Increased expression of the oligopeptidase THOP1 is a neuroprotective response to Aβ toxicity

التفاصيل البيبلوغرافية
العنوان: Increased expression of the oligopeptidase THOP1 is a neuroprotective response to Aβ toxicity
المؤلفون: Renza Roncarati, Andrea Caricasole, Anna Fiorentini, Stefano Gotta, Roberto Raggiaschi, Georg C. Terstappen, Letizia Magnoni, Jeroen J.M. Hoozemans, Giuseppe Pollio, Tamara Seredenina, Daniela Diamanti, Elise S. van Haastert, Annemieke J.M. Rozemuller, Claus A. Andersen, Maria Cristina Rosi, Fiorella Casamenti
المساهمون: Pathology, Neuroscience Campus Amsterdam 2008
المصدر: Neurobiology of Disease, Vol 31, Iss 1, Pp 145-158 (2008)
Pollio, G, Hoozemans, J J M, Andersen, C A, Roncarati, R, Rosi, M C, van Haastert, E S, Seredenina, T, Diamanti, D, Gotta, S, Fiorentini, A, Magnoni, L, Raggiaschi, R, Rozemuller, A J M, Casamenti, F, Caricasole, A & Terstappen, G C 2008, ' Increased expression of the oligopeptidase THOP1 is a neuroprotective response to A beta toxicity ', Neurobiology of Disease, vol. 31, no. 1, pp. 145-158 . https://doi.org/10.1016/j.nbd.2008.04.004Test
Neurobiology of Disease, 31(1), 145-158. Academic Press Inc.
بيانات النشر: Elsevier, 2008.
سنة النشر: 2008
مصطلحات موضوعية: Genetically modified mouse, Male, Amyloid, Phosphoproteomics, Blotting, Western, Oligopeptidase, Gene Expression, Thimet oligopeptidase, Mice, Transgenic, Plaque, Amyloid, Pharmacology, Biology, Transfection, Neuroprotection, lcsh:RC321-571, Rats, Sprague-Dawley, Mice, RNA interference, Alzheimer Disease, Animals, Humans, RNA, Small Interfering, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Cells, Cultured, Aged, Aged, 80 and over, Cerebral Cortex, Neurons, Gene knockdown, Amyloid beta-Peptides, Microscopy, Confocal, Reverse Transcriptase Polymerase Chain Reaction, Metalloendopeptidases, Middle Aged, Alzheimer's disease, Immunohistochemistry, Rats, TgCRND8 mouse, Neurology, RNAi, Toxicity, Female, THOP1, Neuroscience
الوصف: In a comprehensive proteomics study aiming at the identification of proteins associated with amyloid-beta (Abeta)-mediated toxicity in cultured cortical neurons, we have identified Thimet oligopeptidase (THOP1). Functional modulation of THOP1 levels in primary cortical neurons demonstrated that its overexpression was neuroprotective against Abeta toxicity, while RNAi knockdown made neurons more vulnerable to amyloid peptide. In the TgCRND8 transgenic mouse model of amyloid plaque deposition, an age-dependent increase of THOP1 expression was found in brain tissue, where it co-localized with Abeta plaques. In accordance with these findings, THOP1 expression was significantly increased in human AD brain tissue as compared to non-demented controls. These results provide compelling evidence for a neuroprotective role of THOP1 against toxic effects of Abeta in the early stages of AD pathology, and suggest that the observed increase in THOP1 expression might be part of a compensatory defense mechanism of the brain against an increased Abeta load.
اللغة: English
تدمد: 0969-9961
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d1c110ec09431d10d89afae578124d1bTest
http://www.sciencedirect.com/science/article/pii/S0969996108000740Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....d1c110ec09431d10d89afae578124d1b
قاعدة البيانات: OpenAIRE