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As forests burn, can we replant trees ready for a warmer world?
Ecologists testing “assisted migration” are pushing seedlings to the limits—and finding that location matters
Scientists find an immune “false alarm” that may drive rapid aging
Scientists have discovered that some severe genetic disorders linked to rapid aging may be driven not just by damaged DNA, but by the body’s overreaction to that damage. When broken DNA fragments leak into the wrong part of a cell, an immune sensor called cGAS can mistake them for signs of a viral infection, triggering chronic inflammation and even interfering with DNA repair itself.
Scientists find the whole grain “sweet spot” for better heart health
Eating four to six servings of whole grains a day may deliver meaningful benefits for heart health, according to a large review of 87 clinical trials. Researchers found improvements in body weight, waist size, blood pressure, cholesterol, blood sugar, triglycerides, and some markers of inflammation.
Scientists recreated what mice saw from brain activity alone
Scientists reconstructed videos from the brain activity of mice, producing 10-second clips based only on signals from neurons in the visual cortex. The breakthrough could help reveal how the brain reshapes what we see before it becomes our perception of reality.
Human neurons flourish in mouse brains, offering a new view of neurodevelopmental disorders
Method of replacing much of the mouse cortex with human “organoids” enables studies of brain diseases in a living nervous system
Associations of physical fitness with brain structure, pathology and cognition in cognitively normal older adults
The role of physical fitness in cognitive reserve and brain maintenance remains unclear. We investigated the associations of muscular and aerobic fitness (VO(2)max) with markers of brain health and cognition in 353 cognitively unimpaired older adults (mean age = 72.77 ± 7.95 years; 177 females). Muscular fitness comprised handgrip strength, appendicular skeletal muscle mass, and Timed-Up-and-Go performance. Blood biomarkers of Alzheimer's pathology (Aβ(1-42)/Aβ(1-40), p-tau(217), GFAP) and...
APOE genotypes differentially remodel the astrocytic lipid droplet proteome to shape lipid droplet dynamics
Lipid droplets are dynamic cellular organelles that store neutral lipids and coordinate metabolic and stress-response pathways. In the brain, lipid droplets in glial cells, including astrocytes, have been implicated in Alzheimer's disease, but how genetic risk factors influence their composition and turnover remains poorly understood. APOE is the strongest genetic modulator of late-onset Alzheimer's disease and exists in common variants that confer decreased, neutral, or increased risk. Here we...
Map of brain 'microproteins' could offer new clues to Alzheimer's disease
No abstract
Sex-specific biological aging clocks across organs and omics
Sex differentially shapes aging, neurodevelopment and neurodegenerative diseases such as Alzheimer's disease (AD). However, most biological aging clocks (artificial intelligence-predicted age minus chronological age) were trained on sex-pooled samples and implicitly assume sex invariance.Here we developed 38 sex-specific biological aging clocks across 15 organ systems. We first demonstrate the importance of sex-stratified training for constructing sex-specific healthy normative references and...
HMGA1-HP1beta axis regulates premature aging in Hutchinson-Gilford progeria syndrome through chromatin remodeling
Hutchinson‑Gilford progeria syndrome (HGPS) is a rare premature aging disorder caused by mutations in the LMNA gene. High mobility group A1 (HMGA1) exhibits differential expression patterns across aging models. However, its roles and mechanisms in aging remain unclear. Here, we show a positive correlation between HMGA1 and the heterochromatin protein HP1β in multiple tissues of Lmna^(G609G/G609G), a classic genetic mouse model of HGPS to recapitulate typical premature aging features, and...
Cell senescence emerges as a hallmark and therapeutic target of chronic intracellular infection
Intracellular pathogens are ideal candidates for modelling the pathophysiology of chronic infection, as they hide within host cells and avoid immune clearance by reshaping cellular fate. This study unveils how the intracellular pathogen Mycobacterium abscessus (Mab) reprograms alveolar macrophages towards a senescent state -a multifaced phenotype marked by proliferative arrest, distinctive morphological shifts, activation of DNA damage signalling cascade, and secretion of senescence-associated...
CK2alpha restriction of STING accumulation underlies systemic aging
Chronic activation of the cGAS-STING pathway drives inflammaging and cellular senescence. Although nuclear envelope (NE) barrier failure leading to cytoplasmic chromatin leakage is a key trigger, the molecular mechanisms governing STING activity at the NE during aging remain poorly understood. Here, we identify lamin A/C (LMNA) as a critical NE scaffold that orchestrates STING regulation by recruiting both STING and Casein Kinase 2 (CK2α). We demonstrate that LMNA facilitates the phosphorylation...
Quantitative proteomics reveals coordinated changes in the proteome during replicative senescence
Cellular senescence is a state of irreversible cell cycle arrest triggered by telomere erosion, persistent DNA damage or chronic stress. The accumulation of senescent cells disrupts tissue function and contributes to aging and disease. Here, we employ mass spectrometry-based proteomics to systematically interrogate dynamic proteome changes at multiple levels during the progression of replicative cellular senescence. We demonstrate that proteome changes during senescence occur in a coordinated...
Map of brain 'microproteins' could offer new clues to Alzheimer's disease
No abstract
Publisher Correction: Three-dimensional mapping of intact ovaries reveals the aging dynamics of the ovarian reserve
No abstract
Sex-specific biological aging clocks across organs and omics
Sex differentially shapes aging, neurodevelopment and neurodegenerative diseases such as Alzheimer's disease (AD). However, most biological aging clocks (artificial intelligence-predicted age minus chronological age) were trained on sex-pooled samples and implicitly assume sex invariance.Here we developed 38 sex-specific biological aging clocks across 15 organ systems. We first demonstrate the importance of sex-stratified training for constructing sex-specific healthy normative references and...
The TyrRS cascade: circadian gating of neuronal DNA repair and its collapse in aging
Age-related neurodegenerative diseases are characterized by progressive DNA damage in post-mitotic neurons against a backdrop of deteriorating circadian rhythms, yet the molecular link between these conjoined features of brain aging remains unclear. We propose the TyrRS cascade as that link: a signaling architecture in which the noncanonical nuclear functions of tyrosyl-tRNA synthetase (TyrRS/YARS1) schedule neuronal genome maintenance across the day through three coregulated streams,...
Age-dependent changes in lipid droplet distribution and vascularization in naked mole rat vs. mouse hippocampus
The accumulation of lipid droplets in microglia has been reported to increase in response to ageing and age-related diseases like Alzheimer's disease. The present study investigates changes in lipid droplet dynamics with increasing age in the mouse and the similarly sized long-lived rodent, the naked mole rat (Heterocephalus glaber). We show that the naked mole rat contains large amounts of microglial lipid droplets in the CA1 and CA3 region of the hippocampus with an age-dependent increase in...
Adaptive hypergraph learning reveals high-order functional network alterations in mild cognitive impairment
Mild cognitive impairment (MCI) is an important prodromal stage of Alzheimer's disease, and its early identification is critical for risk assessment and timely intervention. Resting-state functional magnetic resonance imaging (rs-fMRI) can noninvasively characterize brain functional activity and connectivity. However, most existing methods rely on static second-order functional connectivity, limiting their ability to capture dynamic coordination and high-order interactions among multiple brain...
Inflection points and transitions in Alzheimer's disease
Alzheimer's disease is widely depicted as a linear cascade from amyloid-β accumulation to Tau pathology and neurodegeneration. We propose instead that the disease unfolds through discrete molecular, cellular and network phases organized around biological inflection points. At these thresholds, stress-driven loss of homeostasis produces qualitative shifts in cellular behavior that alters disease progression. These altered states spread across local tissue-domains, accumulate as a mosaic across...