Special Issue "Neuroprotective Strategies 2012"

Guest Editor
Dr. Katalin Prokai-Tatrai
Department of Pharmacology & Neuroscience, University of North Texas Health Science Center, 3500 Camp Bowie Blvd, Fort Worth, TX 76107, USA
Website: http://www.hsc.unt.edu/faculty/biography.cfm?id=538
E-Mail: kprokai@hsc.unt.edu
Phone: +1 871 735-0617
Fax: +1 817 735 2118
Interests: Medicinal chemistry: drug design of central nervous system agents; neuropeptides and peptidomimetics; prodrugs for CNS delivery; oxidative stress; estrogens and other phenolic antioxidants; protein carbonylation

Dear Colleagues,

This special issue is aimed at both the basic science and clinical aspects of neuroprotective approaches to acute (e.g., brain or spinal cord trauma, stroke), and chronic neurodegenerative (e.g., Alzheimer's and Parkinson's diseases, age-related macular degeneration) diseases. Potential and existing interventions, either as reviews or original papers, to prevent neuronal cell death in the CNS and in the periphery are welcome to this special issue. The concept of neuroprotection in therapeutic terms may be best described by Shouldon (Science, 1998; 282:1072) as "pharmacological interventions that produce enduring benefits by favorably influencing underlying etiology or pathogenesis and thereby forestalling onset of disease or clinical decline." Our life span has increased and it brought about a significant increase in the incidence of neurodegenerative diseases. While each neurodegenerative disease has its own characteristics and clinical manifestations, some common markers have been recognized. Among others, increased levels of oxidative/nitrosative damage to DNA, RNA, mitochondria, membranes, and proteins, etc. have been detected in connection with situations of neuronal damage. The wide variety of approaches to rescue neurons includes free radical scavenging antioxidants, ion channel modulators, excitatory amino acid antagonists and neurotrophic factors. Stem-cell based approaches may also represent a new opportunity to treat neurodegenerative diseases. I wish to thank all the authors for their contribution to this special issue.

Dr. Katalin Prokai-Tatrai
Guest Editor

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Type of Paper: Review
Title: Anti-Oxidant Treatment Approaches as New Neuroprotective Option in Autoimmmune Demyelination
Authors: De-Hyung Lee and Ralf Linker
Affiliation: Department of Neurology, University of Erlangen, Germany; E-Mails: De-Hyung.Lee@uk-erlangen.de (D.H.L.); Ralf.Linker@uk-erlangen.de (R.L.)
Abstract: Axonal loss displays the final stage of tissue damage in multiple sclerosis (MS). Oxidative damage might be a main culprit responsible for the degenerative mechanisms which are harmful for neuronal cells. Recently, it became clear that mitochondrial damage and subsequent energy failure are among the major factors driving such tissue injury. Immune cell derived glutamate excitotoxicity may additionally contribute to tissue destruction. In experimental autoimmune encephalomyelitis (EAE), a model disease mimicking many aspects of MS, an AMPA/kainate antagonist showed protective effects and reduced tissue injury. Thus prevention or minimizing oxidative stress as well as excitotoxicity in the central nervous system came into the focus of interest as new concept for the protection of glial cells as well as axons and neurons in MS. Such options comprise anti-glutamatergic therapies and, most recently in the focus of interest, fumaric acid esters. In EAE, application of fumaric acid esters led to activation of the transcription factor nuclear factor (erythroid-derived 2) related factor (Nrf-2) and accumulation of NADP(H) quinoline reductase-1 as a target gene, which augments the antioxidative response and exerts neuroprotective effects. The efficacy of BG00012, an oral formulation of dimethylfumaric acid, was successfully tested in a in a multi-center, double blind, placebo controlled phase II study and showed beneficial effects on MRI parameters of tissue destruction. At present, the compound is tested in two ongoing multi-center, double blind, placebo controlled phase III trials. In summary, the ability of fumaric acid to activate Nrf-2 may offer a novel cytoprotective modality that augments the natural antioxidant response in MS tissue, a mechanism that is not targeted by other MS therapies so far.