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Can academia handle my religious faith?
This robot hand detaches and walks by itself
Briefing Chat: What Brazilian centenarians could reveal about the science of ageing
Largest galaxy survey yet confirms that the Universe is not clumpy enough
Publisher Correction: <i>Nanotyrannus</i> and <i>Tyrannosaurus</i> coexisted at the close of the Cretaceous
Publisher Correction: A domed pachycephalosaur from the early Cretaceous of Mongolia
Light-powered bacteria become living chemical factories
Traces of ancient seafloor cataclysms turn up in the Himalayas
Vast undersea eruptions may be undercounted source of extinctions through Earth’s history
Trump slump? Attendance plummets at some science meetings, but others hold steady
Amid travel bans, a government shutdown, and funding crunches, 2025 was a turbulent year for U.S. scientific societies
Snakes on a train? Deadly reptiles may be hopping railcars in India
Trains may be transporting cobras and other venomous snakes to new parts of the country
CRISPR screens in iPSC-derived neurons reveal principles of tau proteostasis
Aggregation of the protein tau defines tauopathies, the most common age-related neurodegenerative diseases, which include Alzheimer's disease and frontotemporal dementia. Specific neuronal subtypes are selectively vulnerable to tau aggregation, dysfunction, and death. However, molecular mechanisms underlying cell-type-selective vulnerability are unknown. To systematically uncover the cellular factors controlling the accumulation of tau aggregates in human neurons, we conducted a genome-wide...
Anti-TLR2 immunotherapy modulates neuron-to-oligodendrocyte propagation of α-synuclein in mouse and human models
Intracellular accumulation of α-synuclein (αSyn) aggregates is a hallmark of synucleinopathies, such as Parkinson's disease (PD) and multiple system atrophy (MSA). In MSA, αSyn aggregates form glial cytoplasmic inclusions (GCIs) in oligodendrocytes, despite their low expression of αSyn. Here, we demonstrate that neuron-to-oligodendrocyte propagation of αSyn, via Toll-like receptor 2 (TLR2) contributes to GCI formation. Male transgenic mice expressing the A53T mutant human αSyn exclusively in...
Spinal cord stimulation therapy for gait impairment in Parkinson's disease: a double-blinded, randomised feasibility trial with an open extension
A trial of spinal cord stimulation (SCS) was performed in people with gait-impaired Parkinson's (ClinicalTrials.gov: NCT05110053). Fourteen patients underwent gait assessments and [^(18)F]-FDG and [^(18)F]-FEOBV PET at baseline, six, and twelve months after SCS. Twelve participants were randomised to six-month MicroBurst or sham, followed by six-month extension with stimulation. The primary outcomes were feasibility and safety, as captured by the trial process measures and nature and frequency...
Cytokine-induced senescence in tumors is based on sustained activation of STAT1- and NFkappaB-dependent gene regulatory signatures
Senescence is a tripartite cellular phenotype characterized by permanent growth arrest, resistance to apoptosis, and high secretory activity. Besides its physiological role in embryonic development and pathophysiological contribution to age-related tissue degeneration, in the context of tumor development senescence is an important suppressor mechanism, that counteracts accelerated proliferation. Among the many stressors that induce senescence is the external stimulation by cytokines. Although...
Exploring the nexus between inflammation and mobility through the lens of healthy aging: current scenario and future perspectives
Aging is characterized by a progressive decline in physiological resilience and functional capacity, often accompanied by chronic, low-grade systemic inflammation, a phenomenon termed "inflammaging". This persistent inflammatory milieu contributes significantly to musculoskeletal degeneration, impaired neuromotor coordination, and reduced mobility, collectively diminishing quality of life, particularly among older adults. Key biological drivers of inflammaging include cellular senescence, immune...
Muscle stem cells trade functionality for survival
During aging, stem cell persistence is favored over functionality, resulting in delayed responses to injury.
Rethinking the heritability of aging
The genetic contribution to human longevity is greater than previously thought.
Heritability of intrinsic human life span is about 50% when confounding factors are addressed
How heritable is human life span? If genetic heritability is high, longevity genes can reveal aging mechanisms and inform medicine and public health. However, current estimates of heritability are low-twin studies show heritability of only 20 to 25%, and recent large pedigree studies suggest it is as low as 6%. Here we show that these estimates are confounded by extrinsic mortality-deaths caused by extrinsic factors such as accidents or infections. We use mathematical modeling and analyses of...
DNA-protein cross-links promote cGAS-STING-driven premature aging and embryonic lethality
DNA-protein cross-links (DPCs) are highly toxic DNA lesions that block replication and transcription, but their impact on organismal physiology is unclear. We identified a role for the metalloprotease SPRTN in preventing DPC-driven immunity and its pathological consequences. Loss of SPRTN activity during replication and mitosis lead to unresolved DNA damage, chromosome segregation errors, micronuclei formation, and cytosolic DNA release that activates the cyclic GMP-AMP synthase...
Aging drives a program of DNA methylation decay in plant organs
Plants display a wide range of life spans and aging rates. Although dynamic changes to DNA methylation are a hallmark of aging in mammals, it is unclear whether similar molecular signatures reflect rates of aging and organism life span in plants. In this work, we show that the short-lived model plant Arabidopsis thaliana exhibits a loss of epigenetic integrity during aging, which causes DNA methylation decay and the expression of transposable elements. We show that the rate of epigenetic aging...