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dc.contributor.authorSoto-Rojas, Luis O.
dc.contributor.authorPacheco-Herrero, Mar
dc.contributor.authorMartínez-Gómez, Paola A.
dc.contributor.authorCampa-Córdoba, B. Berenice
dc.contributor.authorApátiga-Pérez, Ricardo
dc.contributor.authorVillegas-Rojas, Marcos M.
dc.contributor.authorHarrington, Charles R.
dc.contributor.authorCruz, Fidel de la
dc.contributor.authorGarcés-Ramírez, Linda
dc.contributor.authorLuna-Muñoz, José
dc.date.accessioned2021-04-07T20:09:02Z
dc.date.available2021-04-07T20:09:02Z
dc.date.issued2021-02-16
dc.identifier.citationSoto-Rojas LO, Pacheco-Herrero M, Martínez-Gómez PA, Campa-Córdoba BB, Apátiga-Pérez R, Villegas-Rojas MM, Harrington CR, Cruz, F dela, Garcés-Ramírez L, Luna-Muñoz J. The Neurovascular Unit Dysfunction in Alzheimer’s Disease. Int. J. Mol. Sci. [En línea]. 2021. [consultado día mes año]; 22, 2022 : 1-28. Disponible en: https://doi.org/ 10.3390/ijms2204202https://doi.org/10.3390/ijms22042022en_US
dc.identifier.urihttps://repositorio.unphu.edu.do/handle/123456789/3451
dc.description.abstractAlzheimer’s disease (AD) is the most common neurodegenerative disease worldwide. Histopathologically, AD presents with two hallmarks: neurofibrillary tangles (NFTs), and aggregates of amyloid peptide (A ) both in the brain parenchyma as neuritic plaques, and around blood vessels as cerebral amyloid angiopathy (CAA). According to the vascular hypothesis of AD, vascular risk factors can result in dysregulation of the neurovascular unit (NVU) and hypoxia. Hypoxia may reduce A clearance from the brain and increase its production, leading to both parenchymal and vascular accumulation of A . An increase in A amplifies neuronal dysfunction, NFT formation, and accelerates neurodegeneration, resulting in dementia. In recent decades, therapeutic approaches have attempted to decrease the levels of abnormal A or tau levels in the AD brain. However, several of these approaches have either been associated with an inappropriate immune response triggering inflammation, or have failed to improve cognition. Here, we review the pathogenesis and potential therapeutic targets associated with dysfunction of the NVU in AD.en_US
dc.language.isoenen_US
dc.publisherInternational Journal o f Molecular Sciencesen_US
dc.rightsAtribución 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectEnfermedad de Alzheimeren_US
dc.subjectPlaca Amiloideen_US
dc.subjectAmiloidosisen_US
dc.subjectDemenciaen_US
dc.subjectPéptidos beta-Amiloidesen_US
dc.titleThe neurovascular unit dysfunction in Alzheimer’s diseaseen_US
dc.typeArticleen_US


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Atribución 4.0 Internacional
Except where otherwise noted, this item's license is described as Atribución 4.0 Internacional