H
Henrik Wilms
Researcher at Texas Tech University Health Sciences Center
Publications - 40
Citations - 2706
Henrik Wilms is an academic researcher from Texas Tech University Health Sciences Center. The author has contributed to research in topics: Microglia & Neuroinflammation. The author has an hindex of 22, co-authored 37 publications receiving 2477 citations. Previous affiliations of Henrik Wilms include Texas Tech University & Heidelberg University.
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Dimethylfumarate inhibits microglial and astrocytic inflammation by suppressing the synthesis of nitric oxide, IL-1β, TNF-α and IL-6 in an in-vitro model of brain inflammation
TL;DR: Pretreatment with DMF decreased synthesis of the proinflammatory mediators iNOS, TNF-α, IL-1β and IL-6 at the RNA level in activated microglial and astrocytes in vitro, associated with a decrease in ERK phosphorylation in microglia.
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Activation of microglia by human neuromelanin is NF-κB dependent and involves p38 mitogen-activated protein kinase: implications for Parkinson’s disease
TL;DR: A crucial role of NM is demonstrated in the pathogenesis of PD by augmentation of microglial activation, leading to a vicious cycle of neuronal death, exposure of additional neuromelanin, and chronification of inflammation.
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Neuromelanin of the substantia nigra: a neuronal black hole with protective and toxic characteristics
TL;DR: Intraneuronal neuromelanin could play a protective role during its synthesis by preventing the toxic accumulation of cytosolic catechol derivatives and, in addition, by its ability to scavenge reactive metals, pesticides and other toxins to form stable adducts.
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The pathophysiology of parkinsonian tremor: a review.
TL;DR: Parkinsonian tremor is most likely due to oscillating neuronal activity within the CNS, but the neuronal mechanisms underlying these oscillations are not yet clear and three hypotheses would be compatible with the presently available data from animal models and data recorded in patients.
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Inflammation in Parkinson's diseases and other neurodegenerative diseases: cause and therapeutic implications.
TL;DR: A crucial role of NM is demonstrated in the pathogenesis of Parkinson's disease by augmentation of microglial activation, leading to a vicious cycle of neuronal death, exposure of additional neuromelanin and chronification of inflammation.