Microglia and brain macrophages in the molecular age: from origin to neuropsychiatric disease

By Marco Prinz, Josef Priller. Nature Reviews Neuroscience, 2014

1,271 citations recorded by the source corpus.

Subfields: Developmental Neuroscience, Immunology, Neurology

View Paper: https://www.semanticscholar.org/paper/0a7da3129843d344677790b5fff056442f2cfcc5

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Citations in the corpus

A Unique Microglia Type Associated with Restricting Development of Alzheimer's Disease. (2017, neutral): “For example, in AD, as in many other neurodegenerative diseases, the local neuroinflammation that is associated with cytotoxicity and disease escalation has often been attributed mainly to microglia (Mosher and Wyss-Coray, 2014; Prinz and Priller, 2014; Wang et al., 2015, 2016; Yuan et al., 2016).”
Depression as a microglial disease. (2015, background): “However, the specific role of microglia in major depression is only beginning to be explicated [4–7] and will be the topic of the current review.”
Microglial brain region-dependent diversity and selective regional sensitivities to ageing (2016, neutral): “Key findings include that (1) transcriptional networks controlling microglial bioenergetic and immunoregulatory functions contribute prominently to heterogeneity in the young adult, (2) immunophenotypic variation suggests a more immune vigilant state of cerebellar microglia, (3) networks of gene co-”
TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer’s disease mouse models (2015, background): “The potential role of peripherally derived macrophages in AD has been controversial (Prinz and Priller, 2014), but it is well accepted that CD45hiLy6C+CCR2+ monocytes enter the central nervous system (CNS) and modulate pathology in other disease contexts (Mildner et al.”
TREM2-mediated early microglial response limits diffusion and toxicity of amyloid plaques (2016, background): “Given that brain-resident microglia are capable of self-renewal and expansion (Gomez Perdiguero et al., 2013; Greter and Merad, 2013; Prinz and Priller, 2014), we next sought to determine if microglia associated with plaques resulted from the proliferation of resident microglia.”
Role of intestinal microbiota and metabolites on gut homeostasis and human diseases (2017, background): “Microglia, as the tissue macrophages of the brain, are crucial for maintaining tissue homeostasis, for scavenging dying cells/components, and for eradicating pathogens through microbial associated molecular pattern receptor-dependent and -independent mechanisms [185].”
Host microbiota constantly control maturation and function of microglia in the CNS (2015, methodology): “Using exome sequencing to reveal mutations in TREM2 presenting as a frontotemporal dementia-like syndrome without bone involvement. JAMA Neurol. 70, 78–84 (2013). 7.”
iPSC-derived human microglia-like cells to study neurological diseases (2017, neutral): “EMPs further develop to early primitive macrophages that migrate into the developing neural tube, and become microglial progenitors (Kierdorf et al., 2013, Prinz and Priller, 2014).”