English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/180401
Share/Impact:
Statistics
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:
Title

Microglia in Alzheimer’s Disease: Activated, Dysfunctional or Degenerative

AuthorsNavarro, Victoria; Sánchez-Mejias, Elisabeth; Jiménez, Sebastián; Muñoz-Castro, Clara; Sánchez-Varo, Raquel; Dávila, José C.; Vizuete, Marisa; Gutiérrez, Antonia; Vitorica, Javier
KeywordsAlzheimer disease
Microglia
APP models
Inflamation
Abeta plaques
Issue Date11-May-2018
PublisherFrontiers Media
CitationFrontiers in Aging Neuroscience 10: 140 (2018)
AbstractMicroglial activation has been considered a crucial player in the pathological process of multiple human neurodegenerative diseases. In some of these pathologies, such as Amyotrophic Lateral Sclerosis or Multiple Sclerosis, the immune system and microglial cells (as part of the cerebral immunity) play a central role. In other degenerative processes, such as Alzheimer’s disease (AD), the role of microglia is far to be elucidated. In this “mini-review” article, we briefly highlight our recent data comparing the microglial response between amyloidogenic transgenic models, such as APP/PS1 and AD patients. Since the AD pathology could display regional heterogeneity, we focus our work at the hippocampal formation. In APP based models a prominent microglial response is triggered around amyloid-beta (Aβ) plaques. These strongly activated microglial cells could drive the AD pathology and, in consequence, could be implicated in the neurodegenerative process observed in models. On the contrary, the microglial response in human samples is, at least, partial or attenuated. This patent difference could simply reflect the lower and probably slower Aβ production observed in human hippocampal samples, in comparison with models, or could reflect the consequence of a chronic long-standing microglial activation. Beside this differential response, we also observed microglial degeneration in Braak V–VI individuals that, indeed, could compromise their normal role of surveying the brain environment and respond to the damage. This microglial degeneration, particularly relevant at the dentate gyrus, might be mediated by the accumulation of toxic soluble phospho-tau species. The consequences of this probably deficient immunological protection, observed in AD patients, are unknown.
Publisher version (URL)https://doi.org/10.3389/fnagi.2018.00140
URIhttp://hdl.handle.net/10261/180401
DOI10.3389/fnagi.2018.00140
E-ISSN1663-4365
Appears in Collections:(IBIS) Artículos
Files in This Item:
File Description SizeFormat 
fnagi-10-00140.pdf2,12 MBAdobe PDFThumbnail
View/Open
Show full item record
Review this work
 

Related articles:


WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.