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dc.contributor.authorSoto Rojas, Luis O.
dc.contributor.authorCampa Córdoba, Berenice
dc.contributor.authorHarrington, Charles R.
dc.contributor.authorSalas Casas, Andrés
dc.contributor.authorHernandes Alejandro, Mario
dc.contributor.authorVillanueva Fierro, Ignacio
dc.contributor.authorBravo Muñoz, Marely
dc.contributor.authorGarcés Ramírez, Linda
dc.contributor.authorCruz López, Fidel de la
dc.contributor.authorOntiveros Torres, Miguel Ángel
dc.contributor.authorGevorkian, Goar
dc.contributor.authorPacheco Herrero, Mar
dc.contributor.authorLuna Muñoz, José
dc.date.accessioned2021-06-11T00:41:03Z
dc.date.available2021-06-11T00:41:03Z
dc.date.issued2021-04-01
dc.identifier.citationSoto Rojas LO, Campa Córdoba BB, Harrington CR, Salas Casas A, Hernandes Alejandro M. Villanueva Fierro I, et al. Insoluble Vascular Amyloid Deposits Trigger Disruption of the Neurovascular Unit in Alzheimer’s Disease Brains. Int. J. Mol. Sci. 2021, 22, 3654. https:// doi.org/10.3390/ijms22073654en_US
dc.identifier.urihttps://repositorio.unphu.edu.do/handle/123456789/3632
dc.description.abstractAlzheimer’s disease (AD) is a neurodegenerative disease, characterized histopathologically by intra-neuronal tau-related lesions and by the accumulation of amyloid -peptide (A ) in the brain parenchyma and around cerebral blood vessels. According to the vascular hypothesis of AD, an alteration in the neurovascular unit (NVU) could lead to A vascular accumulation and promote neuronal dysfunction, accelerating neurodegeneration and dementia. To date, the effects of insoluble vascular A deposits on the NVU and the blood–brain barrier (BBB) are unknown. In this study, we analyze different A species and their association with the cells that make up the NVU. We evaluated post-mortem AD brain tissue. Multiple immunofluorescence assays were performed against different species of A and the main elements that constitute the NVU. Our results showed that there are insoluble vascular deposits of both full-length and truncated A species. Besides, insoluble aggregates are associated with a decrease in the phenotype of the cellular components that constitute the NVU and with BBB disruption. This approach could help identify new therapeutic targets against key molecules and receptors in the NVU that can prevent the accumulation of vascular fibrillar A in AD.en_US
dc.language.isoesen_US
dc.publisherInt. J. Mol. Scien_US
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectDemenciaen_US
dc.subjectEnfermedad de Alzheimeren_US
dc.subjectEnfermedades Neurodegenerativasen_US
dc.titleInsoluble vascular amyloid deposits trigger disruption of the neurovascular unit in Alzheimer’s disease brains.en_US
dc.typeArticleen_US


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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivatives 4.0 Internacional