RT Conference Proceedings
T1 The effect of different amyloid seeds and animal hosts on amyloid propagation in Alzheimer's Disease
A1 Andreo-López, Juana
A1 Cantero-Molina, Francisco
A1 Bettinetti-Luque, Miriam
A1 Do Huynh, Kelly
A1 Thu Nguyen, Marie Minh
A1 Cheung, Alwin
A1 Pham Tran, Janine
A1 Trujillo-Estrada, Laura Isabel
A1 Núñez-Díaz, Cristina
A1 Martini, Alessandra C.
A1 Forner, Stefania
A1 Gutiérrez-Pérez, Antonia
A1 LaFerla, Frank
A1 Baglietto-Vargas, David
K1 Alzheimer, Enfermedad de
AB Abstract text: Alzheimer's Disease is a neurodegenerative proteinopathy in which 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 show that Aβ deposition can be induced by the intracerebral infusion of seed-containingbrain homogenates, and that the characteristics of both the seeding agent and the host, influence the pathologic signature ofthe Aβ seeds. However, it is still unknown which Aβ-misfolded species are most efficient in triggering the aggregation process and which is the effect of amyloid seeds on different AD models. Methods: Amyloid seeds from AD patients (stage C foramyloid) from the Alzheimer’s Disease Research Center (ADRC) at UCI were administered into 7-8-month-old hAβ-KI mice and 3xTg-AD mice. Next, we intracerebrally injected brain homogenates from the human AD patient and 25mo-3xTg-AD miceinto the hippocampus of 7-month-old 3xTg-AD mice, which were analyzed at 18 months of age. Results: Our findings demonstrated that amyloid deposition differentially occurs in 3xTg-AD and hAβ-KI mice, and the Aβ aggregates aredeveloped earlier in the familial model. Moreover, the amyloid seeds from the human patient induce more aggressive amyloidpathology compared to seeds from aged 3xTg-AD mice. Conclusion: These results suggest that multiple factors such as theseed, recipient model and time are critical factors that can modulate the amyloid pathology onset and progression. Thus,more profound understanding of these factors will provide key insight on how amyloid pathology progresses in AD.
YR 2022
FD 2022-07-13
LK https://hdl.handle.net/10630/24855
UL https://hdl.handle.net/10630/24855
LA eng
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 20 ene 2026