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Amyloid- β reduces the expression of neuronal FAIM-L, thereby shifting the inflammatory response mediated by TNF α from neuronal protection to death / Carriba, Paulina (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Jimenez, S. (Universidad de Sevilla. Departamento de Bioquimica y Biologia Molecular) ; Navarro, V (Universidad de Sevilla. Departamento de Bioquimica y Biologia Molecular) ; Moreno-Gonzalez, I (Universidad de Malaga. Departamento de Biologia Celular, Genetica y Fisiologia) ; Barneda Zahonero, Bruna (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Moubarak, Rana S. (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; López-Soriano, Joaquín (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Gutiérrez Pérez, Antonia (Universidad de Malaga. Departamento de Biologia Celular, Genetica y Fisiologia) ; Vitorica, Javier (Universidad de Sevilla. Departamento de Bioquimica y Biologia Molecular) ; Comella i Carnicé, Joan Xavier 1963- (Hospital Universitari Vall d'Hebron. Institut de Recerca) ; Universitat Autònoma de Barcelona
The brains of patients with Alzheimer's disease (AD) present elevated levels of tumor necrosis factor- α (TNF α), a cytokine that has a dual function in neuronal cells. On one hand, TNF α can activate neuronal apoptosis, and on the other hand, it can protect these cells against amyloid- β (A β) toxicity. [...]
2015 - DOI (Digital Object Identifier)

10.1038/cddis.2015.6
Cell death and disease, Vol. 6 (02 2015) , p. e1639

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