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Byron D. Ford

Researcher at University of California, Riverside

Publications -  66
Citations -  2105

Byron D. Ford is an academic researcher from University of California, Riverside. The author has contributed to research in topics: Neuroprotection & Neuregulin 1. The author has an hindex of 25, co-authored 65 publications receiving 1851 citations. Previous affiliations of Byron D. Ford include National Institutes of Health & Morehouse School of Medicine.

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Neuregulins Increase α7 Nicotinic Acetylcholine Receptors and Enhance Excitatory Synaptic Transmission in GABAergic Interneurons of the Hippocampus

TL;DR: Pharmacologic experiments indicated that the shower of PSCs was mediated by glutamate, with a small minority caused by the action of GABA.
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Translational Stroke Research: Vision and Opportunities

TL;DR: Pharmacodynamics, pharmacokinetics, and target engagement in the human brain need to be further developed and optimized for stroke interventions so that drug level in brain tissue, time to initiation, and duration of treatment can be accurately measured in clinical trials.
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Neuroprotection by neuregulin-1 following focal stroke is associated with the attenuation of ischemia-induced pro-inflammatory and stress gene expression

TL;DR: It is demonstrated that NRG-1 can regulate inflammatory and stress gene expression and may give new insight to the molecular mechanisms involved in the neuroprotective role of neuregulins in stroke.
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Neuregulin-1 is neuroprotective and attenuates inflammatory responses induced by ischemic stroke

TL;DR: It is shown that a single intravascular injection of neuregulin-1beta reduced cortical infarct volume by >98% when given immediately before middle cereral artery occlusion, and that this effect protects neurons from delayed, ischemia-induced apoptotic cell death in the cortex by inhibiting pro-inflammatory responses.
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Regulation of inflammatory responses by neuregulin-1 in brain ischemia and microglial cells in vitro involves the NF-kappa B pathway

TL;DR: Findings suggest that NRG-1 may be a potential therapeutic treatment for treating stroke and other neuroinflammatory disorders and the differential regulation of NF-kB signaling pathways in microglia.