000151474 001__ 151474
000151474 005__ 20251017144620.0
000151474 0247_ $$2doi$$a10.3390/pathogens10050596
000151474 0248_ $$2sideral$$a126668
000151474 037__ $$aART-2021-126668
000151474 041__ $$aeng
000151474 100__ $$0(orcid)0000-0001-8385-0219$$aGarcés M.
000151474 245__ $$aNovel morphological glial alterations in the spectrum of prion disease types: A focus on common findings
000151474 260__ $$c2021
000151474 5060_ $$aAccess copy available to the general public$$fUnrestricted
000151474 5203_ $$aHuman prion diseases are a group of rare fatal neurodegenerative diseases with sporadic, genetic, and acquired forms. They are neuropathologically characterized by pathological prion protein accumulation, neuronal death, and vacuolation. Classical immunological response has long been known not to play a major in prion diseases; however, gliosis is known to be a common feature although variable in extent and poorly described. In this investigation, astrogliosis and activated microglia in two brain regions were assessed and compared with non-neurologically affected patients in a representative sample across the spectrum of Creutzfeldt–Jakob disease (CJD) forms and subtypes in order to analyze the influence of prion strain on pathological processes. In this report, we choose to focus on features common to all CJD types rather than the diversity among them. Novel pathological changes in both glial cell types were found to be shared by all CJD types. Microglial activation correlated to astrogliosis. Spongiosis, but not pathological prion protein deposition, correlated to both astrogliosis and microgliosis. At the ultrastructural level, astrocytic glial filaments correlated with pathological changes associated with prion disease. These observations confirm that neuroglia play a prominent role in the neurodegenerative process of prion diseases, regardless of the causative prion type.
000151474 536__ $$9info:eu-repo/grantAgreement/ES/UZ/2017-BIO-04
000151474 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttps://creativecommons.org/licenses/by/4.0/deed.es
000151474 590__ $$a4.531$$b2021
000151474 591__ $$aMICROBIOLOGY$$b58 / 137 = 0.423$$c2021$$dQ2$$eT2
000151474 592__ $$a0.901$$b2021
000151474 593__ $$aImmunology and Allergy$$c2021$$dQ2
000151474 593__ $$aMolecular Biology$$c2021$$dQ2
000151474 593__ $$aMicrobiology (medical)$$c2021$$dQ2
000151474 593__ $$aImmunology and Microbiology (miscellaneous)$$c2021$$dQ2
000151474 594__ $$a3.5$$b2021
000151474 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000151474 700__ $$0(orcid)0000-0001-9773-7460$$aGuijarro I.M.
000151474 700__ $$aRitchie D.L.
000151474 700__ $$0(orcid)0000-0002-7173-7216$$aBadiola J.J.$$uUniversidad de Zaragoza
000151474 700__ $$0(orcid)0000-0002-2787-9671$$aMonzón M.$$uUniversidad de Zaragoza
000151474 7102_ $$11009$$2773$$aUniversidad de Zaragoza$$bDpto. Patología Animal$$cÁrea Sanidad Animal
000151474 7102_ $$11003$$2443$$aUniversidad de Zaragoza$$bDpto. Anatom.Histolog.Humanas$$cArea Histología
000151474 773__ $$g10, 5 (2021), 596 [16 pp.]$$pPathogens$$tPathogens$$x2076-0817
000151474 8564_ $$s6242520$$uhttps://zaguan.unizar.es/record/151474/files/texto_completo.pdf$$yVersión publicada
000151474 8564_ $$s2800650$$uhttps://zaguan.unizar.es/record/151474/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000151474 909CO $$ooai:zaguan.unizar.es:151474$$particulos$$pdriver
000151474 951__ $$a2025-10-17-14:21:34
000151474 980__ $$aARTICLE