000060957 001__ 60957 000060957 005__ 20171211140548.0 000060957 0248_ $$2sideral$$a98403 000060957 037__ $$aART-2016-98403 000060957 041__ $$aeng 000060957 100__ $$aGarcés, M. 000060957 245__ $$aMorphological changes of glia in prion and a prion-like disorder 000060957 260__ $$c2016 000060957 5060_ $$aAccess copy available to the general public$$fUnrestricted 000060957 5203_ $$aSeveral neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Huntington’s are considered to be prion-like disorders in that they are all proteinopathies where in aberrant proteins spread throughout the brain during disease progression, and thus they may share molecular basis and mechanisms of propagation. Therefore, studies elucidating mechanisms of prion propagation may be relevant to other neurodegenerative diseases. While substantial progress has been made, the pathogenesis of these neurodegenerative diseases is still largely unknown, and as consequence, to date no truly effective treatments that prevent onset or delay progression of these diseases have been identified. In addition to propagation of misfolded proteins, these diseases all induce a host response that includes activation of astrocytes and microglial cells. However, in our opinion, the glial response in each of these diseases has not been well-defined. Since a role for glial response in prion disease has been clearly demonstrated in a previous study concerning Scrapie in sheep, a similar approach to analysis of astrocytic gliosis has been taken here for Creutzfeldt-Jakob (CJD) and Alzheimer’s Diseases (AD). Here, morphological analysis of glial cells in cerebella from CJD and AD patients (as the most common prion and prion-like disorders, respectively) was performed. The results presented in this study support the involvement of glial cells not only in the pathogenesis of CJD, but also of AD. A relationship between intensity and morphology is observed in astroglia from the molecular layer in both pathologies. By contrast, the involvement of microgliosis in AD-affected samples showed a lower relevance from that observed in CJD, since reactive microglia were much more abundant in prion disease. Further analysis of the role of gliosis in CJD and AD, as well as other neurodegenerative diseases, may well advance knowledge of the mechanisms underlying these diseases and may also provide new targets for therapeutic intervention. 000060957 536__ $$9info:eu-repo/grantAgreement/ES/UZ/UZ2014-BIO-4 000060957 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/ 000060957 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion 000060957 700__ $$aToledano, A 000060957 700__ $$0(orcid)0000-0002-7173-7216$$aBadiola, J.J.$$uUniversidad de Zaragoza 000060957 700__ $$0(orcid)0000-0002-2787-9671$$aMonzón, M.$$uUniversidad de Zaragoza 000060957 7102_ $$11009$$2773$$aUniversidad de Zaragoza$$bDepartamento de Patología Animal$$cSanidad Animal 000060957 7102_ $$11003$$2443$$aUniversidad de Zaragoza$$bDepartamento de Anatomía e Histología Humanas$$cHistología 000060957 773__ $$g2, 1 (2016), [4 pp.]$$tHSOA Journal of Alzheimer’s and Neurodegenerative Diseases 000060957 8564_ $$s2850776$$uhttps://zaguan.unizar.es/record/60957/files/texto_completo.pdf$$yVersión publicada 000060957 8564_ $$s125068$$uhttps://zaguan.unizar.es/record/60957/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada 000060957 909CO $$ooai:zaguan.unizar.es:60957$$particulos$$pdriver 000060957 951__ $$a2017-12-11-14:02:31 000060957 980__ $$aARTICLE