Cognitive impairment affects over one billion people globally, with elderly individuals in institutions in China being particularly impacted. This study involved 60 elderly participants with mild cognitive impairment, who were randomly assigned to one of two groups: 30 in a control group receiving traditional programs from the elderly institution and 30 in an intervention group receiving socio-therapeutic methods. Cognitive function was assessed before the intervention, and at the end of the first, second, and third months (with unsupervised interventions in the third month). Initially, both groups had similar low MMSE scores. However, the socio-therapeutic intervention led to significant cognitive improvements in the intervention group after the first and second months, with results remaining higher than the control group by the end of the third month. The study highlights the effectiveness of socio-therapeutic interventions in enhancing cognitive function and suggests that such programs should be adopted in elderly care institutions. Further research is needed to explore long-term effects and optimal program components, with personalized interventions and family/community involvement recommended to maximize benefits.

The aging of pancreatic beta cells is closely associated with various diseases, such as impaired glucose tolerance, yet the underlying regulatory mechanisms remain unclear. In this study, we screened young and aged mouse pancreatic beta cells' high-throughput sequencing data from the GEO public database. Utilizing bioinformatics techniques, we identified the key regulatory factor YY1 in the aging process of pancreatic islets. We observed a significant decrease in the expression of YY1 in a D-gal-induced mouse model of pancreatic aging and an HO-induced MIN6 cell model of aging. Moreover, both vivo and vitro models, we found that the YY1 agonist eudesmin (EDN) improved glucose intolerance in mice, alleviated aging of pancreatic beta cells, and downregulated the expression of cell cycle protein P21. Mechanistically, we discovered that EDN inhibited the P38/JNK MAPK pathway in aging cells. In summary, our study confirms the regulatory role of the transcription factor YY1 in the aging process of pancreatic beta cells. This finding may provide a new approach for the clinical treatment of pancreatic aging-related diseases such as impaired glucose tolerance or diabetes.

This study aimed to investigate the effects of swimming exercise on cartilage, inflammatory markers, subchondral bone structure, and stride length in mice with knee osteoarthritis induced by anterior cruciate ligament (ACL) transection, and to explore the role of miR-143-3p in these effects.

To investigate the effect of optimal diastolic blood pressure (DBP) level on cardiovascular disease (CVD) events, considering different age groups. And the nonlinear relationship between DBP and CVD events by age were evaluated.

Sarcopenia is closely associated with cardiovascular disease. We aimed to examine the association of Life's Essential 8 (LE8), the recently updated measurement of cardiovascular health (CVH), with the presence of sarcopenia among US adults.

Exercise is a common strategy for disease prevention or management, including for diabetes and cardiac dysfunction. However, exercise response varies immensely between individuals, and in humans, the same exercise treatment can lead both to positive and negative responses. Drosophila melanogaster is an established model for exercise research that can be leveraged to understand this variation in exercise response. Here, we investigated how two early life exercise treatments differing in duration (5 and 20 days) impact the animals' health- and lifespan in four genotypes. Specifically, we measured lifespan, activity level, body condition, physical ability, and reproductive output in this exploratory study to gain insights into potential trade-offs. For most measures, we found both immediate and long-term effects, with some effects persisting weeks past the cessation of exercise. The effect of the exercise treatment was context-dependent, with treatment, sex, and genotype interactions determining phenotypes. For example, the 20-day treatment did not exhibit a consistently larger effect than the 5-day treatment. Similarly, neither the 5-day nor the 20-day treatment impacted lifespan, but two specific genotype/sex combinations showed altered lifespan after exercise. The 20-day treatment decreased climbing performance compared to controls up to several weeks after treatment ended in some genotypes. Together, our results highlight the complex, interacting factors controlling exercise response and demonstrate that early life exercise can have long-lasting effects in the Drosophila exercise model even though most individual groups show no response.

Structured and supervised physical exercise and cognitive training are two efficient ways to enhance cognition in older adults. Performing both within a combined intervention could maximize their effect on cognition due to their potential synergy on brain functions. During the COVID-19 pandemic, these interventions were particularly relevant due to the collateral impact of social restrictions regarding physical activity and the level of cognitive stimulation. However, the benefits of remotely monitored intervention combining physical exercise and cognitive training for older adult cognition remain to be demonstrated.

Elevated circulatory phosphate levels are linked to age-related muscle dysfunction, yet the mechanisms remain unclear. This study investigated the hypothesis that inflammation plays a role in connecting elevated phosphate levels to muscular dysfunction in middle-aged and older individuals and explored potential sex-based differences in these associations.

This study investigates the distribution of osteoporosis (OP) and its associated comorbidities across different demographic factors. Furthermore, this study seeks to develop a statistically-based diagnostic model leveraging demographic and health indicators to provide personalized risk assessments for OP.

Aging is an invincible phenomenon that is a risk factor for the development of neurological disorders such as anxiety, depression, and memory decline that are prominent in aging. The present study aims to evaluate the effect of Niacin (Nn) on D-galactose (D-Gal)-induced behavioral deficits and memory impairment in rats. In the experiment, forty-eight male albino Sprague dwaley rats were divided on a random basis into six groups (n = 8): Veh + Veh, Veh + Nn (low dose), Veh + Nn (high dose), Veh + D-Gal, D-Gal+Nn (low dose), D-Gal+Nn (high dose). 300 mg/kg/mL drug doses of D-Gal, while low doses (25 mg/kg/mL) and high doses (50 mg/kg/mL) of Nn were used in this study. Animals received their respective treatment for 14 days (intraperitoneally, once daily). After 14 days, animals were subjected to different behavioral tests including light-dark box activity, elevated plus maze test (for anxiety), and tail suspension test (for depression). A Morris water maze test was performed to evaluate short-term and long-term memory performance. After behavioral tests, decapitation was performed and brains were collected and stored for biochemical and neurochemical analysis. Behavioral analysis revealed that Nn alleviated the anxiety and depression-like symptoms and memory decline induced by D-Gal. D-Gal-induced decreased antioxidant enzymes, and acetylcholine levels, while increased oxidative stress markers, neuro-inflammatory cytokines, serotonin metabolism, and acetylcholinesterase (AChE) activity were prevented by Nn administration at both doses. In-silico studies showed that Nn has a potential to inhibit AChE activity with a binding affinity of -5.0 kcal/mol. In conclusion, Nn as an antioxidant and neuromodulator could be helpful for treating aging and associated psychiatric illnesses.

This comprehensive review examines the relationship between osteoarthritis (OA) and osteoporosis (OP), two common disorders in the elderly. OA involves joint cartilage degeneration and pain, while OP leads to fractures due to reduced bone mass. Despite different pathologies, both conditions share risk factors such as age and genetics. Studies reveal mixed results: some show higher bone mineral density (BMD) in OA patients, suggesting an inverse relationship, while others find no significant link. Proposed mechanisms include mechanical loading, bone remodeling, and inflammation. Clinical strategies focus on maintaining bone health in OA and monitoring joint health in OP, with treatments like bisphosphonates and exercise. Understanding these interactions is crucial for developing integrated treatments to improve patient outcomes and quality of life. Further research is needed to clarify these complex mechanisms.

Diabetes mellitus (DM) patients are at increased risk of cognitive impairment. The precise mechanisms underlying the association between DM and cognitive impairment remain unclear. Spleen tyrosine kinase (SYK), a crucial regulator of signal transduction, has been implicated in microglial pyroptosis in experimental ischemic stroke models. The present study investigated the potential role of SYK in DM-associated cognitive impairment.

Dementia and mild cognitive impairment (MCI) present both health and economic challenges on a global scale, thus affecting millions of people, and is projected to increase significantly by the year 2050. Early language processing deficits are evident in those diagnosed with Alzheimer's disease and MCI. Recent advances in pharmacologic and non-pharmacologic interventions, including cognitive rehabilitation and training, show promising effects on cognitive functions. Articulation training, particularly, is highlighted for its potential in addressing the communication difficulties which those experiencing dementia and MCI face, based on the transmission deficit hypothesis. This study aimed to perform a voxel-wise comparison of morphological changes in grey matter volume as well as white matter integrity to represent the plastic changes in response to articulation training among older, healthy Japanese adults.

Older adults are more likely to acquire the severe manifestation of COVID-19 and the hospitalised survivors experience significant functionality loss. Thus, we aimed to identify the level of functionality in older adults hospitalised due to COVID-19, and the effect of inpatient rehabilitation upon functional recovery.

The aim of this study is to investigate the early prognostic efficacy of plasma soluble urokinase-type plasminogen activator receptor (suPAR), soluble tumor necrosis factor receptor 1 (sTNFR1), and soluble tumor necrosis factor receptor 2 (sTNFR2) in complicated acute kidney injury (AKI) in patients with coronavirus disease 2019 (COVID-19), and to analyze the relevant factors contributing to complicated AKI in these patients.

Aging is a dynamic process that requires a continuous response and adaptation to internal and external stimuli over the life course. This eventually results in people aging differently and women aging differently than men. The "gender paradox" describes how women experience greater longevity than men, although linked with higher rates of disability and poor health status. Recently, the concept of frailty has been incorporated into this paradox giving rise to the "sex-frailty paradox" which describes how women are frailer because they manifest worse health status but, at the same time, appear less susceptible to death than men of the same age. However, very little is known about the biological roots of this sex-related difference in frailty. Inflamm-aging, the chronic low-grade inflammatory state associated with age, plays a key pathophysiological role in several age-related diseases/conditions, including Alzheimer's disease (AD), for which women have a higher lifetime risk than men. Interestingly, inflamm-aging develops at a different rate in women compared to men, with features that could play a critical role in the development of AD in women. According to this view, a continuum between aging and age-related diseases that probably lacks clear boundaries can be envisioned in which several shared biological mechanisms that progress at different pace may lead to different aging trajectories in women than in men. It therefore becomes urgent to consider a holistic approach in the study of aging, declining it from a gender medicine perspective that can also consider the biological roots of the sex-frailty paradox.

Skeletal muscle atrophy is one of the main side effects of high-dose or continuous use of glucocorticoids (such as dexamethasone). However, there are limited studies on dexamethasone-induced skeletal muscle atrophy in zebrafish and even fewer explorations of the underlying molecular mechanisms. This study aimed to construct a model of dexamethasone-induced skeletal muscle atrophy in zebrafish and to investigate the molecular mechanisms.

The purposes of this study were to explore the impact of obesity on postoperative cognitive dysfunction (POCD) and to investigate the underlying mechanism by which obesity exacerbates POCD. In this study, fifteen-month-old male C57BL/6 J mice were fed a High-fat diet for three months to establish obesity models. Internal fixation of tibial fractures under isoflurane inhalation was performed to construct a POCD animal model. Three days after surgery, mice were subjected to the Morris water maze (MWM) experiment to evaluate their learning and memory abilities. The findings from the MWM experiment revealed that in comparison to the Ad Libitum Surgical group (ALS), mice in the High-fat Surgical group (HFS) exhibited prolonged escape latencies and reduced platform crossings. These outcomes suggest the potential exacerbating role of obesity in cognitive impairment within the POCD mouse models. Immunofluorescence (IF) findings demonstrate that obesity intensifies anesthesia and surgery-induced oxidative stress levels within the hippocampus. Compared to the Ad Libitum Control group (ALC), an elevation in PARP1 expression and a reduction in the NAD/NADH ratio and SIRT1 expression were observed in the hippocampus of mice from the ALS. Moreover, when contrasting the HFS group with the ALS group, increased PARP1 expression along with decreased NAD/NADH ratio and SIRT1 expression were evident. In vitro studies found that compared with the Control group (CON), oil red staining and BODIPY probe staining showed significant lipid droplet aggregation in the palmitic acid (PA) group. IF results demonstrated that HT22 cells in the PA group experienced oxidative stress and activation of the PARP1/NAD/SIRT1 axis in contrast to the CON group. Moreover, manipulation of PARP1 expression in HT22 cells through PARP1 lentivirus-based silencing or overexpression revealed a converse relationship between PARP1 expression levels and the NAD/NADH ratio as well as SIRT1 expression levels. This study concludes that obesity may exacerbate POCD by triggering activation of the oxidative stress-induced PARP1/NAD/SIRT1 axis.