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Bonnie L. Robinson
Researcher at National Center for Toxicological Research
Publications - 35
Citations - 1521
Bonnie L. Robinson is an academic researcher from National Center for Toxicological Research. The author has contributed to research in topics: Neurotoxicity & Dopaminergic. The author has an hindex of 14, co-authored 34 publications receiving 1289 citations. Previous affiliations of Bonnie L. Robinson include Food and Drug Administration.
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Journal ArticleDOI
Expression of genes related to oxidative stress in the mouse brain after exposure to silver-25 nanoparticles.
M.F. Rahman,J. Wang,Tucker A. Patterson,U.T. Saini,Bonnie L. Robinson,Glenn D. Newport,Richard C. Murdock,John J. Schlager,Saber M. Hussain,Syed F. Ali +9 more
TL;DR: The data suggest that Ag-25 nanoparticles may produce neurotoxicity by generating free radical-induced oxidative stress and by altering gene expression, producing apoptosis and neurotoxicity.
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Silver nanoparticle induced blood-brain barrier inflammation and increased permeability in primary rat brain microvessel endothelial cells.
William J. Trickler,Susan M. Lantz,Richard C. Murdock,Amanda M. Schrand,Bonnie L. Robinson,Glenn D. Newport,John J. Schlager,Steven J. Oldenburg,Merle G. Paule,William Slikker,Saber M. Hussain,Syed F. Ali +11 more
TL;DR: It is suggested that Ag-NPs may interact with the cerebral microvasculature producing a proinflammatory cascade, if left unchecked; these events may further induce brain inflammation and neurotoxicity.
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Effects of copper nanoparticles on rat cerebral microvessel endothelial cells.
William J. Trickler,Susan M. Lantz,Amanda M. Schrand,Bonnie L. Robinson,Glenn D. Newport,John J. Schlager,Merle G. Paule,William Slikker,Alexandru S. Biris,Saber M. Hussain,Syed F. Ali +10 more
TL;DR: It is suggested that Cu-NPs can induce rBMEC, proliferation at low concentrations and/or induce blood-brain barrier toxicity and potential neurotoxicity at high concentrations.
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Post-treatment with an ultra-low dose of NADPH oxidase inhibitor diphenyleneiodonium attenuates disease progression in multiple Parkinson’s disease models
Qingshan Wang,Li Qian,Shih Heng Chen,Chun Hsien Chu,Belinda Wilson,Esteban A. Oyarzabal,Syed F. Ali,Bonnie L. Robinson,Deepa Rao,Jau-Shyong Hong +9 more
TL;DR: Filtration of ultra-low dose diphenyleneiodonium potently reduced microglia-mediated chronic neuroinflammation by selectively inhibiting nicotinamide adenine dinucleotide phosphate oxidase and halted the progression of neurodegeneration in mouse models of Parkinson's disease.
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Neurotoxic-related changes in tyrosine hydroxylase, microglia, myelin, and the blood-brain barrier in the caudate-putamen from acute methamphetamine exposure
TL;DR: A major BBB disruption within the CPu does not directly contribute to neurotoxicity in this single high‐dose METH exposure, however, seizure activity produced or exacerbated by amygdalarBBB disruption can significantly increase CPu somatic neurodegeneration (but not affect dopamine (DA) terminal damage).