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Will Gates and other funders save massive public health database at risk from Trump cuts?
Obesity drugs show promise for treating a new ailment: migraine
Did the US wipe out Iran's nuclear programme? What researchers know
Gating and noelin clustering of native Ca<sup>2+</sup>-permeable AMPA receptors
Modular arene functionalization by differential 1,2-diborylation
Comprehensive evaluation of plasma tau biomarkers for detecting and monitoring Alzheimer’s disease in a multicenter and multiethnic aging population
Sarcosine decreases in sarcopenia and enhances muscle regeneration and adipose thermogenesis by activating anti-inflammatory macrophages
Tardigrade-obsessed: meet the researchers trying to turn water bears into neuroscience models
‘Natural history museums can save the world’: anti-colonialism, conservation and climate change
Medical AI can transform medicine — but only if we carefully track the data it touches
First images from world’s largest digital camera leave astronomers in awe
Ice society: looking for life at unlikely altitudes
What scientists need to know about sharing—and protecting—their published work
With research papers becoming increasingly free to read and use, understanding open-access licenses is key
How many PhDs does the world need? Doctoral graduates vastly outnumber jobs in academia
Multinational evaluation of AnthropoAge as a measure of biological age in the USA, England, Mexico, Costa Rica, and China: a population-based longitudinal study
We validated AnthropoAge, a biological age (BA) metric, for prediction of mortality and age-related outcomes using harmonized data from the US, England, Mexico, Costa Rica, and China. We estimated AnthropoAge and AnthropoAgeAccel as proxies of BA and age acceleration using body mass index and waist-to-height ratio. We compared mortality prediction of AnthropoAge vs. chronological age (CA) using Cox models and assessed its association with age-related outcomes with generalized estimating...
Mechano-energetic uncoupling in heart failure
Heart failure (HF) is a major global and life-threatening disease. Despite advances in therapies, the prevalence of HF is increasing owing to an ageing population and the pervasive pandemic of obesity and metabolic disorders, which have transformed the pathophysiology of HF. Changes in cardiac energy metabolism and the related energy deficit crucially contribute to the severity and type of HF. Furthermore, perturbations in excitation-contraction coupling, mitochondrial function and oxidative...
Cardiac intermediary metabolism in heart failure: substrate use, signalling roles and therapeutic targets
The number of patients with heart failure is expected to rise sharply owing to ageing populations, poor dietary habits, unhealthy lifestyles and improved survival rates from conditions such as hypertension and myocardial infarction. Heart failure is classified into two main types: heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). These forms fundamentally differ, especially in how metabolism is regulated, but they also have shared...
The future of biomarkers for vascular contributions to cognitive impairment and dementia (VCID): proceedings of the 2025 annual workshop of the Albert research institute for white matter and cognition
Advances in biomarkers and pathophysiology of vascular contributions to cognitive impairment and dementia (VCID) are expected to bring greater mechanistic insights, more targeted treatments, and potentially disease-modifying therapies. The 2025 Annual Workshop of the Albert Research Institute for White Matter and Cognition, sponsored by the Leo and Anne Albert Charitable Trust since 2015, focused on novel biomarkers for VCID. The meeting highlighted the complexity of dementia, emphasizing that...
ACLY links mutant α-synuclein to metabolism, autophagy and neurodegeneration
In this issue of Neuron, Son et al.¹ reveal how pathologic α-synuclein inhibits autophagy, leading to neurodegeneration. Their work highlights the key roles of the acetyl-CoA-producing enzyme ACLY and aberrant cytoplasmic p300 acetylation, uncovering new therapeutic strategies for Parkinson's disease.
Astrocytes have no CLU they contribute to Alzheimer's disease
Clusterin (CLU) is a recognized genetic risk factor for Alzheimer's disease. In this issue of Neuron, Lish et al.¹ found that lower CLU levels in astrocytes, caused by the CLU risk allele, heightened inflammation and reduced synaptic functions, potentially increasing risk for cognitive decline.