Distinct inflammatory phenotypes of microglia and monocyte-derived macrophages in Alzheimer's disease models: effects of aging and amyloid pathology. (Q37591996)

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scientific article published on 08 October 2016

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English	Distinct inflammatory phenotypes of microglia and monocyte-derived macrophages in Alzheimer's disease models: effects of aging and amyloid pathology.	scientific article published on 08 October 2016

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25 March 2020

Distinct inflammatory phenotypes of microglia and monocyte-derived macrophages in Alzheimer's disease models: effects of aging and amyloid pathology (English)

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25 March 2020

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Alzheimer's disease

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Cécile Delarasse

4

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25 March 2020

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Elodie Martin

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25 March 2020

Céline Boucher

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Bertrand Fontaine

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8 October 2016

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25 March 2020

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25 March 2020

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25 March 2020

1

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27-38

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25 March 2020

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Differential roles of microglia and monocytes in the inflamed central nervous system

1 reference

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Accelerated microglial pathology is associated with Aβ plaques in mouse models of Alzheimer's disease

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Microglial dysfunction in brain aging and Alzheimer's disease

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CD36 coordinates NLRP3 inflammasome activation by facilitating intracellular nucleation of soluble ligands into particulate ligands in sterile inflammation

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Functional impairment of microglia coincides with Beta-amyloid deposition in mice with Alzheimer-like pathology

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Microglia: scapegoat, saboteur, or something else?

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The fractalkine receptor but not CCR2 is present on microglia from embryonic development throughout adulthood

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Age-related alterations in the dynamic behavior of microglia

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Neuroinflammatory processes in Alzheimer's disease

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CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer

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Formation and maintenance of Alzheimer's disease beta-amyloid plaques in the absence of microglia

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CD14 and toll-like receptors 2 and 4 are required for fibrillar A{beta}-stimulated microglial activation.

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Microglial dysfunction and defective beta-amyloid clearance pathways in aging Alzheimer's disease mice

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The NALP3 inflammasome is involved in the innate immune response to amyloid-beta

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Abeta42-driven cerebral amyloidosis in transgenic mice reveals early and robust pathology

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Microglia in the aging brain

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Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase

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CD36 mediates the innate host response to beta-amyloid

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Isolation and direct characterization of resident microglial cells from the normal and inflamed central nervous system

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Microglia Versus Myeloid Cell Nomenclature during Brain Inflammation

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Ly-6G+CCR2- myeloid cells rather than Ly-6ChighCCR2+ monocytes are required for the control of bacterial infection in the central nervous system

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1 reference

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Identifiers

10.1111/ACEL.12522

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25 March 2020

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