The treatment reduced oxidative stress, suppressed inflammation, and remodeled the gut microbiome in naturally aging mice while prolonging survival in nematodes.
Multi-omics profiling in Drosophila links chromatin regulation to increased ATP, higher NAD-to-NADH ratios, and altered lipid metabolism in aged heads.
Loss of the cGAMP-degrading enzyme ENPP1 allows microglia-derived signaling molecules to trigger STING-dependent inflammation across multiple brain cell types.
Aged male mice showed far larger proteomic shifts than females following microglial removal, including alterations in synaptic and mitochondrial proteins.
bioRxiv : the preprint server for biology · Beganovic A et al.
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 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.
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.
Neutrophil-coated nanoparticles crossed the blood-brain barrier, altered microglial metabolism, and improved cognitive performance after surgery in older mice.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Huang L et al.
Clearing these peripheral myeloid cells remodeled brain macrophages and improved cognitive performance without requiring the engineered immune cells to enter the brain.
Researchers identified ghrelin as a key metabolic factor that reduces microglial senescence and inflammation through the SHBG/JNK1/Beclin1 signaling axis.
An immune risk score tracking immunosenescence correlated with markers of neural injury and neuroinflammation rather than classical amyloid or tau pathology.
Inactivating the ligase HOIL-1 solidifies dynamic protein condensates and impairs the autophagic clearance of tau, amyloid-beta, and alpha-synuclein aggregates.
Loss of the chaperone mediator in human astrocytes disrupts autophagy, proteasomes, and retromer traffic while impairing amyloid-beta proteostasis in neuron cocultures.
Proceedings of the National Academy of Sciences of the United States of America · Augur ZM et al.