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Neurovascular dysfunction and vascular amyloid accumulation as early events in Alzheimer's disease
dc.contributor.author | Apatiga Pérez, Ricardo | |
dc.contributor.author | Soto Rojas, Luis O. | |
dc.contributor.author | Campa Córdoba, B. Berenice | |
dc.contributor.author | Luna Viramontes, Nabil Itzi | |
dc.contributor.author | Cuevas, Elvis | |
dc.contributor.author | Villanueva‑Fierro, Ignacio | |
dc.contributor.author | Ontiveros Torres, Miguel Angel | |
dc.contributor.author | Bravo Múñoz, Marely | |
dc.contributor.author | Flores Rodríguez, Paola | |
dc.contributor.author | Garces Ramírez, Linda | |
dc.contributor.author | Cruz, Fidel de la | |
dc.contributor.author | Montiel Sosa, José Francisco | |
dc.contributor.author | Pacheco Herrero, Mar | |
dc.contributor.author | Luna Muñoz, José | |
dc.date.accessioned | 2021-09-18T19:12:06Z | |
dc.date.available | 2021-09-18T19:12:06Z | |
dc.date.issued | 2021-07 | |
dc.identifier.citation | Apatiga 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/s11011-021-00814-4 | en_US |
dc.identifier.uri | https://repositorio.unphu.edu.do/handle/123456789/3871 | |
dc.description.abstract | Alzheimer'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.iso | es | en_US |
dc.publisher | Metabolic Brain Disease | en_US |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Enfermedad de Alzheimer | en_US |
dc.subject | Angiopatía amiloide cerebral | en_US |
dc.subject | Trastornos cerebrovasculares | |
dc.title | Neurovascular dysfunction and vascular amyloid accumulation as early events in Alzheimer's disease | en_US |
dc.type | Article | en_US |