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Keith M. Erikson
Researcher at University of North Carolina at Greensboro
Publications - 83
Citations - 5772
Keith M. Erikson is an academic researcher from University of North Carolina at Greensboro. The author has contributed to research in topics: Neurotoxicity & Iron deficiency. The author has an hindex of 42, co-authored 80 publications receiving 5239 citations. Previous affiliations of Keith M. Erikson include Pennsylvania State University & Wake Forest University.
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Manganese Dosimetry: Species Differences and Implications for Neurotoxicity
TL;DR: A review on the essentiality and toxicity of manganese and its transport across the blood-brain barrier, and its distribution within the central nervous system (CNS) is presented in this article.
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Iron Deficiency Decreases dopamine D1 and D2 receptors in rat brain
TL;DR: In this paper, the extent of functional alterations in dopamine receptors in two dopaminergic tracts in young, growing, iron-deficient rats were determined, and the results showed abnormal dopamine receptor density and functioning in several brain regions that are related to brain regional iron loss.
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Manganese and its Role in Parkinson's disease: from Transport to Neuropathology.
TL;DR: This review discusses inflammatory activation of glia in neuronal injury and how disruption of synaptic transmission and glial-neuronal communication may serve as underlying mechanisms of Mn-induced neurodegeneration commensurate with the cross-talk between glia and neurons.
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Iron deficiency alters dopamine transporter functioning in rat striatum
TL;DR: Elevated levels of extracellular DA in the striatum of iron-deficient rats is likely to be the result of decreased DAT functioning and not increased rates of release, supporting evidence that iron deficiency anemia in early life produces profound changes in both in vivo and in vitro evaluations of dopamine functioning.
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Regional Brain Iron, Ferritin and Transferrin Concentrations during Iron Deficiency and Iron Repletion in Developing Rats
TL;DR: The hippocampus had the most dramatic Tf response to iron deficiency with elevations of approximately 100%, whereas other regions, except striatum, were unaffected, and brain transferrin concentrations in REPL rats, however, were significantly above the levels of controls.