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Integrative multiomics reveals common endotypes across PSEN1, PSEN2, and APP mutations in familial Alzheimer's disease.
Alzheimers Res Ther
January 2025
Department of Bioengineering, University of California, San Diego, La Jolla, CA, 92093, USA.
Background: PSEN1, PSEN2, and APP mutations cause Alzheimer's disease (AD) with an early age at onset (AAO) and progressive cognitive decline. PSEN1 mutations are more common and generally have an earlier AAO; however, certain PSEN1 mutations cause a later AAO, similar to those observed in PSEN2 and APP.
Methods: We examined whether common disease endotypes exist across these mutations with a later AAO (~ 55 years) using hiPSC-derived neurons from familial Alzheimer's disease (FAD) patients harboring mutations in PSEN1, PSEN2, and APP and mechanistically characterized by integrating RNA-seq and ATAC-seq.
Genetic analysis of chlorantraniliprole resistance in the non-target bio-control agent Trichogrammachilonis.
Chemosphere
December 2024
Department of Entomology, Faculty of Agricultural Sciences and Technology, Bahauddin Zakariya University, Multan, 60800, Pakistan. Electronic address:
Trichogramma chilonis (Ishii) (Hymenoptera: Trichogrammatidae), a widely used egg parasitoid of lepidopteran pests in various crops, has developed very high levels of resistance when treated with chlorantraniliprole under laboratory conditions. This study assessed and characterized its mode of inheritance, degree of dominance, realized heritability (h), and cross-resistance. Toxicity bioassays were performed on T.
View Article and Find Full Text PDFCSF proteomics identifies early changes in autosomal dominant Alzheimer's disease.
Cell
October 2024
Department of Psychiatry, Washington University, St. Louis, MO 63110, USA; NeuroGenomics and Informatics, Washington University, St. Louis, MO 63110, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address:
In this high-throughput proteomic study of autosomal dominant Alzheimer's disease (ADAD), we sought to identify early biomarkers in cerebrospinal fluid (CSF) for disease monitoring and treatment strategies. We examined CSF proteins in 286 mutation carriers (MCs) and 177 non-carriers (NCs). The developed multi-layer regression model distinguished proteins with different pseudo-trajectories between these groups.
View Article and Find Full Text PDFMatrix stiffness regulates the triad communication of adipocytes/macrophages/endothelial cells through CXCL13.
J Lipid Res
September 2024
Department of Biosignals and Inheritance, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan; Division of Biomedical Engineering for Health and Welfare, Graduate School of Biomedical Engineering, Tohoku University, Sendai, Japan; Frontier Research Institute for Interdisciplinary Sciences, Tohoku University, Sendai, Japan; Department of Medicine and Science in Sports and Exercise, Tohoku University School of Medicine, Sendai, Japan. Electronic address:
Adipose tissue remodeling and plasticity are dynamically regulated by the coordinated functions of adipocytes, macrophages, and endothelial cells and extracellular matrix (ECM) that provides stiffness networks in adipose tissue component cells. Inflammation and fibrosis are crucial exogenous factors that dysregulate adipose tissue functions and drastically change the mechanical properties of the ECM. Therefore, communication among the ECM and adipose tissue component cells is necessary to understand the multifaceted functions of adipose tissues.
View Article and Find Full Text PDFGeneration of a gene-corrected human isogenic iPSC line from an Alzheimer's disease iPSC line carrying the PSEN1 H163R mutation.
Stem Cell Res
September 2024
Department of Anatomy and Physiology, the University of Melbourne, Parkville, VIC 3010, Australia; Department of Surgery, Royal Melbourne Hospital, the University of Melbourne, Parkville, VIC 3010, Australia. Electronic address:
We report the generation of a gene-edited human induced pluripotent stem cell (iPSC) line from an Alzheimer's disease patient-derived iPSC line harbouring the PSEN1 H163R mutation. This line demonstrates pluripotent stem cell morphology, expression of pluripotency markers, and maintains a normal karyotype.
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