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ASEMV 2019 Annual Meeting on Exosomes & Microvesicles—Final Day (Day 5), Thursday, October 10

Thursday was the last day of the 2019 ASEMV meeting and a number of interesting topics were presented. Two are reported on here. Louis Laurent, MD, PhD, of the University of California-San Diego (UCSD), spoke on the “Discovery and Verfication of Extracelular miRNA Biomarkers for Non-Invasive Prediction of Preeclampsia in Asymptomatic Women.” Dr. Laurent said that she and colleagues performed small RNA-seq of maternal serum exRNAs to discover and verify miRNAs differentially expressed in patients who later developed preeclammpsia. Serum collected from 73 preeclampsia cases and 139 controls between 17-28 weeks gestational age, divided into separate Discovery and Verification cohorts, was analyzed by small RNA seq. Discovery and verification of univariate and bivariate miRNA biomarkers revealed that bivariate biomarkers verified at a markedly higher rate than univariate markers. The majority of verified biomarkers contained miR-155-5p, which has been reported to mediate the preeclampsia-associated repression of eNOS by TNF-alpha. Deconvolution analysis revealed that several verified miRNA biomarkers came from the placenta and were likely carried by placenta-specific EVs. Norman Haughey, PhD, Johns Hopkins University School of Medicine, presented a talk entitled “Astrocyte-Derived EVs Shed in Response to IL-1 Promote Stabilization of APP Translation Through Ligand-Independent Activation of the Wnt Pathway in Neurons.” In his introduction, Dr. Haughey noted that chronic inflammation is thought to contribute to the pathogenesis of Alzheimer’s disease (AD) by upregulating amyloidogenic processing of APP. Based on previous findings that inflammatory stimuli modify the cargo of astrocyte-derived EVs (ADEV), Dr. Haughey and colleagues sought to determine if ADEVs released in response to IL-1b (ADEV-IL-1b) contain cargo that regulate amyloidogenic processing neurons. Their work generated data suggesting that neuroimflammatory stimuli modify ADEV cargo to enhance amyloidogenic processing of APP in neurons by a mechanism that involves a ligand-independent activation of Wnt signaling in neurons