000070332 001__ 70332
000070332 005__ 20190709135608.0
000070332 0247_ $$2doi$$a10.1097/MD.0000000000010320
000070332 0248_ $$2sideral$$a105916
000070332 037__ $$aART-2018-105916
000070332 041__ $$aeng
000070332 100__ $$0(orcid)0000-0002-2787-9671$$aMonzón, M.$$uUniversidad de Zaragoza
000070332 245__ $$aGlial alterations in human prion diseases
000070332 260__ $$c2018
000070332 5060_ $$aAccess copy available to the general public$$fUnrestricted
000070332 5203_ $$aBackground: Neuroinflammation has recently been proposed to be a major component of neurodegenerative diseases. The aim of this study was to determine how the interaction between microglia and astroglia, which are the primary immune cell populations in the brain, and pathological prion protein (PrPsc) could influence the development and propagation of this neurodegenerative disease. Because a relevant role for glial response in prion disease has been clearly demonstrated in our previous studies using the natural animal model, a similar approach has been taken here using the natural human model. 
Methods: A morphological approach has been developed to analyze cerebellar samples from patients with Creutzfeldt-Jakob disease (CJD) in comparison with healthy control cases. Histopathological lesions were assessed, and PrPsc, glial fibrillary acidic protein (GFAP) and reactive microglia were immunolabelled by specific antibodies. Furthermore, co-location studies using confocal microscopy were performed to determine the possible relationships between both types of glial cells in all samples. 
Results: The results presented in this study support the involvement of both types of glial cells in CJD. Evidence of increased astrocyte and microglia reactivity can be observed in all CJD cases, and a close relationship between the types of glia is demonstrated by co-location studies. 
Conclusion: Proteinopathies such as Alzheimer, Parkinson, and Huntington diseases, where aberrant proteins spread throughout the brain during disease progression, may share a molecular basis and mechanisms of propagation. Therefore, studies elucidating the interaction between gliosis and prion propagation may be relevant to these other neurodegenerative diseases and may provide new targets for therapeutic intervention.
000070332 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000070332 590__ $$a1.87$$b2018
000070332 591__ $$aMEDICINE, GENERAL & INTERNAL$$b69 / 159 = 0.434$$c2018$$dQ2$$eT2
000070332 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000070332 700__ $$0(orcid)0000-0002-3423-0846$$aHernández, R.S.
000070332 700__ $$aGarcés, M.$$uUniversidad de Zaragoza
000070332 700__ $$aSarasa, R.
000070332 700__ $$0(orcid)0000-0002-7173-7216$$aBadiola, J.J.$$uUniversidad de Zaragoza
000070332 7102_ $$11003$$2443$$aUniversidad de Zaragoza$$bDpto. Anatom.Histolog.Humanas$$cArea Histología
000070332 7102_ $$11009$$2773$$aUniversidad de Zaragoza$$bDpto. Patología Animal$$cÁrea Sanidad Animal
000070332 7102_ $$11007$$2610$$aUniversidad de Zaragoza$$bDpto. Medicina, Psiqu. y Derm.$$cArea Medicina
000070332 773__ $$g97, 15 (2018), e0320$$pMedicine (Baltim.)$$tMedicine$$x0025-7974
000070332 8564_ $$s2883144$$uhttp://zaguan.unizar.es/record/70332/files/texto_completo.pdf$$yVersión publicada
000070332 8564_ $$s123224$$uhttp://zaguan.unizar.es/record/70332/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000070332 909CO $$ooai:zaguan.unizar.es:70332$$particulos$$pdriver
000070332 951__ $$a2019-07-09-12:21:26
000070332 980__ $$aARTICLE