A large genomic analysis reveals over 800 inherited variants and structural features that alter how frequently chromosomes missegregate in aging individuals.
medRxiv : the preprint server for health sciences · Si Y et al.
Why it mattersMosaic chromosomal aneuploidies in blood commonly emerge as people age. Identifying the genetic factors behind mitotic errors provides tools to assess how clonal somatic mutations influence health and aging biology.
Mosaic chromosomal aneuploidies in blood commonly emerge as people age. Identifying the genetic factors behind mitotic errors provides tools to assess how clonal somatic mutations influence health and aging biology.
Why it matters
Mosaic chromosomal aneuploidies in blood commonly emerge as people age. Identifying the genetic factors behind mitotic errors provides tools to assess how clonal somatic mutations influence health and aging biology.
Cortical neurons gain mutations at similar yearly rates across six species, leaving aged humans with uniquely high mutational burdens and transcriptomic dysregulation.
bioRxiv : the preprint server for biology · Caglayan E et al.
Reversible oxidation of a single cysteine residue enables core autophagosome formation and prevents severe tissue pathology during nutrient limitation in mice.
bioRxiv : the preprint server for biology · Shin S et al.
The senolytic combination improved liver fibrosis without disease worsening in nearly half of treated participants while lowering cellular senescence markers.
A genome-scale screen in retinal cells identified NKX2-5 variants that conferred oxidative resilience and improved physical function without detectable toxicity.
Loss of the cGAMP-degrading enzyme ENPP1 allows microglia-derived signaling molecules to trigger STING-dependent inflammation across multiple brain cell types.
In cultured fibroblasts and mice, apolipoprotein D triggers SUN1 accumulation, reinforcing a signaling cycle that alters gene expression and cellular polarity.
bioRxiv : the preprint server for biology · Chen M et al.
Multi-omics clocks across fourteen organs reveal divergent molecular programs and uncover thirteen candidate genes separating age acceleration from mortality.
Researchers identified a transient senescent-like monocyte state governed by the transcription factor AP-1 that primes cells toward inflammatory and sepsis-associated states.
bioRxiv : the preprint server for biology · Vasilopoulos T et al.
Researchers linked poor auditory nerve synchrony and myelin degradation to amplified communication difficulties in older humans, beyond standard hearing thresholds.
medRxiv : the preprint server for health sciences · Harris KC et al.
A multi-omic analysis shows that defective luteal resolution and CHK2-driven inflammation drive ovarian aging, but drug inhibition restores oocyte maturation.
In cells expressing progerin, the nucleolus sequesters released lamina-associated domains to preserve gene repression and prevent worsening DNA damage.
Human neurons from frontotemporal lobar degeneration patients showed ultra-low-frequency TARDBP variants that were less abundant in individuals who died at older ages.
bioRxiv : the preprint server for biology · Bidhan V et al.
Researchers found that expanding polyglutamine tracts in the androgen receptor shift binding toward senescence-linked enhancers, driving muscle atrophy in cells and mice.
Single-nucleus sequencing reveals disrupted signaling between satellite cells and fibro-adipogenic progenitors during muscle regrowth in older females.
bioRxiv : the preprint server for biology · Skiles CM et al.
While lifelong depletion reduced muscle strength, short-term deficiency in adult mice induced hypertrophy without degrading muscle quality or contractile performance.
bioRxiv : the preprint server for biology · Son W et al.
Researchers found that senescent epithelial cells secrete TGF-beta1 to reprogram fibroblasts into a matrix-remodeling state, which senolytic treatment can blunt.
