RT Conference Proceedings
T1 Human amyloid seeds aggregate more efficient than seeds from old 3xtg-ad mice
A1 Andreo-López, Juana
A1 Cantero-Molina, Francisco
A1 Bettinetti-Luque, Miriam
A1 Huynh, Kelly
A1 Thu Nguyen, Marie Minh
A1 Cheung, Alwin
A1 Tran, Janine Pham
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
K1 Modelos animales en investigación
AB Aims: Most age-associated neurodegenerative disorders involve the aggregation of specific proteins within the nervous system, as occurs in Alzheimer’s disease (AD). Recent evidence indicates that Aβ can misfold and aggregate into seeds that structurally corrupt native proteins, mimicking a prion-like process of template protein corruption or seeding. In fact, studies in animal models show that the injection of brain homogenates from AD patients or from aged APP-transgenic mice containing Aβ aggregates, can induce some of the neuropathological hallmarks of AD. However, it is still unknown which Aβ-misfolded species are most efficient in triggering the aggregation process. Here, we seek to perform a comparative study to determine whether Aβ seeds from humans vs a familial AD line (the 3xTg-AD model) is more efficient to generate amyloid aggregates. Methods: We employed histological and molecular approaches to determine amyloid level, species and aggregative capacity of brain homogenates from an AD patient (stage C for amyloid, from the Alzheimer’s Disease Research Center at UCI) vs old-3xTg-AD mice (25-month-old). Such brain homogenates were injected into the hippocampus of 7-month-old 3xTg-AD mice and the mice were analyzed at 18 months of age. Results: Our findings demonstrated that amyloid seeds from the human patient have more capacity to generate Aβ plaques vs seeds from aged 3xTg-AD mice. Conclusions: These results suggest that seeds from human patients seem to be more amyloidogenic than from aged 3xTg-AD mice. Thus, more profound understanding these factors will provide key insight on how amyloid pathology progress in AD.
YR 2022
FD 2022
LK https://hdl.handle.net/10630/23894
UL https://hdl.handle.net/10630/23894
LA eng
NO Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 3 mar 2026