Special Issue "Neuroprotection against Ischemic Brain Injury"

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A special issue of Brain Sciences (ISSN 2076-3425).

Deadline for manuscript submissions: closed (28 February 2015)

Special Issue Editor

Guest Editor
Dr. Bruno Meloni
Australian Neuromuscular Research Institute (ANRI), The University of Western Australia (M518), 35 Stirling Highway, CRAWLEY WA 6009, Australia
Website: https://www.socrates.uwa.edu.au/Staff/StaffProfile.aspx?Person=BrunoMeloni
E-Mail: bruno.meloni@anri.uwa.edu.au
Phone: +61 9346 3535
Fax: +61 9346 3487
Interests: neuroprotection; stroke and rat stroke models; hypothermia; sodium calcium exchanger; neuroprotective proteins/peptides; adenoviral vectors and magneisum

Special Issue Information

Dear Colleagues,

Ischemic brain injury is a principal pathology in survivors of ischemic stroke and cardiac arrest, two of the most significant diseases of the developed world. At present, acute treatment options to minimise ischemic brain injury are limited. For ischemic stroke, tPA thrombolysis to restore cerebral blood flow is considered the best available treatment. However, due to tPA’s narrow therapeutic window (3–4.5 h), its use is restricted.

Presently, only moderate hypothermia (33 °C; 12–24 h) has neuroprotective efficacy based on improvements in neurological outcomes following cardiac arrest. Current ongoing phase 3 trials will soon determine if mild-moderate hypothermia (33–35 °C; 24 h) will improve outcome in stroke. Despite these promising interventions there is still an urgent need to develop neuroprotective agents that can be given to a wider patient population and/or can boost the effectiveness of currently available treatments.

The purpose of this special issue is to compile a number of selected articles that provide an overview of pre-clinical and clinical neuroprotective interventions that are currently being investigated or used.

Dr. Bruno Meloni
Guest Editor

Keywords

  • stroke
  • cardiac arrest
  • cerebral ischemia
  • neuroprotection
  • tPA
  • thrombolysis
  • hypothermia
  • blood brain barrier
  • neurovascular unit
  • neuroprotective proteins/peptides
  • combination therapy

Published Papers (20 papers)

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Displaying article 1-20
p. 130-143
by , ,  and
Brain Sci. 2015, 5(2), 130-143; doi:10.3390/brainsci5020130
Received: 11 March 2015 / Revised: 1 April 2015 / Accepted: 13 April 2015 / Published: 21 April 2015
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 1415-1416
by
Brain Sci. 2013, 3(3), 1415-1416; doi:10.3390/brainsci3031415
Received: 20 August 2013 / Accepted: 20 August 2013 / Published: 24 September 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 1395-1414
by  and
Brain Sci. 2013, 3(3), 1395-1414; doi:10.3390/brainsci3031395
Received: 16 July 2013 / Revised: 10 August 2013 / Accepted: 14 August 2013 / Published: 23 September 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 1325-1356
by
Brain Sci. 2013, 3(3), 1325-1356; doi:10.3390/brainsci3031325
Received: 23 June 2013 / Revised: 30 July 2013 / Accepted: 14 August 2013 / Published: 5 September 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
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p. 1095-1108
by  and
Brain Sci. 2013, 3(3), 1095-1108; doi:10.3390/brainsci3031095
Received: 5 May 2013 / Revised: 18 June 2013 / Accepted: 27 June 2013 / Published: 22 July 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 1043-1059
by , ,  and
Brain Sci. 2013, 3(3), 1043-1059; doi:10.3390/brainsci3031043
Received: 16 April 2013 / Revised: 14 May 2013 / Accepted: 26 June 2013 / Published: 10 July 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 1013-1022
by , ,  and
Brain Sci. 2013, 3(3), 1013-1022; doi:10.3390/brainsci3031013
Received: 17 May 2013 / Revised: 2 June 2013 / Accepted: 7 June 2013 / Published: 25 June 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 877-907
by ,  and
Brain Sci. 2013, 3(2), 877-907; doi:10.3390/brainsci3020877
Received: 15 February 2013 / Revised: 14 May 2013 / Accepted: 17 May 2013 / Published: 3 June 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 599-614
by ,  and
Brain Sci. 2013, 3(2), 599-614; doi:10.3390/brainsci3020599
Received: 31 January 2013 / Revised: 12 April 2013 / Accepted: 12 April 2013 / Published: 23 April 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 561-598
by  and
Brain Sci. 2013, 3(2), 561-598; doi:10.3390/brainsci3020561
Received: 31 January 2013 / Revised: 14 March 2013 / Accepted: 20 March 2013 / Published: 22 April 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 540-560
by , ,  and
Brain Sci. 2013, 3(2), 540-560; doi:10.3390/brainsci3020540
Received: 8 March 2013 / Revised: 8 April 2013 / Accepted: 9 April 2013 / Published: 19 April 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 521-539
by , , , , , , , ,  and
Brain Sci. 2013, 3(2), 521-539; doi:10.3390/brainsci3020521
Received: 14 February 2013 / Revised: 26 March 2013 / Accepted: 28 March 2013 / Published: 12 April 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 460-503
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Brain Sci. 2013, 3(2), 460-503; doi:10.3390/brainsci3020460
Received: 15 January 2013 / Revised: 23 March 2013 / Accepted: 26 March 2013 / Published: 8 April 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 360-395
by , , , , , ,  and
Brain Sci. 2013, 3(1), 360-395; doi:10.3390/brainsci3010360
Received: 28 December 2012 / Revised: 19 February 2013 / Accepted: 6 March 2013 / Published: 20 March 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 344-359
by ,  and
Brain Sci. 2013, 3(1), 344-359; doi:10.3390/brainsci3010344
Received: 10 December 2012 / Revised: 19 February 2013 / Accepted: 7 March 2013 / Published: 19 March 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 239-261
by , , , ,  and
Brain Sci. 2013, 3(1), 239-261; doi:10.3390/brainsci3010239
Received: 7 December 2012 / Revised: 22 February 2013 / Accepted: 26 February 2013 / Published: 7 March 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 215-238
by , , , , , , , ,  and
Brain Sci. 2013, 3(1), 215-238; doi:10.3390/brainsci3010215
Received: 6 January 2013 / Revised: 21 February 2013 / Accepted: 22 February 2013 / Published: 7 March 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 177-190
by , ,  and
Brain Sci. 2013, 3(1), 177-190; doi:10.3390/brainsci3010177
Received: 22 December 2012 / Revised: 16 February 2013 / Accepted: 21 February 2013 / Published: 5 March 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 191-214
by , ,  and
Brain Sci. 2013, 3(1), 191-214; doi:10.3390/brainsci3010191
Received: 7 January 2013 / Revised: 13 February 2013 / Accepted: 22 February 2013 / Published: 5 March 2013
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(This article belongs to the Special Issue Neuroprotection against Ischemic Brain Injury)
p. 123-142
by  and
Brain Sci. 2013, 3(1), 123-142; doi:10.3390/brainsci3010123
Received: 5 January 2013 / Revised: 23 January 2013 / Accepted: 23 January 2013 / Published: 30 January 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: Article
Title: Potential of the Neuropeptide PACAP38 Therapy for Brain Ischemia: Insights from Bioinformatics Analysis of the High-throughput DNA Microarray Analyses Data in PMCAO Mouse Model
Authors: Motohide Hori 1,2, Tomoya Nakamachi 2,3, Junko Shibato 2,4, Randeep Rakwal 2,5,*, Seiji Shioda 2,* and Satoshi Numazawa 1
Affiliations:
1. Division of Toxicology, Department of Pharmacology, Toxicology and Therapeutics, School of Pharmacy, Showa University 1-5-8 Hatanodai, Shinagawa, Tokyo 142-8555, Japan
2. Department of Anatomy, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa, Tokyo 142-8555, Japan;
E-Mails: plantproteomics@gmail.com (R.R.); shioda@med.showa-u.ac.jp (S.S.)
3. Laboratory of Regulatory Biology, Graduate School of Science and Engineering, University of Toyama, Toyama, Toyama 930-8555, Japan
4. Laboratory of Exercise Biochemistry and Neuroendocrinology, Institute of Health and Sports Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8574, Japan
5. Organization for Educational Initiatives, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba 305-8577, Ibaraki, Japan
Abstract:
Permanent middle cerebral artery occlusion (PMCAO) mouse model has been established and used by our group with a focus on systematically investigating effects of the neuropeptide pituitary adenylate-cyclase activating polypeptide (PACAP38) on the ischemic brain. Using an intracerebroventrically PACAP38 (1 pmol) injection over a control saline (0.9% sodium chloride, NaCl) treatment, we have been successful in generating a vast inventory of gene expression data in both whole hemispheres and specific brain regions of infract/ischemic core and penumbra with high-throughput Agilent whole genome 4 × 44 K oligo DNA microarray chips. These differential gene expressions generated from these various analyses have revealed the importance of both whole hemisphere and region-specific analyses in genome-wide identification of target molecular factors that might play a role in the neuroprotective function of PACAP38, providing a great resource for further study by the scientific community. In this study, we specifically utilize the Ingenuity Pathway Analysis (IPA; Ingenuity® Systems, www.ingenuity.com) bioinformatics tool to generate biological function and network analysis from our studies, and present new insight into the potential mechanism behind PACAP38 neuroprotective function in the ischemic brain.
Keywords:
brain ischemia; hemispheres; infract core and penumbra; genomics; proteomics; PACAP38

Type of Paper: Article
Title: Sex Differences in Behavioral Outcomes Following Mild Temperature Modulation during Induced Neonatal Hypoxic Ischemic Injury in Rats
Author: Amanda Smith
Affiliation: Department of Psychology, Behavioral Neuroscience Division, University of Connecticut,
Storrs, CT 06269, USA, Email: amanda.smith205@gmail.com
Abstract:A common injury resulting from premature birth is hypoxia ischemia (HI; reduced oxygen and/or blood flow to the brain). This injury can cause various degrees of tissue damage, as well as subsequent cognitive/behavioral deficits such as motor, learning/memory, and auditory impairments. Data suggests that there is a sex difference in HI outcome, with males more adversely affected by HI as compared to similarly injured females. Body temperatures may play a role in the severity of an HI insult, with lower temperatures during an insult yielding more favorable anatomical and behavioral outcomes.
The current study utilized a postnatal day (P) 7 rodent model of HI injury to assess the effect of temperature on each sex. We hypothesized that female P7 rats would benefit more from lower body temperatures as compared to male P7 rats, or that rats kept at slightly higher temperatures would show enhanced HI effects that might override intrinsic female protection and mask sex differences.
By using a rota-rod, auditory discrimination, and spatial/non-spatial tasks, our results revealed a significant benefit of temperature reduction in females. However, males also seemed to benefit from temperature reduction on an auditory and non-spatial task. Our data suggest that temperature reduction benefits both sexes from the deleterious effects of HI injury, but task and sex specific patterns are seen.

Title: Growth Factors for the Treatment of Ischemic Brain Injury
Author: Fernando Gonzalez, et al. Email: Fernando.Gonzalez@ucsf.edu
Abstract: In recent years growth factor therapy has emerged as apotential treatment for ischemic brain injury. The efficacy of therapies that either directly produce or stimulate local production of growth factors and growth factor receptors in damaged brain tissue has been tested in a multitude of models for different CNS diseases. These growth factors include erythropoietin (EPO), vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), and insulin-like growth factor (IGF-1), among others. Despite the promise of these experimental therapies in animal models, the particular growth factors that should be used to maximize both brain protection and repair, and the therapeutic time window, are not well-defined. We will review current pre-clinical and clinical evidence for growth factor therapies in treating different causes of brain injury, as well as issues thatneed to addressed prior to their use in humans.

Last update: 2 February 2015

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