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Rodney M. Ritzel

Researcher at University of Maryland, Baltimore

Publications -  51
Citations -  2694

Rodney M. Ritzel is an academic researcher from University of Maryland, Baltimore. The author has contributed to research in topics: Microglia & Neuroinflammation. The author has an hindex of 20, co-authored 42 publications receiving 1705 citations. Previous affiliations of Rodney M. Ritzel include University of Connecticut Health Center & University of Connecticut.

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Journal Article

Microglia and ischemic stroke: a double-edged sword.

TL;DR: Fine-tuning immunomodulatory interventions based on the heterogeneous profiles of microglia are urgently needed for ischemic stroke.
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Functional differences between microglia and monocytes after ischemic stroke

TL;DR: The resident microglia population is vulnerable to the effects of severe ischemia, show compromised cell cycle progression, and adopt a largely pro-inflammatory phenotype after stroke, suggesting that the early wave of infiltrating monocytes may be beneficial to stroke repair.
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Microglial Depletion with CSF1R Inhibitor During Chronic Phase of Experimental Traumatic Brain Injury Reduces Neurodegeneration and Neurological Deficits.

TL;DR: It is shown that short-term elimination of microglia during the chronic phase of TBI followed by repopulation results in long-term improvements in neurological function, suppression of neuroinflammatory and oxidative stress pathways, and a reduction in persistent neurodegenerative processes.
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Old Maids: Aging and Its Impact on Microglia Function

TL;DR: The impact of normal aging on microglial function is outlined, the potential mechanisms underlying age-related changes in microglia are highlighted, and how aging can shape the recovery process following injury is discussed.
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Age-Associated Resident Memory CD8 T Cells in the Central Nervous System Are Primed To Potentiate Inflammation after Ischemic Brain Injury.

TL;DR: A novel population of resident memory, immunosurveillant CD8 T cells that represent a hallmark of CNS aging and appear to modify microglia homeostasis under normal conditions, but are primed to potentiate inflammation and leukocyte recruitment following ischemic injury is identified.