Phospho-Tau Accumulation and Structural Alterations of the Golgi Apparatus of Cortical Pyramidal Neurons in the P301S Tauopathy Mouse Model
Publisher
IOS PressDate
2017-01-01Citation
10.3233/JAD-170332
Journal of Alzheimer's Disease 60.2 (2017): 651-661
ISSN
1387-2877 (print); 1875-8908 (online)DOI
10.3233/JAD-170332Funded by
This work was supported by grants from the following entities: SAF 2015-66603-P and BFU-2016-77885-P from the Ministerio de Economía y Competitividad; Centro de Investigación en Red sobre Enfermedades Neurodegenerativas (CIBERNED, CB06/05/0066, Spain); and a grant from the Alzheimer’s Association (ZEN-15-321663). J. M-R was supported by a predoctoral fellowship from La Caixa foundation. This project received funding from the European Union’s Horizon 2020 research and innovation program under grant agreement No. 720270.Project
info:eu-repo/grantAgreement/EC/H2020/720270/EU//ATTRACTEditor's Version
https://doi.org/10.3233/JAD-170332Subjects
Golgi apparatus; hippocampus; neocortex; neurofibrillary tangles; tauopathies; Biología y Biomedicina / BiologíaRights
© 2017 - IOS Press and the authorsAbstract
The Golgi apparatus (GA) is a highly dynamic organelle involved in the processing and sorting of cellular proteins. In Alzheimer's disease (AD), it has been shown to decrease in size and become fragmented in neocortical and hippocampal neuronal subpopulations. This fragmentation and decrease in size of the GA in AD has been related to the accumulation of hyperphosphorylated tau. However, the involvement of other pathological factors associated with the course of the disease, such as the extracellular accumulation of amyloid-β (Aβ) aggregates, cannot be ruled out, since both pathologies are present in AD patients. Here we use the P301S tauopathy mouse model to examine possible alterations of the GA in neurons that overexpress human tau (P301S mutated gene) in neocortical and hippocampal neurons, using double immunofluorescence techniques and confocal microscopy. Quantitative analysis revealed that neurofibrillary tangle (NFT)-bearing neurons had important morphological alterations and reductions in the surface area and volume of the GA compared with NFT-free neurons. Since in this mouse model there are no Aβ aggregates typical of AD, the present findings support the idea that the progressive accumulation of phospho-tau is associated with structural alterations of the GA, and that these changes may occur in the absence of Aβ pathology
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Google Scholar:Antón Fernández, Alejandro
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Merchán-Rubira, Jesús
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Ávila, Jesús
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Hernández Pérez, Félix
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Defelipe, Javier
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Muñoz, Alberto
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