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Science, Volume 390, Issue 6776, Page 954-954, November 2025.

Science, Volume 390, Issue 6776, Page 945-950, November 2025.

Science, Volume 390, Issue 6776, Page 905-910, November 2025.

Science, Volume 390, Issue 6776, Page 935-939, November 2025.

Science, Volume 390, Issue 6776, Page 925-929, November 2025.

Science, Volume 390, Issue 6776, Page 918-924, November 2025.

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Science, Volume 390, Issue 6776, Page 940-944, November 2025.

Science, Volume 390, Issue 6776, Page 888-888, November 2025.

Science, Volume 390, Issue 6776, Page 887-887, November 2025.

Specialized appendage responds to female sex hormones, allowing males to find sex organs in the dark

Government pledges to more than triple research spending by 2030

CONCLUSION: Exercise can simultaneously impact insulin resistance and Alzheimer's disease pathology in animal models. Results from human research are limited, and no robust evaluation of the potential mediating role of insulin resistance in the physical activity - Aβ or tau relationship exists. Future research should focus on identifying the mediating pathways that may link physical activity to biomarkers of Alzheimer's disease.

Biomolecular condensates, membrane-less assemblies formed by phase separation, are implicated in neurodegenerative disease, but their role in Alzheimer's disease (AD) remains unclear. Here, we report that in the brain of AD patients and animal models, an elevation of poly(C)-binding protein 2 (PCBP2) correlates with biomolecular condensation that involves phase separation. These condensates sequester large numbers of mitochondrial and mRNA-binding proteins, leading to the outside impairment of...

Genome-wide association studies have identified many loci for brain disorders, but most non-coding variants fail to colocalize with bulk expression quantitative trait loci. Single-cell expression quantitative trait loci studies capture cell-type-specific regulation but are often underpowered. We developed Bulk And Single cell expression quantitative trait loci Integration across Cell states (BASIC) to combine bulk and single-cell expression quantitative trait loci through "axis-quantitative...

Aging and age-related diseases share convergent pathways at the proteome level. Here, using plasma proteomics and machine learning, we developed organismal and ten organ-specific aging clocks in the UK Biobank (n = 43,616) and validated their high accuracy in cohorts from China (n = 3,977) and the USA (n = 800; cross-cohort r = 0.98 and 0.93). Accelerated organ aging predicted disease onset, progression and mortality beyond clinical and genetic risk factors, with brain aging being most strongly...

Humans are living longer and experiencing more age-related diseases, many of which involve metabolic dysregulation, but how metabolism changes in multiple organs during aging is not known. Answering this could reveal new mechanisms of aging and therapeutics. Here, we profile metabolic changes in 12 organs in male and female mice at 5 different ages. We also develop organ-specific metabolic aging clocks that identify metabolic drivers of aging, including alpha-ketoglutarate, previously shown to...

Aging is one of the factors for the decline in adipose tissue browning and, consequently, age-related metabolic disorders. Metabolic disorders will in turn accelerate aging and lead to a vicious circle. Therefore, the research on the reduced browning of adipose tissue that occurs with aging, that is, adipose tissue browning aging, is necessary and of great significance for the development of metabolically healthy aging. In this study, we performed a bibliometric analysis of 2527 published...

Fuellen et al. (2025) highlighted the essential role of explainable AI methods, particularly principal component analysis (PCA), in evaluating interventions for aging and longevity. However, this paper raises significant concerns regarding PCA's linear and parametric nature, which can misrepresent complex, nonlinear data common in geroscience research. As biological relationships often defy simplistic interpretations, reliance on PCA may obscure vital insights, leading to potential...

The core mechanism of skeletal aging lies in the comprehensive disruption of microenvironmental homeostasis, involving a multidimensional interactive network comprising immune cells, mesenchymal stem cells, and their differentiated lineages. Although osteoporosis (OP) and osteoarthritis (OA) have traditionally been viewed as distinct degenerative disorders, recent breakthroughs in osteoimmunology reveal their shared immune-aging mechanism: immune cell dysfunction within the bone marrow...