Scientific Communications: biomarkers 06.00 - NOVEL TARGET/ EXPERIMENTAL FIDINGS TO CLINICAL TRANSLATION - 06.02 - GENETICS, OMICS AND BIOMARKERS O - ESOC25-1221 NOVEL EPIGENETIC INSIGHTS INTO CEREBRAL SMALL VESSEL DISEASE: AN EWAS OF EXTREME-cSVD UNSING METHYL-C SEQUENCING Ilana Caro 1 , Aniket Mishra 1 , Bing Ge 2 , Nicola Armstrong 3 , Qiong Yang 4,5 , Andrew Simpkin 6 , Karen Mather 7 , Sudha Seshadri 5,8 , Hans Grabe 9 , Elin Grundberg 10,11 , Tomi Pastinen 10,11 , Mark Lathrop 2 , Stphanie Debette 1 1 Bordeaux Population Health research center - Universit de Bordeaux, Bordeaux, France, 2 Victor Phillip Dahdaleh Institute of Genomic Medicine, McGill University, Montral, Canada, 3 Department of Mathematics and Statistics, Curtin University, Perth, Australia, 4 Department of Biostatistics, Boston University School of Public Health, Boston, United States, 5 The Framingham Heart Study, Framingham, United States, 6 School of Mathematical and Statistical Sciences, National University of Ireland, Galway, Ireland, 7 Centre for Healthy Brain Ageing (CHeBA), Discipline of Psychiatry and Mental Health, School of Clinical Medicine, University of New South Wales, Sydney, Australia, 8 Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, University of Texas Health Sciences Center, San Antonio, United States, 9 Department of Psychiatry and Psychotherapy, University Medicine Greifswald, Greifswald, Germany, 10 Genomic Medicine Center, Department of Pediatrics, Children's Mercy Kansas City, Kansas, United States, 11 UKMC School of Medicine, University of Missouri Kansas City, Kansas City, United States Background and Aims: Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia, yet no specific mechanism-based treatment to date is available and its underlying molecular mechanisms remain poorly understood
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Sluggish Liver Function and Toxicity: Glutathione is the primary agent used by the liver to bind to heavy metals, mold toxins, and metabolic waste
PeerJ 11 , e15060 (2023)
Also, UCMSCs-derived exosomal miR-451a may inhibit epithelial-mesenchymal transition in HCC by targeting ADAM10, contributing to ferroptosis [186]
