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Prodrug nanoplatform for triggering ferroptosis to eliminate senescent cells in age-associated pathologies

Accumulation of senescent cells is associated with age-related diseases. Here, the authors present a prodrug nanoplatform to trigger ferroptosis specifically and exclusively in senescent cells.

Physical and Cognitive Activities and Trajectories of AD Neuroimaging BiomarkersLongitudinal Analysis in the Mayo Clinic Study of Aging

Background and ObjectivesEngagement in physical and cognitive activities is associated with a decreased risk of mild cognitive impairment (MCI) and dementia, but the association with Alzheimer disease (AD) neuroimaging biomarkers is less clear. We thus…

Cardiovascular Disease Biomarker Deep Dive (Test #7 In 2025)

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Pineal gland senescence: an emerging ageing-related pathology?

An ageing-related pathology has recently been described as one that develops and/or progresses with increasing chronological age, that is associated with, or contributes to, functional decline and that is evidenced by studies in humans. The pineal gland is a photo-neuroendocrine organ whose primary function is to produce and secrete melatonin in response to light-dark cycle environmental cues. The gland may undergo ageing-related structural and morphological changes, including calcification, gliosis, cyst formation, and reduced density of β-adrenergic receptors, which are hypothesised to reduce melatonin secretion.

Model-Informed Dose Optimization of Spironolactone in Neonates and Infants

Background/Objectives: Spironolactone (SP) has been used off-label in pediatrics since its approval, but its use is challenged by limited pharmacokinetic (PK) data in adults and especially in children. Methods: Physiologically based pharmacokinetic (PBPK) models for SP and its active metabolites, canrenone (CAN) and 7α thio-methyl spironolactone (TMS), in adults were developed. These models aim to enhance understanding of SP’s PK and provide a basis for predicting PK and optimizing SP dosing in infants and neonates. Given SP’s complex metabolism, we assumed complete conversion to CAN and TMS by CES1 enzymes, fitting CES1-mediated metabolism to the parent-metabolite model using PK data. We incorporated ontogeny for CES1 and CYP3A4 and other age-related physiological changes into the model to anticipate PK in the pediatric population.

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