000120952 001__ 120952
000120952 005__ 20240319081013.0
000120952 0247_ $$2doi$$a10.3390/ijms232012609
000120952 0248_ $$2sideral$$a131239
000120952 037__ $$aART-2022-131239
000120952 041__ $$aeng
000120952 100__ $$0(orcid)0000-0002-6806-9990$$aHernaiz, Adelaida$$uUniversidad de Zaragoza
000120952 245__ $$aEpigenetic Changes in Prion and Prion-like Neurodegenerative Diseases: Recent Advances, Potential as Biomarkers, and Future Perspectives
000120952 260__ $$c2022
000120952 5060_ $$aAccess copy available to the general public$$fUnrestricted
000120952 5203_ $$aPrion diseases are transmissible spongiform encephalopathies (TSEs) caused by a conformational conversion of the native cellular prion protein (PrPC) to an abnormal, infectious isoform called PrPSc. Amyotrophic lateral sclerosis, Alzheimer’s, Parkinson’s, and Huntington’s diseases are also known as prion-like diseases because they share common features with prion diseases, including protein misfolding and aggregation, as well as the spread of these misfolded proteins into different brain regions. Increasing evidence proposes the involvement of epigenetic mechanisms, namely DNA methylation, post-translational modifications of histones, and microRNA-mediated post-transcriptional gene regulation in the pathogenesis of prion-like diseases. Little is known about the role of epigenetic modifications in prion diseases, but recent findings also point to a potential regulatory role of epigenetic mechanisms in the pathology of these diseases. This review highlights recent findings on epigenetic modifications in TSEs and prion-like diseases and discusses the potential role of such mechanisms in disease pathology and their use as potential biomarkers.
000120952 536__ $$9info:eu-repo/grantAgreement/ES/DGA/A19-20R$$9info:eu-repo/grantAgreement/ES/DGA-FEDER/Construyendo Europa desde Aragón$$9info:eu-repo/grantAgreement/ES/DGA-FSE/IIU-2023-2017$$9info:eu-repo/grantAgreement/ES/MINECO/AGL2015-67945-P
000120952 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000120952 590__ $$a5.6$$b2022
000120952 592__ $$a1.154$$b2022
000120952 591__ $$aBIOCHEMISTRY & MOLECULAR BIOLOGY$$b66 / 285 = 0.232$$c2022$$dQ1$$eT1
000120952 593__ $$aMedicine (miscellaneous)$$c2022$$dQ1
000120952 591__ $$aCHEMISTRY, MULTIDISCIPLINARY$$b52 / 178 = 0.292$$c2022$$dQ2$$eT1
000120952 593__ $$aPhysical and Theoretical Chemistry$$c2022$$dQ1
000120952 593__ $$aComputer Science Applications$$c2022$$dQ1
000120952 593__ $$aInorganic Chemistry$$c2022$$dQ1
000120952 593__ $$aSpectroscopy$$c2022$$dQ1
000120952 593__ $$aOrganic Chemistry$$c2022$$dQ1
000120952 593__ $$aMolecular Biology$$c2022$$dQ2
000120952 593__ $$aCatalysis$$c2022$$dQ2
000120952 594__ $$a7.8$$b2022
000120952 655_4 $$ainfo:eu-repo/semantics/review$$vinfo:eu-repo/semantics/publishedVersion
000120952 700__ $$0(orcid)0000-0002-7243-1737$$aToivonen, Janne Markus$$uUniversidad de Zaragoza
000120952 700__ $$0(orcid)0000-0002-2746-3932$$aBolea, Rosa$$uUniversidad de Zaragoza
000120952 700__ $$0(orcid)0000-0001-6016-4726$$aMartín-Burriel, Inmaculada$$uUniversidad de Zaragoza
000120952 7102_ $$11001$$2420$$aUniversidad de Zaragoza$$bDpto. Anatom.,Embri.Genét.Ani.$$cÁrea Genética
000120952 7102_ $$11009$$2773$$aUniversidad de Zaragoza$$bDpto. Patología Animal$$cÁrea Sanidad Animal
000120952 773__ $$g23, 20 (2022), 12609 [28 pp.]$$pInt. j. mol. sci.$$tInternational Journal of Molecular Sciences$$x1661-6596
000120952 8564_ $$s1027278$$uhttps://zaguan.unizar.es/record/120952/files/texto_completo.pdf$$yVersión publicada
000120952 8564_ $$s2790815$$uhttps://zaguan.unizar.es/record/120952/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
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000120952 951__ $$a2024-03-18-15:22:21
000120952 980__ $$aARTICLE