Please use this identifier to cite or link to this item:
Title: Prion protein oligomers cause neuronal cytoskeletal damage in rapidly progressive Alzheimer’s disease
Author: Shafiq, Mohsin
Zafar, Saima
Younas, Neelam
Noor, Aneeqa
Puig, Berta
Altmeppen, Hermann Clemens
Schmitz, Matthias
Matschke, Jakob
Ferrer, Isidro (Ferrer Abizanda)
Glatzel, Markus
Zerr, Inga
Keywords: Malaltia d'Alzheimer
Proteïnes citosquelètiques
Alzheimer's disease
Cytoskeletal proteins
Issue Date: 22-Feb-2021
Publisher: BioMed Central
Abstract: Background: High-density oligomers of the prion protein (HDPs) have previously been identified in brain tissues of patients with rapidly progressive Alzheimer's disease (rpAD). The current investigation aims at identifying interacting partners of HDPs in the rpAD brains to unravel the pathological involvement of HDPs in the rapid progression. Methods: HDPs from the frontal cortex tissues of rpAD brains were isolated using sucrose density gradient centrifugation. Proteins interacting with HDPs were identified by co-immunoprecipitation coupled with mass spectrometry. Further verifications were carried out using proteomic tools, immunoblotting, and confocal laser scanning microscopy. Results: We identified rpAD-specific HDP-interactors, including the growth arrest specific 2-like 2 protein (G2L2). Intriguingly, rpAD-specific disturbances were found in the localization of G2L2 and its associated proteins i.e., the end binding protein 1, α-tubulin, and β-actin. Discussion: The results show the involvement of HDPs in the destabilization of the neuronal actin/tubulin infrastructure. We consider this disturbance to be a contributing factor for the rapid progression in rpAD.
Note: Reproducció del document publicat a:
It is part of: Molecular Neurodegeneration, 2021, vol. 16
Related resource:
Appears in Collections:Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))

Files in This Item:
File Description SizeFormat 
s13024-021-00422-x.pdf2.09 MBAdobe PDFView/Open

This item is licensed under a Creative Commons License Creative Commons