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Background And Objectives: Chronic kidney disease (CKD) is known to be associated with increased plasma phosphorylated tau217 (p-tau217) concentrations, potentially confounding the utility of plasma p-tau217 measurements as a marker of amyloid pathology in individuals with suspected Alzheimer disease (AD). In this study, we quantitatively investigate the relationship of plasma p-tau217 concentrations vs estimated glomerular filtration rate (eGFR) in individuals with CKD with and without amyloid pathology.

Methods: This was a retrospective examination of data from 2 observational cohorts from either the Mayo Clinic Study of Aging or the Alzheimer's Disease Research Center cohorts.

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Knee exoskeletons have been developed to assist, stabilize, or improve human movement or recovery. However, exoskeleton designers must implement transparency (i.e.

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Resilience-the ability of socio-ecological systems to withstand and recover from shocks-is a key research and policy focus. Definitions of resilience differ between disciplines, however, and the term remains inadequately operationalized. Resilience is the outcome of variable behavioral decisions, yet the process itself and the strategies behind it have rarely been addressed quantitatively.

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Two versatile yet simple methods, colorimetric and spectrofluorimetric, were utilized for the quantitation of nonchromophore neomycin using silver nanoparticles modified with fluorescein. Fluorescein was excited at 485 nm (emission at 515 nm); when it is deposited on the surface of silver nanoparticles, its fluorescence intensity at 515 nm is quenched. Neomycin restores the fluorescence level at 515 nm by displacing fluorescein from nanoparticle binding sites.

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Design and validation of cell-based potency assays for frataxin supplementation treatments.

Mol Ther Methods Clin Dev

December 2024

Department of Neurology, O'Donnell Brain Institute, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390, USA.

Friedreich's ataxia (FRDA) is a multisystem, autosomal recessive disorder caused by mutations in the frataxin () gene. As FRDA is considered an FXN deficiency disorder, numerous therapeutic approaches in development or clinical trials aim to supplement FXN or restore endogenous expression. These include gene therapy, protein supplementation, genome editing or upregulation of transcription.

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