The binding of many pathogens and toxins to human cells can be inhibited by (1) depleting host cells of their surface glycosphingolipids; (2) coating the binding sites on pathogens (adhesins) with glycosphingolipid-like substances (decoys); (3) coating the host's glycosphingolipids with substances that compete with the pathogen for binding. Details of using these methods are described.
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http://dx.doi.org/10.1016/j.micinf.2005.09.005 | DOI Listing |
PLoS One
January 2025
Department of Microbiology, UT Southwestern Medical Center, Dallas, TX, United States of America.
Unraveling the metabolism of Treponema pallidum is a key component to understanding the pathogenesis of the human disease that it causes, syphilis. For decades, it was assumed that glucose was the sole carbon/energy source for this parasitic spirochete. But the lack of citric-acid-cycle enzymes suggested that alternative sources could be utilized, especially in microaerophilic host environments where glycolysis should not be robust.
View Article and Find Full Text PDFJ Cell Biol
March 2025
Department of Pulmonary Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Epithelial cells can become polyploid upon tissue injury, but mechanosensitive cues that trigger this state are poorly understood. Using an Madin Darby Canine Kidney (MDCK) cell knock-out/reconstitution system, we show that α-catenin mutants that alter force-sensitive binding to F-actin or middle (M)-domain promote cytokinesis failure and binucleation, particularly near epithelial wound-fronts. We identified Leucine Zipper Tumor Suppressor 2 (LZTS2), a factor previously implicated in abscission, as a conformation sensitive proximity partner of α-catenin.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Penn Frontotemporal Degeneration Center, Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Background: Frontotemporal lobar degeneration (FTLD) is defined neuropathologically by misfolded tau (FTLD-tau) or TAR DNA-binding protein of 43 kDa (FTLD-TDP). However, we lack biomarkers that can distinguish them in vivo which is a major barrier to effective disease-modifying treatment trials. Based on neuropathological evidence of distinct patterns of cellular degeneration, more prominent in white matter (WM) for FTLD-tau relative to FTLD-TDP, we hypothesized that diffusion MRI (dMRI) measures of white matter microstructure would help dissociate FTLD-tau and FTLD-TDP during life.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Psychiatry, School of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
Background: Plasma phospho-tau217 (p-tau217) is a promising blood-based biomarkers for Alzheimer's disease (AD). However, the accessibility of pTau217 tests for both research and clinical applications has been constrained. Previous studies focused on highly-phenotyped cohorts that differ substantially from the wider population.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Clinical Memory Research Unit, Department of Clinical Sciences, Lund University, and Memory Clinic, Skåne University Hospital, Malmö, Sweden.
Background: Alzheimer's disease (AD) is the leading cause of cognitive impairment and dementia with rising prevalence, morbidity, and mortality. Limited treatment options highlight a significant unmet need. AD is characterized pathologically by extracellular accumulation of Aβ peptide-containing plaques and intracellular neurofibrillary tangles containing aggregates of the microtubule-associated protein tau, leading to neuronal and synaptic loss, neuroinflammation, and brain atrophy.
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