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Paul A. Rosenberg

Researcher at Johns Hopkins University School of Medicine

Publications -  249
Citations -  19965

Paul A. Rosenberg is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Glutamate receptor & Excitotoxicity. The author has an hindex of 69, co-authored 225 publications receiving 18397 citations. Previous affiliations of Paul A. Rosenberg include University of Pittsburgh & New York University.

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Excitatory amino acids as a final common pathway for neurologic disorders.

TL;DR: In many neurologic disorders, injury to neurons may be caused at least in part by overstimulation of receptors for excitatory amino acids, including glutamate and aspartate.
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Activation of innate immunity in the CNS triggers neurodegeneration through a Toll-like receptor 4-dependent pathway

TL;DR: A mechanistic link among innate immunity, TLRs, and neurodegeneration is demonstrated and microglia is identified as the major lipopolysaccharide-responsive cell in the CNS.
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Ferrostatins inhibit oxidative lipid damage and cell death in diverse disease models.

TL;DR: A mechanistic model to explain the activity of Fer-1 was developed, which guided the development of ferrostatins with improved properties, and that lipid peroxidation mediates diverse disease phenotypes are suggested.
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The Toll-Like Receptor TLR4 Is Necessary for Lipopolysaccharide-Induced Oligodendrocyte Injury in the CNS

TL;DR: The data provide a general mechanistic link between (1) lipopolysaccharide and similar microbial molecular motifs and (2) injury to oligodendrocytes and myelin as occurs in periventricular leukomalacia and multiple sclerosis.
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Maturation-Dependent Vulnerability of Oligodendrocytes to Oxidative Stress-Induced Death Caused by Glutathione Depletion

TL;DR: It is reported here that OLs demonstrate maturation-dependent differences in survival when subjected to free radical-mediated injury induced by glutathione depletion, and that oligodendroglial maturation is associated with decreased susceptibility to oxidative stress.