Microglia and Synapse: Interactions in Health and Neurodegeneration
A series of discoveries spanning for the last few years has challenged our view of microglial function, the main form of immune defense in the brain. The surveillance of neuronal circuits executed by each microglial cell overseeing its territory occurs in the form of regular, dynamic interactions. M...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2013/425845 |
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| author | Zuzana Šišková Marie-Ève Tremblay |
| author_facet | Zuzana Šišková Marie-Ève Tremblay |
| author_sort | Zuzana Šišková |
| collection | DOAJ |
| description | A series of discoveries spanning for the last few years has challenged our view of microglial function, the main form of immune defense in the brain. The surveillance of neuronal circuits executed by each microglial cell overseeing its territory occurs in the form of regular, dynamic interactions. Microglial contacts with individual neuronal compartments, such as dendritic spines and axonal terminals, ensure that redundant or dysfunctional elements are recognized and eliminated from the brain. Microglia take on a new shape that is large and amoeboid when a threat to brain integrity is detected. In this defensive form, they migrate to the endangered sites, where they help to minimize the extent of the brain insult. However, in neurodegenerative diseases that are associated with misfolding and aggregation of synaptic proteins, these vital defensive functions appear to be compromised. Many microglial functions, such as phagocytosis, might be overwhelmed during exposure to the abnormal levels of misfolded proteins in their proximity. This might prevent them from attending to their normal duties, such as the stripping of degenerating synaptic terminals, before neuronal function is irreparably impaired. In these conditions microglia become chronically activated and appear to take on new, destructive roles by direct or indirect inflammatory attack. |
| format | Article |
| id | doaj-art-49c3aef3e63b4c50b735f544e62e7eb8 |
| institution | Kabale University |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-49c3aef3e63b4c50b735f544e62e7eb82025-02-03T07:26:10ZengWileyNeural Plasticity2090-59041687-54432013-01-01201310.1155/2013/425845425845Microglia and Synapse: Interactions in Health and NeurodegenerationZuzana Šišková0Marie-Ève Tremblay1German Center for Neurodegenerative Diseases (DZNE), Ludwig-Erhard-Allee 2, 53175 Bonn, GermanyAxe Neurosciences, Centre de Recherche du CHU de Québec, Département de Médecine Moléculaire, Université Laval, 2705 Boulevard Laurier, Québec, QC, G1V 4G2, CanadaA series of discoveries spanning for the last few years has challenged our view of microglial function, the main form of immune defense in the brain. The surveillance of neuronal circuits executed by each microglial cell overseeing its territory occurs in the form of regular, dynamic interactions. Microglial contacts with individual neuronal compartments, such as dendritic spines and axonal terminals, ensure that redundant or dysfunctional elements are recognized and eliminated from the brain. Microglia take on a new shape that is large and amoeboid when a threat to brain integrity is detected. In this defensive form, they migrate to the endangered sites, where they help to minimize the extent of the brain insult. However, in neurodegenerative diseases that are associated with misfolding and aggregation of synaptic proteins, these vital defensive functions appear to be compromised. Many microglial functions, such as phagocytosis, might be overwhelmed during exposure to the abnormal levels of misfolded proteins in their proximity. This might prevent them from attending to their normal duties, such as the stripping of degenerating synaptic terminals, before neuronal function is irreparably impaired. In these conditions microglia become chronically activated and appear to take on new, destructive roles by direct or indirect inflammatory attack.http://dx.doi.org/10.1155/2013/425845 |
| spellingShingle | Zuzana Šišková Marie-Ève Tremblay Microglia and Synapse: Interactions in Health and Neurodegeneration Neural Plasticity |
| title | Microglia and Synapse: Interactions in Health and Neurodegeneration |
| title_full | Microglia and Synapse: Interactions in Health and Neurodegeneration |
| title_fullStr | Microglia and Synapse: Interactions in Health and Neurodegeneration |
| title_full_unstemmed | Microglia and Synapse: Interactions in Health and Neurodegeneration |
| title_short | Microglia and Synapse: Interactions in Health and Neurodegeneration |
| title_sort | microglia and synapse interactions in health and neurodegeneration |
| url | http://dx.doi.org/10.1155/2013/425845 |
| work_keys_str_mv | AT zuzanasiskova microgliaandsynapseinteractionsinhealthandneurodegeneration AT marieevetremblay microgliaandsynapseinteractionsinhealthandneurodegeneration |