Neurovascular dysfunction and vascular amyloid accumulation as early events in Alzheimer's disease
Fecha
2021-07Autor
Apatiga Pérez, Ricardo
Soto Rojas, Luis O.
Campa Córdoba, B. Berenice
Luna Viramontes, Nabil Itzi
Cuevas, Elvis
Villanueva‑Fierro, Ignacio
Ontiveros Torres, Miguel Angel
Bravo Múñoz, Marely
Flores Rodríguez, Paola
Garces Ramírez, Linda
Cruz, Fidel de la
Montiel Sosa, José Francisco
Pacheco Herrero, Mar
Luna Muñoz, José
Metadatos
Mostrar el registro completo del ítemResumen
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.
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