GeroScience最新文献

Social support has been related to cardiovascular disease (CVD) incidence and mortality in longitudinal cohort analyses, but the biological pathways underpinning this remain underexplored. This exploratory study examined the associations between social support and a wide range of proteomic biomarkers and performed the mediating effect of proteomic biomarkers in the association between social support and CVD and mortality to identify potential biological pathways linking social support to health outcomes. Data from 3141 adults over the age of 50 in the English Longitudinal Study of Ageing who had plasma proteome data were analyzed, with CVD and mortality outcomes followed up for 16 years following through Hospital Episode Statistics and the National Health Service's Central Registry. Linear and Cox regression analyses were used to identify proteins associated with social support, CVD, and mortality. Mediation analysis was then performed on the identified proteins to explore their role as a potential mediator between social support and CVD and mortality risk. Over a median of 15.8-year follow-up, 889 participants have died, and 627 developed CVD. Of 276 plasma proteins measured, greater social support was associated with lower levels of 13 proteins and higher TN-R levels, after adjusting for baseline socioeconomic confounders. We also identified 49 protein-CVD and 70 protein-mortality associations after minimal adjustments, including 11 and 14 proteins simultaneously associated with social support. All the significant proteins together mediated about 20.9% and 26.4% of the associations for CVD and mortality, respectively. The main enriched biological pathways involved death receptor activity and carbohydrate binding. Social support was related to a cluster of proteomic biomarkers, which may be linked to inflammation, apoptosis, and atherosclerosis/vascular pathways. The identified plasma proteins partly mediated the association between social support and CVD and mortality risk, independently and cumulatively. These findings deepen our understanding of the intricate connections between relationship quality, proteomic signatures, and CVD and mortality development.

Age-related hearing loss (ARHL) is a common health problem that impairs auditory perception. However, the dynamic patterns of brain functional connectivity in ARHL during auditory spatial selective attention have not been thoroughly investigated. In this study, 32 older adults were recruited to investigate the dynamic brain functional connectivity in ARHL. First, an experimental paradigm for auditory spatial selective attention was designed, and neural electrical signals were recorded using electroencephalography. Then, a multilayer time-varying brain network was constructed based on multiple time windows, equally dividing each epoch signal to capture dynamic functional connectivity across time scales. Finally, the core layer brain network was identified by the multilayer time-varying brain network properties to investigate the changing patterns of network topology. Behavioral analysis revealed a significant negative correlation between the severity of hearing loss and auditory spatial selective attention performance. Multilayer time-varying brain network analysis revealed that worsening hearing loss was found to lead to increased inter-layer connectivity strength, decreased multilayer modularity and a higher participation coefficient. This suggests that the brain compensates by weakening the independence of local functional modules and enhancing cross-interaction. Core layer analysis further highlighted the critical role of the right parietal lobe in auditory spatial selective attention. It also suggested that connectivity between the right prefrontal and frontal lobes may play a compensatory role in ARHL. In conclusion, these findings provide important neuroscientific insights into the dynamic brain functional connectivity of ARHL, and potential biomarkers and time windows for the development of precision auditory rehabilitation strategies.

The ability to suppress irrelevant or distracting inputs that interfere with goal-driven behavior is known to decline with increasing age. Although noninvasive stimulation of the motor cortices has been shown to modulate age-related changes in motor activity, the findings remain preliminary, and it is unknown whether this effect extends beyond the motor cortex. In this study, 125 healthy adults, categorized into young (20-35 years) and older groups (55-72 years) underwent three visits (i.e., anodal, cathodal, and sham). During each visit, they received 20 min of high-definition transcranial direct current stimulation (HD-tDCS) applied to their left primary motor cortex (M1) and completed a flanker task during high-density magnetoencephalography (MEG). Statistically significant oscillatory responses were imaged and analyzed using voxel-wise, whole-brain, and point of stimulation approaches. Our results showed increased gamma flanker interference effects within the contralateral M1 in older relative to younger adults following anodal stimulation, and after anodal compared to cathodal HD-tDCS in older adults. We also found polarity-based differences in beta and gamma M1-prefrontal connectivity as a function of age group. Critically, these data indicate distinct spectrally- and polarity-dependent effects of M1 HD-tDCS on the local and network-level neurophysiological responses serving motor performance in young versus older healthy adults.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent condition increasingly recognized in aging populations. However, its clinical relevance in older adults-particularly in relation to sarcopenia, cognitive function, and rehabilitation outcomes-remains poorly defined. This retrospective observational study included in-patients admitted for geriatric rehabilitation in 2022 with available abdominal ultrasound. MASLD was defined according to AASLD/EASL criteria. Demographics, comorbidities, medications, and the hepatic steatosis index were recorded. Cognitive function (MMSE, clock-drawing, GDS), hand grip strength, mobility (Tinetti, Timed Up and Go), and functional status (Barthel Index, discharge autonomy) were assessed. Analyses included regression and AUROC, with significance at p below 0.05. MASLD was present in 49.6% of the study population. No significant association was observed between MASLD and cognitive impairment. Patients with higher hand grip strengths showed higher proportions of MASLD (p = 0.01). In this cohort, hepatic steatosis index has poor capacity to detect hepatic steatosis (AUC = 0.503, 95%-CI: 0.437-0.570). Furthermore, MASLD did not predict poorer functional outcomes following the rehabilitation stay. In adjusted models, Barthel Index -but neither MASLD nor hand grip strength- was independently associated with reduced functional autonomy at discharge (p = 0.006). In elderly patients, MASLD was associated with diabetes mellitus and higher hand grip strength, while sarcopenia was linked to a lower prevalence of steatosis. MASLD showed no association with cognitive performance, functional outcomes, or prediction by the hepatic steatosis index. These findings highlight age-specific characteristics of MASLD requiring tailored clinical approaches.

Facial wrinkling is a prominent sign of aging, yet individuals exhibit unique trajectories of biological aging, contributing to the variability in facial appearance. Here, we present a pioneering study exploring the association between lifestyle choices, DNA methylation, and SNP genotypes with a range of facial skin aging phenotypes. The study demonstrated that age-related facial skin phenotypes are influenced by multiple environmental stressors. Epigenome-wide association analyses identified differentially methylated cytosines mapped to 151 loci, including novel genes associated with facial wrinkles, such as EDAR (cg02925966, p = 4.96 × 10^-8) and NRG1 (cg26267340, p = 4.64 × 10^-8), both involved in wound healing. Sensitivity analysis, conditioning on the top meQTLs, showed minor attenuation, suggesting an association independent of genetic variants. Accelerated epigenetic aging, measured in the blood of over 700 Polish individuals, was found to correlate with facial wrinkle area, photoaging, telangiectasias, and perceived facial age, with the GrimAge and FitAge clocks showing the most robust associations. Genome-wide SNP analysis identified rs73943403 (RP11-78F17.1, p = 3.72 × 10^-8) associated with wrinkle area and rs113125564 (ZC3H4, p = 1.23 × 10^-8) associated with perceived facial age, potentially implicating stress response and adiposity in skin aging. Finally, the study revealed the additive value of methylation and SNP data for predicting two continuous skin phenotypes, with 59.0% of the variation explained in facial wrinkle area and 26.2% in perceived facial age. The findings underscore the relevance of genetic and epigenetic factors, revealing novel candidate genes and molecular pathways involved in skin aging. These insights hold substantial translational value for dermatology, the cosmetics industry, and anti-aging strategies.