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Mitochondrial dysfunction and impaired mitophagy are hallmarks of aging and age-related pathologies. Disrupted inter-organellar communication among mitochondria, endoplasmic reticulum (ER), and lysosomes, further contributes to cellular dysfunction. While mitophagy has emerged as a promising target for neuroprotection and geroprotection, its potential to restore age-associated defects in organellar crosstalk remains unclear. Here, we show that mitophagy deficiency deregulates the morphology and...

Time-based diets have gained popularity for their health benefits, but their effects on human longevity remain unclear, with most evidence from short-term human trials and animal studies. We determined the associations between eating window and mortality among U.S. adults. We conducted a prospective cohort study using NHANES 2003-2018 data linked to mortality records through December 2019. The analytic sample included 33,052 adults (aged 20 and above) with two complete 24-h dietary recalls...

Chemotherapy-induced cognitive impairment (CICI), commonly referred to as chemobrain, is a pervasive adverse effect of cancer treatment, characterized by deficits in memory, concentration, and executive function. Several observations have suggested a potential for senescence in mediating CICI. First, chemotherapeutic agents that are implicated in CICI can also trigger senescence in neurons and glial cells, accompanied by the senescence-associated secretory phenotype (SASP), that could propagate...

Background: The Multiracial population is the fastest-growing racial group in the United States but remains underrepresented in cognitive aging research. No national estimates exist for subjective cognitive decline (SCD)-a self-reported indicator of worsening memory associated with dementia risk-among older Multiracial adults. Methods: We used 2019-2023 Behavioral Risk Factor Surveillance System data from states that administered the optional cognitive decline module (n = 599,874 adults aged...

Growing evidence from the past seven decades indicates that atherosclerosis begins in youth and progresses in response to exposure to cardiovascular risk factors, which contribute to the development of cardiovascular disease in later life. A long-term randomized clinical trial lasting at least 50 years and involving screening and follow-up of children across their lifespan would provide the highest level of evidence to determine the lifelong influence of cardiovascular risk factors on...

Biological age (BA) reflects the aging process more accurately than chronological age. This study aimed to evaluate the associations and predictive values of nine BA measures for mortality outcomes. BA measures were developed using data from the Yixing Cohort Study (YCS; N = 4,128) and externally validated in the Jurong Cohort Study (JCS; N = 16,652). Dose-response relationships between the clinical indices and all-cause death were assessed using restricted cubic spline analysis. Statistically...

Retinitis pigmentosa (RP), the leading cause of inherited blindness, lacks therapies because of undefined photoreceptor degeneration mechanisms. While microglia/myeloid cells drive RP progression, their phenotype-regulating determinants remain unclear. Using rd10 mice, we reveal TREM2 as a biphasic RP regulator via STAT2-mediated microglial reprogramming. Early TREM2 loss amplifies neuroinflammation through STAT2 hyperactivation, while late deficiency triggers NF-κB/STAT2-driven microglial...

Immunosenescence is the process of immune dysfunction and gradual deterioration of the immune system associated with aging, while cellular senescence is the stable cell cycle arrest that can occur in non-immune or immune cells in response to stress or damage. Immunosenescence significantly impacts both the innate and adaptive immune responses and is characterised by physical changes in lymphoid organs, as well as dysfunctions in cellular and molecular mechanisms. Key features of immunosenescence...

Peripheral nerve injuries (PNI) present a significant challenge, particularly in aging populations where Schwann cell dysfunction, reduced c-Jun expression, increased senescence, and impaired myelin clearance hinder regeneration. Targeted therapies aim to restore Schwann cell plasticity and improve nerve repair. These include gene therapy to upregulate c-Jun, senolytic agents to eliminate senescent Schwann cells, pharmacological activation of JNK, ferroptosis inhibition, and stem cell-based...

Spiky projections on plant matter may act like “drain snakes,” helping felines dislodge wads of fur

Finding highlights promise, questions about detectors of AI-generated text