Tau enhances α-synuclein aggregation and toxicity in cellular models of synucleinopathy

Background: The simultaneous accumulation of different misfolded proteins in the central nervous system is a common feature in many neurodegenerative diseases. In most cases, co-occurrence of abnormal deposited proteins is observed in different brain regions and cell populations, but, in some instan...

Descripción completa

Detalles Bibliográficos
Autores: Badiola Benito, Nahuai|||0000-0001-9488-5628, de Oliveira, Rita Machado|||0000-0002-0970-4501, Herrera, Federico, Guardia-Laguarta, Cristina|||0000-0003-0811-9068, Gonçalves, Susana A., Pera, Marta|||0000-0003-4317-6623, Suárez-Calvet, Marc|||0000-0002-2993-569X, Clarimón, Jordi|||0000-0002-6824-6942, Outeiro, Tiago Fleming, Lleó, Alberto|||0000-0002-2568-5478
Tipo de recurso: artículo
Fecha de publicación:2011
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:312050
Acceso en línea:https://ddd.uab.cat/record/312050
https://dx.doi.org/urn:doi:10.1371/journal.pone.0026609
Access Level:acceso abierto
Descripción
Sumario:Background: The simultaneous accumulation of different misfolded proteins in the central nervous system is a common feature in many neurodegenerative diseases. In most cases, co-occurrence of abnormal deposited proteins is observed in different brain regions and cell populations, but, in some instances, the proteins can be found in the same cellular aggregates. Co-occurrence of tau and α-synuclein (α-syn) aggregates has been described in neurodegenerative disorders with primary deposition of α-syn, such as Parkinson's disease and dementia with Lewy bodies. Although it is known that tau and α-syn have pathological synergistic effects on their mutual fibrillization, the underlying biological effects remain unclear. Methodology/Principal Findings: We used different cell models of synucleinopathy to investigate the effects of tau on α-syn aggregation. Using confocal microscopy and FRET-based techniques we observed that tau colocalized and interacted with α-syn aggregates. We also found that tau overexpression changed the pattern of α-syn aggregation, reducing the size and increasing the number of aggregates. This shift was accompanied by an increase in the levels of insoluble α-syn. Furthermore, co-transfection of tau increased secreted α-syn and cytotoxicity. Conclusions/Significance: Our data suggest that tau enhances α-syn aggregation and toxicity and disrupts α-syn inclusion formation. This pathological synergistic effect between tau and α-syn may amplify the deleterious process and spread the damage in neurodegenerative diseases that show co-occurrence of both pathologies. © 2011 Badiola et al.