RT Conference Proceedings
T1 Amyloid propagation in a sporadic model of Alzheimer disease
A1 Andreo-López, Juana
A1 Cantero-Molina, Francisco
A1 Bettinetti-Luque, Miriam
A1 Huynh, Kelly
A1 Nguyen, Marie
A1 Cheung, Alwin
A1 Tran, Janine
A1 Da Cunha, Celia
A1 Trujillo-Estrada, Laura Isabel
A1 Núñez-Díaz, Cristina
A1 Cadete-Martini, Alessandra
A1 Forner, Stefania
A1 Gutiérrez-Pérez, Antonia
A1 LaFerla, Frank
A1 Baglietto-Vargas, David
K1 Alzheimer, Enfermedad de
AB Most age-associated neurodegenerative disorders involve the aggregation ofspecific proteins within the nervous system, as occurs in Alzheimer’s disease (AD). Recentevidence indicates that Aβ can misfold and aggregate into seeds that structurally corruptnative proteins, mimicking a prion-like process of template protein corruption or seeding. Infact, studies in FAD-based animal models show that Aβ deposition and cerebral amyloidangiopathy may be induced by intracerebral infusion of brain extracts from AD patients orfrom aged APP-transgenic mice. These studies have shown that the characteristic of boththe seeding agent and the host influence the pathologic signature of the Aβ seeds. In thisregard, the majority of the Aβ-seeding studies have been done in APP-transgenic animalmodels that overproduce APP and/or Aβ. However, it remains to be elucidated whether Aβdeposition can be induced by Aβ seeds in an animal model that does not overexpress APPand produces wild type human Aβ and if these aggregates are similar to the humancondition.Here, we used an innovative animal model to better understand theamyloidogenic events that occur in the sporadic form of the disease. Our model, termedhAβ-KI, expresses wild-type human Aβ under the control of the endogenous mouse APPgene. Thus, amyloid seeds from AD patients (stage C for amyloid) from the Alzheimer’sDisease Research Center (ADRC) at UCI were administered into 7-8-month-old hAβ-KI andas positive controls 3xTg-AD mice were employed.Our findings demonstrated that amyloid seeds differentially occur in 3xTg-AD andhAb-KI mice and these aggregates are developed earlier in the familial model, 3xTg-ADmice.These results suggest that multiple factors such as the seed, recipient modeland time are critical factors that can modulate the amyloid pathology onset andprogression. Thus, more profound understanding these factors will provide key insight onhow amyloid pathology progress in AD.
YR 2021
FD 2021-11-04
LK https://hdl.handle.net/10630/23338
UL https://hdl.handle.net/10630/23338
LA spa
NO Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 20 ene 2026