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dc.contributor.authorApatiga Pérez, Ricardo
dc.contributor.authorSoto Rojas, Luis O.
dc.contributor.authorCampa Córdoba, B. Berenice
dc.contributor.authorLuna Viramontes, Nabil Itzi
dc.contributor.authorCuevas, Elvis
dc.contributor.authorVillanueva‑Fierro, Ignacio
dc.contributor.authorOntiveros Torres, Miguel Angel
dc.contributor.authorBravo Múñoz, Marely
dc.contributor.authorFlores Rodríguez, Paola
dc.contributor.authorGarces Ramírez, Linda
dc.contributor.authorCruz, Fidel de la
dc.contributor.authorMontiel Sosa, José Francisco
dc.contributor.authorPacheco Herrero, Mar
dc.contributor.authorLuna Muñoz, José
dc.date.accessioned2021-09-18T19:12:06Z
dc.date.available2021-09-18T19:12:06Z
dc.date.issued2021-07
dc.identifier.citationApatiga Pérez R, Soto Rojas LO, Campa Córdoba BB, Luna Viramontes NI, Cuevas E, Villanueva Fierro I. [et al.]. Neurovascular dysfunction and vascular amyloid accumulation as early events in Alzheimer's disease. Metabolic Brain Disease ; 2021. Disponible en: https://doi.org/10.1007/s11011-021-00814-4en_US
dc.identifier.urihttps://repositorio.unphu.edu.do/handle/123456789/3871
dc.description.abstractAlzheimer's disease (AD) is clinically characterized by a progressive loss of cognitive functions and short-term memory. AD patients present two distinctive neuropathological lesions: neuritic plaques and neurofibrillary tangles (NFTs), constituted of beta-amyloid peptide (Aβ) and phosphorylated and truncated tau proteins. Aβ deposits around cerebral blood vessels (cerebral amyloid angiopathy, CAA) is a major contributor to vascular dysfunction in AD. Vascular amyloid deposits could be early events in AD due to dysfunction in the neurovascular unit (NVU) and the blood–brain barrier (BBB), deterioration of the gliovascular unit, and/or decrease of cerebral blood flow (CBF). These pathological events can lead to decreased Aβ clearance, facilitate a neuroinflammatory environment as well as synaptic dysfunction and, finally, lead to neurodegeneration. Here, we review the histopathological AD hallmarks and discuss the two-hit vascular hypothesis of AD, emphasizing the role of neurovascular dysfunction as an early factor that favors vascular Aβ aggregation and neurodegeneration. Addtionally, we emphasize that pericyte degeneration is a key and early element in AD that can trigger amyloid vascular accumulation and NVU/BBB dysfunction. Further research is required to better understand the early pathophysiological mechanisms associated with NVU alteration and CAA to generate early biomarkers and timely treatments for AD.en_US
dc.language.isoesen_US
dc.publisherMetabolic Brain Diseaseen_US
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectEnfermedad de Alzheimeren_US
dc.subjectAngiopatía amiloide cerebralen_US
dc.subjectTrastornos cerebrovasculares
dc.titleNeurovascular dysfunction and vascular amyloid accumulation as early events in Alzheimer's diseaseen_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