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The Integrated Care for Older People program of the World Health Organization is intended as a catalyst to empower communities to cocreate personalized interventions and usher in an era of precision healthy longevity, in which the needs, values and preferences of older people are centered. A study from France now presents early screening data and reveals distinct phenotypic trajectories towards adverse outcomes.
In our study, we linked machine-learning-derived biological age gaps (BAGs) to common genetic variants in nine human organ systems, which revealed how these BAGs are causally associated with organ health and chronic diseases such as Alzheimer’s disease and diabetes. The findings provide insights into therapeutic and lifestyle interventions that might enhance organ health.
A study from Ortega-Molina and colleagues uses mouse models with mildly elevated mTOR activity to investigate the stepwise process by which increased nutrient signaling affects healthy aging. These findings show how initial parenchymal damage caused by mTOR activity is followed by secondary myeloid inflammation, a multistage process that culminates in organ deterioration and reduced lifespan.
Our study shows that older adults who survive severe COVID-19 suffer accelerated cognitive decline for 1 year after infection, after which the rate of decline decelerates. Long-lasting cognitive impairment occurs mostly in individuals who had severe COVID-19, showed cognitive impairments at 6 months after infection and had coexisting hypertension.
SARS-CoV-2 infections are typically more severe with increased age. Vaccination can reduce morbidity and mortality, but the age-associated decline in immune function could limit vaccine efficacy in older adults. Dallan, Proietto and colleagues demonstrate robust immunological humoral and cellular memory in older adults who received primary vaccinations using the adenoviral platforms and received subsequent boosting with mRNA vaccine platforms.
Identification of patients at risk for hip fracture is crucial to inform intervention strategies. We developed a plasma protein-based risk score for hip fracture and validated this score in three independent cohorts using two substantially different proteomics platforms. The protein-based risk score, but not available polygenic risk scores, improved hip fracture discrimination.
A study demonstrates the efficacy of immune-checkpoint blockade in prolonging survival and boosting CD8+ T cell function in aged mice after pathogen exposure. These findings highlight how aging-related immune changes may lead to augmented CD8+ T cell responses to checkpoint blockade, which results in improved protection from infection. The findings also highlight the importance of understanding immune aging in future efforts to target immunotherapies to older adults.
A deep learning model accurately predicts 1-year mortality for the entire Finnish population. Despite robust performance and potential as a digital marker of aging, fairness analyses reveal prediction disparities, so integration into public health should be approached cautiously.
Older age is associated with metabolic stress and increases the risk of degeneration of organs that maintain metabolic homeostasis, including the liver. We discovered that aging promotes ferroptosis in hepatocytes, that ferroptotic stress is generally increased in degenerating organs, and that reducing ferroptosis reverses aging-related metabolic dysfunction and liver damage.
We reveal considerable heterogeneity in risk factors for healthy aging in Latin America, which underscores the limitations of existing, unharmonized research models for diverse populations. Our results emphasize the urgent need for region-specific studies that describe particular risks for Latin American aging to develop tailored preventive models and interventions.
Inhibitors of sodium glucose co-transporter 2 (SGLT2) have long been used in the treatment of diabetes and cardiovascular disease, owing to their modulation of glucose levels. Katsuumi and colleagues now show that, in addition to their glycemic effects, SGLT2 inhibitors modulate senescence immune surveillance by downregulating PD-L1 expression on senescent cells.
Small extracellular vesicles (sEVs) derived from the blood of young mice are shown to have the potential to extend lifespan and rejuvenate physiological functions in aged mice. Mechanistically, microRNA (miRNA) cargoes within these sEVs alleviated age-related dysfunction by promoting the expression of PGC1α and enhancing mitochondrial energy metabolism.
A study in Nature Aging on electronic health records from 1.7 million people in New Zealand reveals that most patients with dementia have a history of hospital-treated infection. In a dementia-free population, individuals with a severe infection were at a threefold-higher risk of dementia even 25 years later.
Aging-related DNA methylation changes are numerous. Their precise measurement has opened new avenues to explore aging-related disease pathology, including the construction of chronological and biological age predictors (termed DNA methylation ‘clocks’). Three studies investigate the substantial stochastic contribution to these epigenetic changes and further our understanding of aging biology, as well as of these predictors.
Zou and colleagues design and analyze a health education program that targeted college students (who were grandchildren) to encourage older persons who had already had their first COVID-19 vaccine dose to receive a booster. The program increased the uptake of booster doses, which highlights the fact that family ties can have positive roles in the context of a pandemic.
Zhou and colleagues explore reversing testicular aging and late-onset hypogonadism by targeting lysosomal function in Sertoli cells. The aging-related transformation of Sertoli cells into a lipid-hoarding subtype with dysregulated phagolysosomes and autolysosomes was reversed using the TRPML channel agonist ML-SA1, which demonstrates the potential of this targeted therapy in alleviating testosterone decline and systemic male-aging phenotypes.
Skeletal muscle is a highly heterogenous tissue that comprises multiple cell types. Leveraging single-cell and single-nucleus experiments, we systematically mapped the cellular and molecular changes across different skeletal muscle compartments with age. We identify neuromuscular-junction accessory nuclei that may be pivotal in mitigating denervation and uncovered differences between myofiber and myonucleus aging.
The advent of plaque-clearing antibodies to the amyloid-β as the first disease-modifying treatment for Alzheimer’s disease will change the course of this disease, the most common type of dementia. Related progress will gradually alter the trajectory of human aging.
Our analysis of the spatiotemporal transcriptional features of human ovarian aging at the single-cell level identified the DNA damage response as a fundamental attribute in oocyte senescence. FOXP1, a gatekeeper both in granulosa and in theca and stroma cellular senescence, can be activated by quercetin treatment to delay ovarian aging.
