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Colm Cunningham

Researcher at Trinity College, Dublin

Publications -  116
Citations -  13241

Colm Cunningham is an academic researcher from Trinity College, Dublin. The author has contributed to research in topics: Delirium & Systemic inflammation. The author has an hindex of 53, co-authored 108 publications receiving 10621 citations. Previous affiliations of Colm Cunningham include University of Southampton & University College London.

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Systemic inflammation and disease progression in alzheimer disease

TL;DR: Both acute and chronic systemic inflammation, associated with increases in serum tumor necrosis factor α, is associated with an increase in cognitive decline in Alzheimer disease.
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Systemic infections and inflammation affect chronic neurodegeneration.

TL;DR: Evidence is reviewed to support the hypothesis that in chronic neurodegenerative diseases such as Alzheimer's disease, with an ongoing innate immune response in the brain, systemic infections and inflammation can cause acute exacerbations of symptoms and drive the progression of neurodegenersation.
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Reactive astrocyte nomenclature, definitions, and future directions

Carole Escartin, +88 more
- 15 Feb 2021 - 
TL;DR: In this article, the authors point out the shortcomings of binary divisions of reactive astrocytes into good-vs-bad, neurotoxic vs-neuroprotective or A1-vs.A2.
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Central and Systemic Endotoxin Challenges Exacerbate the Local Inflammatory Response and Increase Neuronal Death during Chronic Neurodegeneration

TL;DR: Both central and peripheral inflammation can exacerbate local brain inflammation and neuronal death, and the finding that a single acute systemic inflammatory event can induce neuronal death in the CNS has implications for therapy in neurodegenerative diseases.
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Microglia and neurodegeneration: The role of systemic inflammation

TL;DR: It is now apparent in multiple chronic disease states, and in ageing, that microglia are primed by prior pathology, or by genetic predisposition, to respond more vigorously to subsequent inflammatory stimulation, thus transforming an adaptive CNS inflammatory response to systemic inflammation, into one that has deleterious consequences for the individual.