Artículo
Microglia in Alzheimer’s Disease: Activated, Dysfunctional or Degenerative
Autor/es | Navarro Garrido, Victoria
Sánchez Mejías, Elisabeth Jiménez Muñoz, Sebastián Muñoz Castro, Clara Sánchez Varo, Raquel María Dávila, José Carlos Vizuete Chacón, María Luisa Gutiérrez, Antonia Vitorica Ferrández, Francisco Javier |
Departamento | Universidad de Sevilla. Departamento de Bioquímica y Biología Molecular |
Fecha de publicación | 2018 |
Fecha de depósito | 2018-09-25 |
Publicado en |
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Resumen | Microglial 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, ... Microglial 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. |
Agencias financiadoras | Instituto de Salud Carlos III Junta de Andalucía |
Identificador del proyecto | PI15/00957
PI15/00796 CTS-2035 |
Cita | Navarro Garrido, V., Sánchez Mejías, ., Jiménez Muñoz, S., Muñoz Castro, ., Sánchez Varo, R.M., Dávila, J.C.,...,Vizuete Chacón, M.L. (2018). Microglia in Alzheimer’s Disease: Activated, Dysfunctional or Degenerative. Frontiers in Aging Neuroscience, 10 (140), 1-8. |
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pubfnagi-10-00140.pdf | 2.073Mb | [PDF] | Ver/ | |