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Age-related sensory decline impairs responses to balance disturbances, increasing fall risk. Evaluating gait and balance under sensory challenges can help reveal how this decline affects instability in older adults. This study (Clinicaltrials.gov NCT06345625) incorporates head movements to evaluate the effect of sensory function - cervical sensorimotor control, vestibular function, and visual acuity - on walking stability in aging and its relationship with falls through a novel augmented-reality...

Aging is a critical risk factor for intervertebral disc degeneration, a major contributor to chronic low back pain. Loss-of-function studies showed that SIRT6, a nuclear NAD^(+)-dependent deacetylase, maintains disc health. We therefore investigated whether long-term SIRT6 activation via systemic delivery of the small-molecular agonist MDL-800 improves disc health in 24-month-old mice. Studies revealed healthy disc morphology, enhanced cell viability, and lower degeneration scores following...

Disruption describes the extent to which a scientific work overturns the prior knowledge on which it builds and leads to a new line of research. A scientist's tendency to produce disruptive work has been found recently to decline over the career. However, the disruption index captures only how strongly a paper overturns prior work and ignores whether that disruption is later accepted or overturned by subsequent research. The persistent disruption (PD) framework adds this second perspective,...

Maternal age is the primary risk factor for aneuploidy in mammalian oocytes, but the molecular mechanisms that preserve meiotic chromosome segregation fidelity during aging remain incompletely understood. Using ultrastructural analysis, we observe that spindle microtubules in aged mouse oocytes tend to exhibit increased misorientation and shorter interaction lengths, whereas microtubule number and density remain largely unchanged. We demonstrate that the levels of the key centromeric components...

Scientists have uncovered an unexpected culprit behind sleep loss in Alzheimer’s disease: overactive immune cells in the brain. By temporarily removing these cells, researchers restored more than two hours of sleep per day in mice, revealing a promising new target for treatment.