Topical Collection "Molecular Research in Neurotoxicology"

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A topical collection in International Journal of Molecular Sciences (ISSN 1422-0067). This collection belongs to the section "Molecular Toxicology".

Editor

Collection Editor
Dr. G. Jean Harry
Neurotoxicology Group, NIEHS and National Toxicology Program, National Institute of Environmental Health Sciences, P.O. Box 12233, Research Triangle Park, NC 27709, USA
Website: http://www.niehs.nih.gov/research/atniehs/labs/ntp/nt/index.cfm
Phone: 919-967-7449
Fax: +1 919 541 4611
Interests: neurotoxicants; aging; development; inflammation; oxidative stress; signal transduction; hormones; neuropathology; pharmaceuticals; alternative models

Topical Collection Information

Dear Colleagues,

Alterations in nervous system functioning as a result of environmental factors, pharmaceuticals, genetic variability, and health status remain an issue of concern for human health. Recent advancements have been made in our understanding of common biological processes related to neurotoxicity associated with disease states and age-related or genetic vulnerabilities. These advances have been possible due to the ability to examine molecular aspects underlying neurodevelopment, neurodegeneration, and associated processes of neurotoxicity. The integration of this molecular data into the field of neurotoxicology, as it applies to the broad spectrum of environmental exposure now offers a mechanistic framework for understanding the dynamics of neurotoxicity. Further work on epigenetic mechanisms associated with nervous system functioning, e.g., learning and memory, provide additional mechanisms by which regulation of the nervous system can be altered by environmental exposure or by which events occurring during early life stages can influence responses later in life. This topical collection will focus on the integration of established biological processes and molecular events as they relate to the regulation of cellular and functional changes within the nervous system and how this may contribute to neurotoxicity. The collection will include aspects of neurological and neurodegenerative disease, neurodevelopmental disorders, and specific neurotoxicity from environmental or pharmaceutical agents. We are seeking novel research and/or review articles highlighting 1) the variety of molecular signals and integrated networks that underlie adverse responses in the nervous system, 2) how these alterations in molecular signaling translate to alterations in the structure or function of the nervous system (biochemical, physiology, behavior), 3) molecular events occurring during early life that can shift susceptibility in the adult, 4) epigenetic regulatory events as they contribute to neurotoxicity and 5) contributions to life stage events influencing human health.

Dr. G. Jean Harry
Collection Editor

Manuscript Submission Information

Manuscripts for the topical collection can be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on this website. The topical collection considers regular research articles, short communications and review articles. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF (Swiss Francs).


Keywords

  • oxidative stress
  • organophosphorus pesticides
  • neuropathy target esterase (nte)
  • animal models
  • transcription factor signaling
  • cell death
  • receptor mediated events
  • neural cell differentiation
  • glia
  • kynurenines
  • quinolinic acid
  • inflammation
  • cytokines
  • heat shock protein 70
  • neurobehavior
  • neuroprotection
  • seizures
  • neurotrophic factors
  • ischemia/hypoxia
  • microglia
  • cyanobacteria
  • heavy metals
  • pharmacological models
  • neurodegeneration
  • ischemia
  • perinatal brain injury
  • neurotoxicants
  • neurodegenerative diseases
  • zinc

Published Papers (22 papers)

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2015  ( 6 papers )


2014  ( 3 papers )


2013  ( 13 papers )


2015
by , , ,  and
Int. J. Mol. Sci. 2015, 16(8), 17422-17444; doi:10.3390/ijms160817422 (registering DOI)
Received: 7 May 2015 / Revised: 19 June 2015 / Accepted: 29 June 2015 / Published: 30 July 2015
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by , , , ,  and
Int. J. Mol. Sci. 2015, 16(5), 10426-10442; doi:10.3390/ijms160510426
Received: 25 January 2015 / Revised: 23 April 2015 / Accepted: 4 May 2015 / Published: 7 May 2015
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by , , , , , , , ,  and
Int. J. Mol. Sci. 2015, 16(4), 8635-8654; doi:10.3390/ijms16048635
Received: 26 January 2015 / Revised: 31 March 2015 / Accepted: 10 April 2015 / Published: 17 April 2015
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by  and
Int. J. Mol. Sci. 2015, 16(3), 5400-5419; doi:10.3390/ijms16035400
Received: 11 December 2014 / Revised: 28 January 2015 / Accepted: 22 February 2015 / Published: 9 March 2015
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by , , ,  and
Int. J. Mol. Sci. 2015, 16(3), 4800-4813; doi:10.3390/ijms16034800
Received: 23 December 2014 / Revised: 16 February 2015 / Accepted: 17 February 2015 / Published: 3 March 2015
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by , , ,  and
Int. J. Mol. Sci. 2015, 16(1), 1221-1231; doi:10.3390/ijms16011221
Received: 22 September 2014 / Accepted: 24 December 2014 / Published: 6 January 2015
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2014
by , , ,  and
Int. J. Mol. Sci. 2014, 15(12), 23672-23704; doi:10.3390/ijms151223672
Received: 4 November 2014 / Revised: 3 December 2014 / Accepted: 6 December 2014 / Published: 18 December 2014
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by , , , , ,  and
Int. J. Mol. Sci. 2014, 15(11), 20607-20637; doi:10.3390/ijms151120607
Received: 16 September 2014 / Revised: 23 October 2014 / Accepted: 30 October 2014 / Published: 10 November 2014
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by , , , , , , ,  and
Int. J. Mol. Sci. 2014, 15(1), 905-926; doi:10.3390/ijms15010905
Received: 14 October 2013 / Revised: 8 December 2013 / Accepted: 17 December 2013 / Published: 9 January 2014
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2013
by , , ,  and
Int. J. Mol. Sci. 2013, 14(12), 24438-24475; doi:10.3390/ijms141224438
Received: 14 October 2013 / Revised: 27 November 2013 / Accepted: 6 December 2013 / Published: 16 December 2013
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by , ,  and
Int. J. Mol. Sci. 2013, 14(11), 23103-23128; doi:10.3390/ijms141123103
Received: 14 August 2013 / Revised: 8 October 2013 / Accepted: 16 October 2013 / Published: 21 November 2013
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by ,  and
Int. J. Mol. Sci. 2013, 14(11), 22163-22189; doi:10.3390/ijms141122163
Received: 30 September 2013 / Revised: 28 October 2013 / Accepted: 28 October 2013 / Published: 8 November 2013
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by  and
Int. J. Mol. Sci. 2013, 14(11), 22067-22081; doi:10.3390/ijms141122067
Received: 18 September 2013 / Revised: 18 October 2013 / Accepted: 22 October 2013 / Published: 7 November 2013
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by ,  and
Int. J. Mol. Sci. 2013, 14(11), 21328-21338; doi:10.3390/ijms141121328
Received: 2 September 2013 / Revised: 2 October 2013 / Accepted: 22 October 2013 / Published: 25 October 2013
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by  and
Int. J. Mol. Sci. 2013, 14(10), 21021-21044; doi:10.3390/ijms141021021
Received: 23 August 2013 / Revised: 30 September 2013 / Accepted: 1 October 2013 / Published: 18 October 2013
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by , , , , ,  and
Int. J. Mol. Sci. 2013, 14(10), 19831-19845; doi:10.3390/ijms141019831
Received: 26 August 2013 / Revised: 22 September 2013 / Accepted: 26 September 2013 / Published: 30 September 2013
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by , , ,  and
Int. J. Mol. Sci. 2013, 14(9), 19054-19066; doi:10.3390/ijms140919054
Received: 19 July 2013 / Revised: 8 August 2013 / Accepted: 14 August 2013 / Published: 16 September 2013
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by  and
Int. J. Mol. Sci. 2013, 14(9), 18284-18318; doi:10.3390/ijms140918284
Received: 3 July 2013 / Revised: 31 July 2013 / Accepted: 9 August 2013 / Published: 5 September 2013
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by , , ,  and
Int. J. Mol. Sci. 2013, 14(8), 16817-16835; doi:10.3390/ijms140816817
Received: 23 July 2013 / Revised: 6 August 2013 / Accepted: 8 August 2013 / Published: 15 August 2013
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by , , , , , ,  and
Int. J. Mol. Sci. 2013, 14(8), 15959-15976; doi:10.3390/ijms140815959
Received: 19 June 2013 / Revised: 25 July 2013 / Accepted: 25 July 2013 / Published: 31 July 2013
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by ,  and
Int. J. Mol. Sci. 2013, 14(8), 15286-15311; doi:10.3390/ijms140815286
Received: 11 April 2013 / Revised: 5 July 2013 / Accepted: 8 July 2013 / Published: 24 July 2013
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by , , ,  and
Int. J. Mol. Sci. 2013, 14(7), 13858-13872; doi:10.3390/ijms140713858
Received: 24 May 2013 / Revised: 14 June 2013 / Accepted: 27 June 2013 / Published: 4 July 2013
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Type of Paper: Review
Title:
The role of astrocytes and microglia in neuroprotection against toxics alkaloids from Prosopis juliflora
Authors:
Victor Diogenes Amaral da Silva, André Mario Mendes da Silva, Silvia Lima Costa
Affiliation:
Laboratório de Neuroquímica e Biologia Celular, Instituto de Ciências da Saúde, Universidade Federal da Bahia, Salvador, Brazil
Abstract:
Glial cells, mainly astrocytes and microglia, are essential for maintaining cerebral functions and present import roles in xenobiotics response, metabolism and detoxification, consisting the first line of defence against changes on central nervous system micro environment. After damage they undergo morphological and or functional alterations which can both facilitate neuronal survival or induces a neurodegenerative state. Prosopis juliflora Sw. DC (mesquite) is a shrub that produces pods rich in carbohydrates and proteins largely used for animal and human nutrition. However, large ingestion has been shown to induce intoxication in animals, characterized by gliosis associated to neurodegeneration and neuromuscular alterations, involving mechanisms that are not yet well understood. We and others demonstrated that extracts and purified compounds of mesquite pods and leaves possess several pharmacological properties, attributed especially to piperidine alkaloids. This review will present the main advances about the mechanisms involved in the toxic effects of active components presents in pods and leaves of P. juliflora related to gliosis and the role of neurons/glial cells interactions in neurotoxicity induced by its piperidine alkaloids.
Keywords:
astrocytes; microglia; piperidine alkaloids; Prosopis juliflora

Type of Paper: Review
Title:
2-Methoxyestradiol, Derivative of 17β-Estradiol, a Missing Link in Neurodegeneration and Cancer?
Authors:
Gorska Magdalena *, Kuban-Jankowska A, Wozniak Michal
Affiliation:
Department of Medical Chesmistry, Medical University of Gdansk, Debinki 1, Gdansk, Poland
Abstract:
2-methoxyestradiol, metabolite of 17β-estradiol, is considered as a potential anticancer agent, currently investigated in several clinical trials. This natural compound was found to be effective towards great number of cancers including colon, breast, lung, osteosarcoma. Interestingly, a recent study suggested that the molecular pathways of neurodegeneration and cancer may overlap. Several neurodegeneration-causing factors like PARK2 parkin, and PARK5 have been recently been evidenced to be involved in cancer development by playing an important role as regulators of cell cycle. Reactive oxygen and reactive nitrogen species play an important role in mediating cell signaling pathways, but their increased concentration leads to nitro-oxidative stress resulting in cell cycle arrest or cell death. Interestingly, increased levels of nitrated proteins and 3-nitrotyrosine have been associated with a variety of neurodegenerative diseases like Parkinson’s disease. Previously, we have suggested that 2-ME is a naturally occurring hormone with potential anti-cancer properties (Gorska et al., 2015). On the other side, we have also determined the potential neurotoxicity and genotoxicity of 2-methoxyestradiol at physiological and pharmacological relevant concentrations (Gorska et al., 2014; 2015a,b-under review Molecular Neurobiology, Molecules). We demonstrated that 2-methoxyestradiol, at pharmacological but also physiological relevant concentrations, increases neuronal nitric oxide synthase, reactive nitrogen species and 3-nitrotyrosine both in cancer and neuronal cells, resulting in cell death. Thus, we are postulating that naturally occurring 2-methoxyestradiol may be considered as a physiological modulator of cancer cells and neuronal cells survival. Moreover, though the mechanisms of 2-ME action is still undefined, the drug is currently under clinical trials as a chemotherapeutic agent. Due to plausible neurotoxic effects towards neuronal cells (especially hippocampal), we hypothesize plausible side effects of chemotherapy with 2-methoxyestradiol like emotional and/or cognitive disorders.

Last update: 2 July 2015

Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert