C
Celia F. Brosnan
Researcher at Albert Einstein College of Medicine
Publications - 216
Citations - 20206
Celia F. Brosnan is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Experimental autoimmune encephalomyelitis & Microglia. The author has an hindex of 77, co-authored 216 publications receiving 19668 citations. Previous affiliations of Celia F. Brosnan include Yeshiva University.
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Microglia and cytokines in neurological disease, with special reference to AIDS and Alzheimer's disease
TL;DR: The results suggest that microglial activation in AD may be secondary to neurodegeneration and that, once activated, microglia may participate in a local inflammatory cascade that promotes tissue damage and contributes to amyloid formation.
Journal Article
Cytokine production by human fetal microglia and astrocytes. Differential induction by lipopolysaccharide and IL-1 beta.
TL;DR: The results demonstrate that cytokine production can be induced in human fetal microglia and astrocytes but that the stimuli for induction differed significantly for the two cell types, and suggest that microglian may be key regulators of astroCyte response, working primarily through the expression of cell-associated IL-1 beta.
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Identification of lymphotoxin and tumor necrosis factor in multiple sclerosis lesions.
TL;DR: Results indicate that LT and TNF may be involved in the immunopathogenesis of MS, and can be detected in both inflammatory cells and cells endogenous to the CNS.
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Proliferation of astrocytes in vitro in response to cytokines. A primary role for tumor necrosis factor.
TL;DR: A role for products of activated inflammatory cells in the development of astrocyte proliferation that may contribute to the reactive gliosis found in white matter diseases of the central nervous system such as multiple sclerosis is supported.
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Quantitative aspects of reactive gliosis: A review
TL;DR: There are different biological mechanisms for induction and maintenance of reactive gliosis, which, depending on the kind of tissue damage, result in different expressions of the gliotic response.