Person: Urdánoz Casado, Amaya
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Urdánoz Casado
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Amaya
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Ciencias de la Salud
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0000-0002-6312-8330
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123923
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Publication Open Access Identificación de circRNAs como biomarcadores epigenéticos candidatos en la enfermedad de Alzheimer(2022) Urdánoz Casado, Amaya; Blanco Luquin, Idoia; Mendióroz Iriarte, Maite; Ciencias de la Salud; Osasun Zientziak; Gobierno de Navarra / Nafarroako GobernuaLa enfermedad de Alzheimer (EA) es una enfermedad neurodegenerativa, crónica y, por el momento, irreversible que representa la primera causa de demencia relacionada con la edad. Su diagnóstico sigue siendo un reto. En los últimos años, se han identificado diferentes biomarcadores diagnósticos pero, debido a su coste o dificultad de acceso, se ha limitado su implantación de rutina en muchos centros sanitarios. Por ello se están investigando nuevos biomarcadores no invasivos en sangre, como los biomarcadores epigenéticos, entre los que se encuentran los RNAs circulares (circRNAs), una clase de RNAs no codificantes. El objetivo de esta tesis es identificar circRNAs con una expresión diferencial en la corteza entorrinal (CE) humana, una región cerebral especialmente vulnerable a la EA, en pacientes con EA respecto a controles.Publication Open Access Profile of TREM2-derived circRNA and mRNA variants in the entorhinal cortex of Alzheimer's disease patients(MDPI, 2022) Urdánoz Casado, Amaya; Sánchez Ruiz de Gordoa, Javier; Robles, Maitane; Roldán, Miren; Zelaya Huerta, María Victoria; Blanco Luquin, Idoia; Mendióroz Iriarte, Maite; Ciencias de la Salud; Osasun Zientziak; Gobierno de Navarra / Nafarroako GobernuaGenetic variants in TREM2, a microglia-related gene, are well-known risk factors for Alzheimer’s disease (AD). Here, we report that TREM2 originates from circular RNAs (circRNAs), a novel class of non-coding RNAs characterized by a covalent and stable closed-loop structure. First, divergent primers were designed to amplify circRNAs by RT-PCR, which were further assessed by Sanger sequencing. Then, additional primer sets were used to confirm back-splicing junctions. In addition, HMC3 cells were used to assess the microglial expression of circTREM2s. Three candidate circTREM2s were identified in control and AD human entorhinal samples. One of the circRNAs, circTREM2_1, was consistently amplified by all divergent primer sets in control and AD entorhinal cortex samples as well as in HMC3 cells. In AD cases, a moderate negative correlation (r = −0.434) was found between the global average area of Aβ deposits in the entorhinal cortex and circTREM2_1 expression level. In addition, by bioinformatics tools, a total of 16 miRNAs were predicted to join with circTREM2s. Finally, TREM2 mRNA corresponding to four isoforms was profiled by RTqPCR. TREM2 mRNA levels were found elevated in entorhinal samples of AD patients with low or intermediate ABC scores compared to controls. To sum up, a novel circRNA derived from the TREM2 gene, circTREM2_1, has been identified in the human entorhinal cortex and TREM2 mRNA expression has been detected to increase in AD compared to controls. Unraveling the molecular genetics of the TREM2 gene may help to better know the innate immune response in AD.