The neurovascular unit dysfunction in Alzheimer’s disease
Fecha
2021-02-16Autor
Soto-Rojas, Luis O.
Pacheco-Herrero, Mar
Martínez-Gómez, Paola A.
Campa-Córdoba, B. Berenice
Apátiga-Pérez, Ricardo
Villegas-Rojas, Marcos M.
Harrington, Charles R.
Cruz, Fidel de la
Garcés-Ramírez, Linda
Luna-Muñoz, José
Metadatos
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Alzheimer’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.
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