Insoluble vascular amyloid deposits trigger disruption of the neurovascular unit in Alzheimer’s disease brains.
Fecha
2021-04-01Autor
Soto Rojas, Luis O.
Campa Córdoba, Berenice
Harrington, Charles R.
Salas Casas, Andrés
Hernandes Alejandro, Mario
Villanueva Fierro, Ignacio
Bravo Muñoz, Marely
Garcés Ramírez, Linda
Cruz López, Fidel de la
Ontiveros Torres, Miguel Ángel
Gevorkian, Goar
Pacheco Herrero, Mar
Luna Muñoz, José
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Alzheimer’s disease (AD) is a neurodegenerative disease, characterized histopathologically
by intra-neuronal tau-related lesions and by the accumulation of amyloid -peptide (A ) in the brain
parenchyma and around cerebral blood vessels. According to the vascular hypothesis of AD, an
alteration in the neurovascular unit (NVU) could lead to A vascular accumulation and promote
neuronal dysfunction, accelerating neurodegeneration and dementia. To date, the effects of insoluble
vascular A deposits on the NVU and the blood–brain barrier (BBB) are unknown. In this study,
we analyze different A species and their association with the cells that make up the NVU. We
evaluated post-mortem AD brain tissue. Multiple immunofluorescence assays were performed
against different species of A and the main elements that constitute the NVU. Our results showed
that there are insoluble vascular deposits of both full-length and truncated A species. Besides,
insoluble aggregates are associated with a decrease in the phenotype of the cellular components that
constitute the NVU and with BBB disruption. This approach could help identify new therapeutic
targets against key molecules and receptors in the NVU that can prevent the accumulation of vascular
fibrillar A in AD.
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