RT Conference Proceedings
T1 Human and mouse seeds differentially affect AB aggregation by modulating the inflammatory response.
A1 Andreo-López, Juana
A1 Cantero-Molina, Francisco
A1 Bettinetti-Luque, Miriam
A1 Do Huynh, Kelly
A1 Minh Thu Nguyen, Marie
A1 Cheung, Alwin
A1 Pham Tran, Janine
A1 Da Cunha, Celia
A1 Morales-Cabello, Mario
A1 Fatuarte Juli, Ivan
A1 Trujillo-Estrada, Laura Isabel
A1 Núñez-Díaz, Cristina
A1 Cadete-Martini, Alessandra
A1 Forner, Stefania
A1 LaFerla, Frank
A1 Gutiérrez-Pérez, Antonia
A1 Baglietto-Vargas, David
K1 Alzheimer, Enfermedad de
K1 Amiloide
AB Abstract text: Alzheimer’s Disease (AD) is a neurodegenerative proteinopathy in which Aβ can misfold and aggregate into seeds that structurally corrupt native proteins, mimicking a prionlike process. These amyloid aggregation and propagation processes are influenced by three factors: the origin of the Aβ seed, time of incubation and host. However, the mechanism underlying the differential effect of each factor is poorly known. Previous studies have shown that the Aβ source is relevant for the amyloid process, since its pathogenicity is different according to its origin. Furthermore, recent evidence suggests that microglia plays a key role in the amyloidogenic event, and can modulate the propagation and 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) are more efficient to generate amyloid aggregates, as well as the role of the microglia in the propagation process.Methods: Amyloid seeds from AD patient (stage C for amyloid; from the Alzheimer’s Disease Research Center at UCI) and 25 mo-3xTg-AD mice were injected into the hippocampus of 7-8- month-old 3xTg-AD mice. They were analyzed 10 months post-surgery for amyloid and microglia markers.Results: Our findings demonstrated that amyloid seeds from the human patient seem to induce a more aggressive amyloid pathology compared to seeds from aged 3xTg-AD mice. Moreover, human and mice seeds differentially affect the presence of plaque-associated microglia in 3xTgAD mice. Conclusion: These results suggest that seeds from human patients seem to be more amyloidogenic than from aged 3xTg-AD mice, and also microglia cells may play a key role in this differential effect. Therefore, more profound understanding these factors will provide keyinsight on how amyloid pathology progresses in AD.
YR 2023
FD 2023
LK https://hdl.handle.net/10630/27521
UL https://hdl.handle.net/10630/27521
LA eng
NO Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech.
DS RIUMA. Repositorio Institucional de la Universidad de Málaga
RD 19 ene 2026