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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 <jats:italic>PSEN1<\/jats:italic>, which causes early\u2010onset AD. Recently, our group identified an E280A carrier who did not develop FAD. The individual was homozygous for the Christchurch mutation R136S in <jats:italic>APOE3<\/jats:italic> (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\u2010like glia, and APOEch displays the mildest astrocytic and vascular alterations despite having the highest burden of A\u03b2. 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.<\/jats:p>","DOI":"10.1111\/bpa.13119","type":"journal-article","created":{"date-parts":[[2022,9,21]],"date-time":"2022-09-21T19:00:51Z","timestamp":1663786851000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3<\/i><\/scp> Christchurch homozygote glioprotection"],"prefix":"10.1111","volume":"33","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4988-5220","authenticated-orcid":false,"given":"Juli\u00e1n","family":"Henao\u2010Restrepo","sequence":"first","affiliation":[{"name":"Instituto de Biolog\u00eda, Facultad de Ciencias Exactas y Naturales Universidad de Antioquia  Medell\u00edn Colombia"},{"name":"\u00c1rea de Neurobiolog\u00eda Celular y Molecular, Grupo de Neurociencias de Antioquia Universidad de 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