Poster preview
ePoster
UNVEILING FAD3T: A GROUNDBREAKING TRANSGENIC MOUSE MODEL FOR ACCELERATING ALZHEIMER’S DISEASE RESEARCH
Rui Fengand 3 co-authors
GemPharmatech Co., Ltd.
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-376
Presentation
Date TBA
Board: PS02-07PM-376
Event Information
Poster Board
PS02-07PM-376
Poster
View posterAbstract
Aims: Alzheimer's disease (AD) presents a formidable challenge in contemporary healthcare. Traditional mouse models not only exhibit a protracted disease course but also fail to fully recapitulate the complete spectrum of clinical phenotypes observed in patients, thereby significantly impeding pharmaceutical discovery and development. To address the limitations of traditional mouse models in Alzheimer's disease (AD) research, this study aimed to develop a novel transgenic mouse model, FAD3T, incorporating three key genetic mutations associated with AD pathogenesis.
Methods: The FAD3T model was created with three genetic mutations central to AD. The model was assessed for AD-like phenotypes, including elevated phosphorylated Tau biomarkers, amyloid deposition, and cognitive deficits through spatial learning and memory tests. Gender differences in symptom manifestation were also examined.
Results: The FAD3T model showed elevated blood levels of diagnostic biomarkers at 1 month, with amyloid deposition and progressive Tau phosphorylation starting at 2 months. Cognitive deficits appeared earlier in female mice than in males, mirroring clinical AD progression. Compared to traditional models, FAD3T exhibited faster disease onset and progression.
Conclusions: The FAD3T model provides a highly reliable tool for studying AD pathophysiology due to its fidelity in mimicking clinical phenotypes. Its accelerated disease progression offers a rapid platform for drug testing, particularly for therapies targeting disease progression. This innovative mouse model holds the potential to enhance our understanding of AD and accelerate the development of therapeutic strategies.
Methods: The FAD3T model was created with three genetic mutations central to AD. The model was assessed for AD-like phenotypes, including elevated phosphorylated Tau biomarkers, amyloid deposition, and cognitive deficits through spatial learning and memory tests. Gender differences in symptom manifestation were also examined.
Results: The FAD3T model showed elevated blood levels of diagnostic biomarkers at 1 month, with amyloid deposition and progressive Tau phosphorylation starting at 2 months. Cognitive deficits appeared earlier in female mice than in males, mirroring clinical AD progression. Compared to traditional models, FAD3T exhibited faster disease onset and progression.
Conclusions: The FAD3T model provides a highly reliable tool for studying AD pathophysiology due to its fidelity in mimicking clinical phenotypes. Its accelerated disease progression offers a rapid platform for drug testing, particularly for therapies targeting disease progression. This innovative mouse model holds the potential to enhance our understanding of AD and accelerate the development of therapeutic strategies.
Recommended posters
UNRAVELING AGE-DEPENDENT BEHAVIORAL AND MOLECULAR FEATURES IN NOVEL MOUSE MODELS OF ALZHEIMER’S DISEASE IN DOWN SYNDROME: IMPLICATIONS FOR PATHOGENESIS AND TARGET IDENTIFICATION
Monika Rataj Baniowska, Paige Mumford, Francesca Prestia, Pauline Stephan, Millie Beament, Marie-Christine Birling, Chiara Lanzillotta, Letizia Ciafardini, Eugenio Barone, Gloria Lau, Claire Chevalier, Chadia Nahy, Nadia Messaddeq, Thais Lestra, Yixing Wu, Valerie Nalesso, Fabio Di Domenico, Frances Wiseman, Yann Herault
A NOVEL INDUCIBLE MODEL TO STUDY TAUOPATHY IN ALZHEIMER’S DISEASE APPLICABLE TO BOTH, MOUSE AND HUMAN NEURAL TISSUES
Nerea Gomez Rivada, Marcos Galán Ganga, Elisa Marín Ordovas, Marta Cervera-Sospedra, Georgina Bombau, Sara Borràs Pernas, Manuel Comabella, Andrés Miguez, Josep M Canals, Albert Giralt
HUMAN CORTICAL ORGANOID MODELS REVEAL AN AMYLOID-BETA-INDEPENDENT RESPONSE PHENOTYPE IN EARLY ALZHEIMER’S DISEASE
Mathilde Colinet, Alessia Cambier, Gerald Masset, Bernard Coumans, Laurent Nguyen, Ira Espuny Camacho
ADVANCING NEUROLOGICAL RESEARCH: MOUSE MODELS WITH HUMANIZED GENES AS TOOLS FOR UNDERSTANDING PATHOPHYSIOLOGY AND DEVELOPING THERAPEUTICS
Ivan Gladwyn-Ng, Morris Cui, Joseph Wekselblatt, Yun Shi, Jingyu Xu, Xing Mou, Qiming Wang
INVESTIGATING THE EARLY FRONTOTEMPORAL DEMENTIA PHENOTYPES IN A MOUSE MODEL OF TDP-43 PROTEINOPATHY
Anna Stuckert, Nicole Johnstone, Mary Everett Toombs, Santiago Mora, Raghavendra Selvan, Ilary Allodi
MODELING ALZHEIMER’S DISEASE WITH HUMAN CEREBRAL ORGANOIDS: RECAPITULATING PATHOLOGY AND PROTEOMIC BIOMARKERS
Patricia Mateos Martínez, Rosa González-Sastre, Milagros González-Flores, Cristina Soriano-Amador, Sabela Martín-Benito, Victoria López-Alonso, Raquel Coronel, Isabel Liste