinase operates within two distinct protein complexes known as mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2), which engage separate downstream signaling pathways impacting diverse cellular processes. Although mTORC1 has been extensively studied as a pro-proliferative factor and a pro-aging hub if activated aberrantly, mTORC2 received less attention, particularly regarding its implication in aging regulation. However, recent studies brought increasing evidence or clues for us, which implies the associations of mTORC2 with aging, as the genetic elimination of unique subunits of mTORC2, such as RICTOR, has been shown to alleviate aging progression in comparison to mTORC1 inhibition. In this review, we first summarized the basic characteristics of mTORC2, including its protein architecture and signaling network. We then focused on reviewing the molecular signaling regulation of mTORC2 in cellular senescence and organismal aging, and proposed the multifaceted regulatory characteristics under senescent and nonsenescent contexts. Next, we outlined the research progress of mTOR inhibitors in the field of antiaging and discussed future prospects and challenges. It is our pleasure if this review article could provide meaningful information for our readers and call forth more investigations working on this topic.

Recent Innovations and Technical Advances in High-Throughput Parallel Single-Cell Whole-Genome Sequencing Methods.

Single-cell whole-genome sequencing (scWGS) detects cell heterogeneity at the aspect of genomic variations, which are inheritable and play an important role in life processes such as aging and cancer progression. The recent explosive development of high-throughput single-cell sequencing methods has enabled high-performance heterogeneity detection through a vast number of novel strategies. Despite the limitation on total cost, technical advances in high-throughput single-cell whole-genome sequencing methods are made for higher genome coverage, parallel throughput, and level of integration. This review highlights the technical advancements in high-throughput scWGS in the aspects of strategies design, data efficiency, parallel handling platforms, and their applications on human genome. The experimental innovations, remaining challenges, and perspectives are summarized and discussed.

Cellular Senescence-Related Long Non-coding RNA Signatures Predict Prognosis in Juvenile Osteosarcoma

AbstractOsteosarcoma is the most common malignant bone tumor and is frequently diagnosed in juvenile. Cellular senescence is a fundamental hallmark of osteosarcoma and plays a vital role in the initiation and progression of aging and tumorigenesis. Long non-coding RNAs (lncRNAs) are implicated in tumorigenesis. In this study, six cellular senescence-related lncRNAs with independent prognostic significance in juvenile osteosarcoma patients were identified through univariate Cox regression analysis, least absolute shrinkage and selection operator (LASSO) regression analysis, and multivariate Cox regression analysis. Prognostic significance was further confirmed by Kaplan–Meier (KM) survival curves, co-expression interaction networks, and sankey diagrams. A prognostic model of cellular senescence-related genes in juvenile osteosarcoma patients was then constructed using multivariate Cox regression analysis based on these six genes. High- and low-risk groups were identified according to the median risk score calculated by the prognostic model. The favorable prognostic significance of this model was demonstrated through survival curves, receiver operating characteristic (ROC) curves, distribution scatter plots and lncRNA expression heatmaps. Furthermore, cellular senescence-related lncRNAs were validated by enrichment analysis, immunological correlation analysis, m6A correlation analysis, and drug sensitivity correlation analysis. These findings are important for improving the prognosis of juvenile osteosarcoma patients and understanding the mechanisms underlying cellular senescence in juvenile osteosarcoma development.

Comparison of dynamic hip screw with anti-rotation screw and femoral neck system internal fixation for the treatment of garden II-IV type femoral neck fractures.

Femoral neck fractures, which are fractures occurring from the femoral head to the base of the femoral neck, are prevalent in the elderly population. With the progression of societal aging, the incidence of femoral neck fractures has been steadily increasing, making it a significant global issue that urgently needs to be addressed. To compare the efficacy and safety of dynamic hip screw (DHS) with anti-rotation screw and femoral neck system (FNS) internal fixation for the treatment of Garden II-IV type femoral neck fractures. A total of 90 patients with Garden II-IV type femoral neck fractures were randomly assigned to either the control group (n= 45) treated with DHS and anti-rotation screw or the experimental group (n= 45) treated with FNS. Surgical outcomes, including incision size, blood loss, operation time, fluoroscopy frequency, and fracture healing time, were compared. Postoperative complication rates, reoperation rates, Harris scores, and visual analogue scale (VAS) scores were also assessed. The experimental group demonstrated significantly reduced incision length, blood loss, operation time, and fluoroscopy frequency compared to the control group (P< 0.01). No significant differences were observed in fracture healing time, Garden classification, or fracture reduction outcomes between the two groups (P> 0.05). At 6 months post-treatment, both groups showed significant improvements in Harris scores and VAS scores compared to pre-treatment (P< 0.05), with no significant differences between the groups (P> 0.05). The rates of internal fixation failure, nonunion, and avascular necrosis of the femoral head, as well as overall incidence of postoperative complications and reoperation rates, showed no significant differences between the two groups (P> 0.05). Both DHS with anti-rotation screw and FNS internal fixation demonstrated comparable efficacy and safety profiles in the treatment of Garden II-IV type femoral neck fractures. The experimental group showed advantages in terms of reduced incision length, blood loss, operation time, and fluoroscopy frequency, while maintaining similar clinical outcomes and complication rates.

Targeting senescence induced by age or chemotherapy with a polyphenol-rich natural extract improves longevity and healthspan in mice

Accumulating senescent cells within tissues contribute to the progression of aging and age-related diseases. Botanical extracts, rich in phytoconstituents, present a useful resource for discovering therapies that could target senescence and thus improve healthspan. Here, we show that daily oral administration of a standardized extract of Salvia haenkei (Haenkenium (HK)) extended lifespan and healthspan of naturally aged mice. HK treatment inhibited age-induced inflammation, fibrosis and senescence markers across several tissues, as well as increased muscle strength and fur thickness compared with age-matched controls. We also found that HK treatment reduced acutely induced senescence by the chemotherapeutic agent doxorubicin, using p16LUC reporter mice. We profiled the constituent components of HK by mass spectrometry, and identified luteolin—the most concentrated flavonoid in HK—as a senomorphic compound. Mechanistically, by performing surface plasmon resonance and in situ proximity ligation assay, we found that luteolin disrupted the p16–CDK6 interaction. This work demonstrates that administration of HK promotes longevity in mice, possibly by modulating cellular senescence and by disrupting the p16–CDK6 interaction.

Understanding the Temporal Dynamics of Accelerated Brain Aging and Resilient Brain Aging: Insights from Discriminative Event-Based Analysis of UK Biobank Data.

The intricate dynamics of brain aging, especially the neurodegenerative mechanisms driving accelerated (ABA) and resilient brain aging (RBA), are pivotal in neuroscience. Understanding the temporal dynamics of these phenotypes is crucial for identifying vulnerabilities to cognitive decline and neurodegenerative diseases. Currently, there is a lack of comprehensive understanding of the temporal dynamics and neuroimaging biomarkers linked to ABA and RBA. This study addressed this gap by utilizing a large-scale UK Biobank (UKB) cohort, with the aim to elucidate brain aging heterogeneity and establish the foundation for targeted interventions. Employing Lasso regression on multimodal neuroimaging data, structural MRI (sMRI), diffusion MRI (dMRI), and resting-state functional MRI (rsfMRI), we predicted the brain age and classified individuals into ABA and RBA cohorts. Our findings identified 1949 subjects (6.2%) as representative of the ABA subpopulation and 3203 subjects (10.1%) as representative of the RBA subpopulation. Additionally, the Discriminative Event-Based Model (DEBM) was applied to estimate the sequence of biomarker changes across aging trajectories. Our analysis unveiled distinct central ordering patterns between the ABA and RBA cohorts, with profound implications for understanding cognitive decline and vulnerability to neurodegenerative disorders. Specifically, the ABA cohort exhibited early degeneration in four functional networks and two cognitive domains, with cortical thinning initially observed in the right hemisphere, followed by the temporal lobe. In contrast, the RBA cohort demonstrated initial degeneration in the three functional networks, with cortical thinning predominantly in the left hemisphere and white matter microstructural degeneration occurring at more advanced stages. The detailed aging progression timeline constructed through our DEBM analysis positioned subjects according to their estimated stage of aging, offering a nuanced view of the aging brain's alterations. This study holds promise for the development of targeted interventions aimed at mitigating age-related cognitive decline.

Space electric field impacts on softening and cell wall modification of strawberry during cold storage

As an emerging non-contact cold chain preservation technology, the impact of the DENBA+ on plant cell wall metabolism and its mechanism of inhibiting softening have not been addressed. In this study, strawberries were used as an experimental model to investigate the effect of space electric field storage on cell wall metabolism. Compared with the control, 500 V DENBA+ treatment was able to reduce the firmness loss of strawberries by 18.3 % on 18 d. Additionally, the DENBA+ exhibited a pronounced ability to suppress fruit softening enzyme (FaPG1 and FaβGal4) expression, delay the rise in polygalacturonates (PG), pectin methyl esterase (PME), cellulase (Cx), and β-galactosidase (β-Gal) activities, postpone the decline in cell wall matrix (CWM), insoluble solid pectin (ISP), and colloidal soluble pectin (CSP) content along with hemicellulose and cellulose levels while attenuating water-soluble pectin (WSP) accumulation during cold storage period. These findings contribute to the maintenance of fruit cell wall structural integrity with the aim of sustaining strawberry firmness and retarding the progression of aging.

Age, sex and Alzheimer’s disease: a longitudinal study of 3xTg-AD mice reveals sex-specific disease trajectories and inflammatory responses mirrored in postmortem brains from Alzheimer’s patients

BackgroundAging and sex are major risk factors for developing late-onset Alzheimer’s disease. Compared to men, women experience worse neuropathological burden and cognitive decline despite living longer with the disease. Similarly, male 3xTg-AD mice, developed to model Alzheimer’s disease, no longer consistently exhibit standard Alzheimer’s neuropathology yet experience higher rates of mortality - providing a unique opportunity to further elucidate this dichotomy. We hypothesized that sex differences in the biological aging process yield distinct pathological and molecular Alzheimer’s disease signatures in males and females, which could be harnessed for therapeutic and biomarker development.MethodsWe aged male and female, 3xTg-AD and B6129 control mice across their respective lifespans (n = 3–8 mice per sex, strain, and age group) and longitudinally assessed neuropathological hallmarks of Alzheimer’s disease, markers of hepatic inflammation, splenic mass and morphology, as well as plasma cytokine levels. We conducted RNA sequencing analysis on bulk brain tissue and examined differentially expressed genes (DEGs) between 3xTg-AD and B6129 samples and across ages in each sex. We also examined DEGs between clinical Alzheimer’s and control parahippocampal gyrus brain tissue samples from the Mount Sinai Brain Bank study in each sex.Results3xTg-AD females significantly outlived 3xTg-AD males and exhibited progressive Alzheimer’s neuropathology, while 3xTg-AD males demonstrated progressive hepatic inflammation, splenomegaly, circulating inflammatory proteins, and minimal Alzheimer’s neuropathological hallmarks. Instead, 3xTg-AD males experienced an accelerated upregulation of immune-related gene expression in the brain relative to females. Our clinical investigations revealed that individuals with Alzheimer’s disease develop similar sex-specific alterations in neuronal and immune function. In diseased males of both species, we observed greater upregulation of complement-related gene expression, and lipopolysaccharide was predicted as the top upstream regulator of DEGs.ConclusionsOur data demonstrate that chronic inflammation and complement activation are associated with increased mortality, indicating that age-related changes in immune response contribute to sex differences in Alzheimer’s disease trajectories. We provide evidence that aging and transgene-driven disease progression trigger a widespread inflammatory response in 3xTg-AD males, which mimics the impact of lipopolysaccharide stimulation despite the absence of infection.

The Citrus flavanone naringenin prolongs the lifespan in C. elegans and slows signs of brain aging in mice

Aging is one of the main risk factors for neurodegenerative disorders, which represent a global burden on healthcare systems. Therefore, identifying new strategies to slow the progression of brain aging is a compelling challenge. In this article, we first assessed the potential anti-aging effects of the Citrus flavanone naringenin (NAR), an activator of the enzyme sirtuin-1 (SIRT1), in a 3R-compliant and short-lived aging model (i.e., the nematode C. elegans). Then, we investigated the preventive effects of a 6-month treatment with NAR (100 mg/kg, orally) against brain aging and studied its mechanism of action in middle-aged mice. We demonstrated that NAR (100 μM) extends lifespan and improves healthspan in C. elegans. In the brain of middle-aged mice, NAR promotes the activity of metabolic enzymes (citrate synthase, cytochrome C oxidase) and increases the expression of the SIRT1 enzyme. Consistently, NAR up-regulates the expression of downstream antioxidant (Foxo3, Nrf2, Ho-1), anti-senescence (p16), and anti-inflammatory (Il-6, Il-18) markers. Our findings support NAR supplementation to slow the signs of brain aging.

Monitoring the Aging and Edible Safety of Pork in Postmortem Storage Based on HSI and Wavelet Transform.

The process of meat postmortem aging is a complex one, in which improved tenderness and aroma coincide with negative effects such as water loss and microbial growth. Determining the optimal postmortem storage time for meat is crucial but also challenging. A new visual monitoring technique based on hyperspectral imaging (HSI) has been proposed to monitor pork aging progress. M. longissimus thoracis from 15 pigs were stored at 4 °C for 12 days while quality indexes and HSI spectra were measured daily. Based on changes in physical and chemical indicators, 100 out of the 180 pieces of meat were selected and classified into rigor mortis, aged, and spoilt meat. Discrete wavelet transform (DWT) technology was used to improve the accuracy of classification. DWT separated approximate and detailed signals from the spectrum, resulting in a significant increase in classification speed and precision. The support vector machine (SVM) model with 70 band spectra achieved remarkable classification accuracy of 97.06%. The study findings revealed that the aging and microbial spoilage process started at the edges of the meat, with varying rates from one pig to another. Using HSI and visualization techniques, it was possible to evaluate and portray the postmortem aging progress and edible safety of pork during storage. This technology has the potential to aid the meat industry in making informed decisions on the optimal storage and cooking times that would preserve the quality of the meat and ensure its safety for consumption.

Active aging and health among older adults in China: a perspective based on downward intergenerational economic support.

In China, the rapid progression of population aging presents significant challenges to society and the economy, drawing widespread attention to the health conditions of older adults. While aging is often seen as a societal burden, the phenomenon of intergenerational economic support reveals the potential for older adults to continue playing an active role within their families. This study delves into how older parents' financial support to their children can reciprocally influence their own health, exploring the potential non-linear relationships involved. This research, utilizing data from the 2018 China Health and Retirement Longitudinal Study, employs instrumental variable techniques and cross-sectional threshold models to examine how financial support provided by older adults to their children affects their health. It particularly highlights the varied impacts of economic support on older adults' health at different levels of support. The findings indicate that moderate intergenerational economic support significantly enhances the health of older adults, while either minimal or excessive financial support does not demonstrate the same positive effect. Additionally, subjective life expectancy plays a mediating role between intergenerational economic support and the health of older adults, further emphasizing the beneficial impact of economic support. The study underscores the importance of moderate intergenerational economic support in improving the health of older adults amidst aging challenges. Future policies and practices should consider how to encourage and optimize such support to address the challenges of an aging society, enhance the welfare of older adults, and promote healthy aging.