Poster preview
ePoster
AΒ42 DRIVES GOLGI FRAGMENTATION IN AN APP KNOCK-IN MOUSE MODEL OF ALZHEIMER’S DISEASE
Subash Chandra Malikand 4 co-authors
Karolinska Institute
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS06-09PM-165
Presentation
Date TBA
Board: PS06-09PM-165
Event Information
Poster Board
PS06-09PM-165
Poster
View posterAbstract
Alzheimer’s disease is characterized by extracellular deposits of the 42 residues long amyloid β-peptide (Aβ42) derived from the amyloid precursor protein (APP). Understanding the processing and trafficking of APP is critical for targeting disease pathology. APP undergoes post-translational modifications in the Golgi apparatus prior to its trafficking to the plasma membrane and the endosomal systems. Transgenic mice overexpressing mutated APP shows Golgi fragmentation, but it is not clear whether this is due to increased Aβ levels or overexpression of APP. Here we studied AppNL‑F, a humanized APP knock-in mouse model exhibiting AD pathology without APP overexpression. Using 2D and 3D Airyscan imaging, we show that the Golgi apparatus is fragmented in AppNL-F primary hippocampal neurons while the APP levels in Golgi are unaltered. Furthermore, we found that addition of Aβ42 to the medium of primary WT neurons resulted in Golgi fragmentation similar to what we observed in the AppNL-F neurons. Thus, Aβ42 drives the Golgi fragmentation in AppNL-F neurons leading to smaller and isolated surfaces that might result in altered sorting and trafficking of proteins along the secretory pathway.
Recommended posters
THE ASSOCIATION BETWEEN TOXIC AΒ SPECIES AND AXONAL GROWTH AND SPROUTING IN ALZHEIMER'S DISEASE
Tosca Doeswijk, Michael Axenhus, Lars Tjernberg, Sophia Schedin Weiss
INVESTIGATING EARLY AΒ-DRIVEN SYNAPTIC DYSFUNCTIONS IN ALZHEIMER’S DISEASE: MORPHOLOGICAL AND FUNCTIONAL ALTERATIONS OF DENDRITIC SPINES OCCUR SIMULTANEOUSLY IN VITRO
Marion Tudury, Eve Borel, Béatrice Blot, Muriel Jacquier Sarlin, Alain Buisson
ALTERATION OF THE G-PROTEIN GΑO SUBUNIT IN THE HIPPOCAMPUS IN AMYLOID-Β AND TAU PATHOLOGY
María de los Llanos Martínez Poyato, Carolina Aguado Rubio, Alejandro Martín Belmonte, Rocío Alfaro-Ruíz, Ana Esther Moreno Martínez, Rafael Luján Miras
ALZHEIMER’S DISEASE MODELS IN IPSC-DERIVED GLUTAMATERGIC NEURONS SHOW INCREASED SECRETION OF PATHOGENIC AMYLOID BETA PEPTIDES
Veronica Acevedo Morejon, Aurora Veteleanu, Tony Oosterveen, Germano Belli Valletta, George Shipley, Hannah Garnett, Christopher Aruthan, Philippa Barton, Stefan Milde, Magdalena Gamperl, Sejla Salic-Hainzl, Tilmann Buerckstuemmer, Amanda Turner, Karl Firth, Oliver Dovey, Will Bernard
SUBCELLULAR PROTEOME CHARACTERISATION OF ALZHEIMER'S DISEASE VULNERABLE NEURONS IN APPNL-F MICE
Christina Tsagkogianni, Patricia Rodriguez Rodriguez
DECODING Β-AMYLOID TOXICITY THROUGH SPATIOTEMPORAL AND INTERACTOMIC PROFILING OF RHO GTPASES
Maximiliano Gabriel Melano, Lorena Paola Neila, Clara Ines Chungara, Martina Aleman, Laura Montroull, Gonzalo Quassollo, Leticia Peris, Mariano Bisbal