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dc.contributor.authorApátiga‑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‑Muñoz, Marely
dc.contributor.authorFlores‑Rodríguez, Paola
dc.contributor.authorGarcés‑Ramirez, Linda
dc.contributor.authorde la Cruz, Fidel
dc.contributor.authorMontiel‑Sosa, José Francisco
dc.contributor.authorPacheco‑Herrero, Mar
dc.contributor.authorLuna‑Muñoz, José
dc.date.accessioned2022-02-13T18:17:28Z
dc.date.available2022-02-13T18:17:28Z
dc.date.issued2021-07
dc.identifier.citationApátiga Pérez R, Soto Rojas LO, Campa Córdoba BB, Luna Viramontes N, Cuevas E, Villanueva Fierro I … et al. Neurovascular dysfunction and vascular amyloid accumulation as early events in Alzheimer's disease. Metab Brain Dis 37, 39–50 (2022). https://doi.org/10.1007/s11011-021-00814-4en_US
dc.identifier.urihttps://repositorio.unphu.edu.do/handle/123456789/4321
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.isoenen_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.subjectDemenciaen_US
dc.subjectAngiopatía amiloide cerebralen_US
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