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dc.contributor.author Henao-Restrepo, Julián
dc.contributor.author López-Murillo, Carolina
dc.contributor.author Valderrama-Carmona, Pablo
dc.contributor.author Orozco-Santa, Natalia
dc.contributor.author Gomez, Johana
dc.contributor.author Gutiérrez-Vargas, Johanna
dc.contributor.author Moraga, Renato
dc.contributor.author Toledo, Jorge
dc.contributor.author Littau, Jessica Lisa
dc.contributor.author Härtel, Steffen
dc.contributor.author Arboleda-Velásquez, Joseph F.
dc.contributor.author Sepulveda-Falla, Diego
dc.contributor.author Lopera, Francisco
dc.contributor.author Cardona-Gómez, Gloria Patricia
dc.contributor.author Villegas, Andrés
dc.contributor.author Posada-Duque, Rafael
dc.date.accessioned 2024-09-26T00:44:00Z
dc.date.available 2024-09-26T00:44:00Z
dc.date.issued 2023-03
dc.identifier.issn 1015-6305
dc.identifier.uri https://repositorio.uss.cl/handle/uss/13303
dc.description Publisher Copyright: © 2022 The Authors. Brain Pathology published by John Wiley & Sons Ltd on behalf of International Society of Neuropathology.
dc.description.abstract In response to brain insults, astrocytes become reactive, promoting protection and tissue repair. However, astroglial reactivity is typical of brain pathologies, including Alzheimer's disease (AD). Considering the heterogeneity of the reactive response, the role of astrocytes in the course of different forms of AD has been underestimated. Colombia has the largest human group known to have familial AD (FAD). This group carries the autosomal dominant and fully penetrant mutation E280A in PSEN1, which causes early-onset AD. Recently, our group identified an E280A carrier who did not develop FAD. The individual was homozygous for the Christchurch mutation R136S in APOE3 (APOEch). Remarkably, APOE is the main genetic risk factor for developing sporadic AD (SAD) and most of cerebral ApoE is produced by astroglia. Here, we characterized astrocyte properties related to reactivity, glutamate homeostasis, and structural integrity of the gliovascular unit (GVU), as factors that could underlie the pathogenesis or protection of AD. Specifically, through histological and 3D microscopy analyses of postmortem samples, we briefly describe the histopathology and cytoarchitecture of the frontal cortex of SAD, FAD, and APOEch, and demonstrate that, while astrodegeneration and vascular deterioration are prominent in SAD, FAD is characterized by hyperreactive-like glia, and APOEch displays the mildest astrocytic and vascular alterations despite having the highest burden of Aβ. Notably, astroglial, gliovascular, and vascular disturbances, as well as brain cell death, correlate with the specific astrocytic phenotypes identified in each condition. This study provides new insights into the potential relevance of the gliovasculature in the development and protection of AD. To our knowledge, this is the first study assessing the components of the GVU in human samples of SAD, FAD, and APOEch. en
dc.language.iso eng
dc.relation.ispartof vol. 33 Issue: no. 2 Pages:
dc.source Brain Pathology
dc.title Gliovascular alterations in sporadic and familial Alzheimer's disease : APOE3 Christchurch homozygote glioprotection en
dc.type Artículo
dc.identifier.doi 10.1111/bpa.13119


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