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Aging reshapes T cell immunity, as evidenced by eroding naive diversity and remodeled memory hierarchies. This generates an experienced yet constrained repertoire, with weakened protection against novel infections and malignancies and blunted vaccine responsiveness. However, the pace and extent of decline vary widely between individuals. Such heterogeneity signals a recalibration of immune priorities that favors persistence over plasticity of memory T cells. Here, we discuss how aging shapes...

Analysis of gravitational waves supports theory that some stars explode without leaving behind black holes

Bristling, multilegged ocean swimmer shows early emergence of claws  

Ambitious effort tested whether more than 100 papers held up on multiple types of “repeatability” tests

Gastrointestinal dysfunction often precedes motor symptoms in Parkinson's disease (PD), suggesting the enteric nervous system (ENS) is central to early pathogenesis. How α-synuclein contributes to ENS dysfunction, and how inflammation modulates this, remains unclear. Here we show that Tumor Necrosis Factor alpha enhances α-synuclein accumulation in induced pluripotent stem cell-derived enteric neurons and glia, and impairs the malate-aspartate shuttle, a key pathway for mitochondrial energy...

Cancer immunotherapy has markedly improved patient outcomes, particularly when combined with conventional treatments such as chemotherapy, radiotherapy, and targeted therapy. Following these therapies, however, a subset of cancer cells can enter a senescent state, ceasing proliferation while remaining metabolically active and persistent within tissues. Such therapy-induced senescent cancer cells (TISCCs) significantly influence antitumor immune responses. TISCCs can enhance tumor immunogenicity...

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Neurons assemble into breathtakingly intricate circuits that govern behavior and often perdure for life. How injured or aged neurons control their complex morphological connections to survive or perish remains an exciting and open question. Using the genetics of Caenorhabditis elegans, Park et al. uncover that lipid biosynthesis is critical for both neuronal regrowth after injury, and for maintaining neuronal morphology during aging. This primer is designed to help students read and understand...

Lipidomic analysis enables the detailed characterization of platelet concentrates from donors of different ages, offering valuable insights into the role of lipid mediators in aging and transfusion-related adverse reactions (AR). In this study, we analyzed lipidomic profiles from a cohort of single-donor apheresis platelet concentrates, classified into three age groups: 20-44, 45-59, and 60-70 years. Total levels of LPC, LPA, S1P, and eicosanoids did not exhibit significant age-related changes....

Nanoscale chromatin domains have emerged as fundamental units of mammalian genome organization during interphase and mitosis. Single-molecule localization microscopy now enables their direct visualization, revealing conserved features including characteristic packing, enrichment of linker histones, and radial stratification of histone marks. These domains act as dynamic regulators of gene activity, remodel in response to developmental and environmental cues, and become disrupted in disease....

Aging impairs vision, but its specific impact on the neural channels underlying pattern processing is unknown. By examining individual differences in behavioral data from 52 younger and 50 older adults, we investigated how aging reorganizes underlying channels for detecting first-order (defined by luminance static or in motion) and second-order (defined by contrast, motion, or orientation) patterns. We identified a key organizational feature in youth on spatial processing: a global factor...

Neurodegeneration shows regional and cell-type-specific patterns in ageing and disease¹, but the underlying mechanisms for cell-type-specific neuronal losses remain poorly understood. Previous studies have shown that upper cortical layer thinning occurs in progressive human multiple sclerosis (MS) and that cortical layer 2 and layer 3 (L2/3) excitatory neurons (L2/3ENs) that express CUT-like homeobox 2 (CUX2) are selectively vulnerable to degeneration². Here we report that L2/3ENs within MS...

The MetaboHealth score, a metabolomics-based biomarker trained on mortality, is associated with ageing-related phenotypes and morbidity, but its heritable component is still uncertain. Understanding genetic versus environmental contributions is essential for its utility as an intervention-responsive biomarker. Hence, the aim of this study was to estimate heritability of the MetaboHealth score in the large Swedish TwinGene cohort and evaluate interactions with modifiable lifestyle factors and...

Synucleinopathies is an umbrella term for multiple neurological disorders, including Parkinson's disease (PD), Lewy body dementia (LBD), and multiple system atrophy (MSA). A central pathological hallmark of synucleinopathies is the aggregation of α-synuclein (αS, a neuronal protein) and its prion-like spread. Therefore, inhibition of αS aggregation and spread is considered a viable therapeutic approach for the treatment of synucleinopathies. Foldamers are synthetic ligands that mimic the...

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CONCLUSIONS: Community-based interventions to improve physical accessibility and dementia awareness may be important avenues for supporting social activity engagement among people in the last stage of life, particularly among older adults living independently in their communities.

Aging is accompanied by progressive functional decline, and nuclear receptors have become significant modulators of the process. Farnesoid X receptor (FXR), a ligand activated nuclear receptor transcription factor that regulates genes involved in bile acid and metabolic homeostasis, has been implicated in aging, yet genetic evidence remains limited. In this study, we demonstrate that FXR knockout (FXR^(-/-)) mice have significantly shorter lifespan and healthspan than WT mice. FXR deficiency led...

Mitochondrial degeneration and dysfunctions are increasingly linked with neurodegenerative diseases, with the greatest risk factor being increased age. Mitochondrial dysfunction is also implicated in sarcopenia, the age-associated weakness and atrophy of striated muscle. Untangling the pathophysiological effects of age-related mitochondrial degeneration and dysfunction is of huge interest in gerontology. In elderly humans and Fischer 344 (F344) rats, motor neuron (MN) death and denervation...