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Special Issue "Neuroinflammation and Cell Death"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (30 May 2019).

Special Issue Editor

Dr. Antonella Scorziello
Website
Guest Editor
Division of Pharmacology, Department of Neuroscience, Federico II University of Naples, School of Medicine, Via Sergio Pansini 5, 80131 Naples, Italy
Interests: cerebral ischemia; in vivo and in vitro models; Parkinson's disease; calcium homeostasis; mitochondria; neruonal metabolism; astrocytes; microglia; mitophagy; apoptosis; neurodegeneration; neuroinflammation.. sodium calcium exchangers; transporters; calcium channels

Special Issue Information

Dear Colleagues,

It is well-established that neuroinflammation plays a key pathogenetic role in a broad range of neurological and neurodegenerative disorders including multiple sclerosis, stroke, neoplasia, Parkinson’s Disease, Alzheimer’s Disease, and traumatic brain injury. In addition, an important role of neuroinflammation in the pathophysiology of several neurodegenerative disorders is emerging and becoming an important topic for the prevention and development of disease-modifying treatments. However, whether the neuroinflammatory processes are a cause or a consequence of neuronal degeneration remains unanswered. Characteristic of neuroinflammation is the activation of brain glial cells, principally microglia and astrocytes that release various soluble factors that can, in turn, accelerate the rate of neurodegeneration, synaptic loss, and synaptic dysfunction. On the other hand, there is evidence that activated microglia might also have neuroprotective effects.

This Special Issue of IJMS provides a comprehensive synopsis of the state-of-the-art of neuroinflammation research from cellular to molecular mechanisms, with the aim of delving deeper into unresolved questions about the relationship between markers of neuroinflammation and clinical indices of neurodegeneration, the causal relationship between these two phenomena, and the identification of biomarkers capable of measuring neuroinflammation in vivo, as well as of tracking its course over time, for prognosis and monitoring of effects of disease-modifying therapies.

You are warmly invited to submit original research and review articles related to any of these aspects.

Dr. Antonella Scorziello
Guest Editor

Manuscript Submission Information

Manuscripts should 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. Manuscripts can be submitted until the deadline. 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 the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neuroinflammation
  • neurodegenerative disorders
  • neuronal death
  • cellular homeostasis
  • apoptosis
  • mitophagy
  • calcium homeostasis
  • oxidative stress
  • cytokines
  • necrosis
  • microglial cells
  • astrocytes
  • magnetic resonance imaging
  • biomarker
  • Parkinson’s disease
  • Alzheimer’s disease
  • stroke
  • multiple sclerosis
  • traumatic brain injury
  • mitochondria
  • metabolic dysfunction
  • inflammasome
  • diagnostic and therapeutical approaches

Published Papers (4 papers)

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Research

Open AccessArticle
Electrical Stimulation of the Mesencephalic Locomotor Region Has No Impact on Blood–Brain Barrier Alterations after Cerebral Photothrombosis in Rats
Int. J. Mol. Sci. 2019, 20(16), 4036; https://doi.org/10.3390/ijms20164036 - 19 Aug 2019
Abstract
Blood–brain barrier (BBB) disruption is a critical event after ischemic stroke, which results in edema formation and hemorrhagic transformation of infarcted tissue. BBB dysfunction following stroke is partly mediated by proinflammatory agents. We recently have shown that high frequency stimulation of the mesencephalic [...] Read more.
Blood–brain barrier (BBB) disruption is a critical event after ischemic stroke, which results in edema formation and hemorrhagic transformation of infarcted tissue. BBB dysfunction following stroke is partly mediated by proinflammatory agents. We recently have shown that high frequency stimulation of the mesencephalic locomotor region (MLR-HFS) exerts an antiapoptotic and anti-inflammatory effect in the border zone of cerebral photothrombotic stroke in rats. Whether MLR-HFS also has an impact on BBB dysfunction in the early stage of stroke is unknown. In this study, rats were subjected to photothrombotic stroke of the sensorimotor cortex and implantation of a stimulating microelectrode into the ipsilesional MLR. Thereafter, either HFS or sham stimulation of the MLR was applied for 24 h. After scarifying the rats, BBB disruption was assessed by determining albumin extravasation and tight junction integrity (claudin 3, claudin 5, and occludin) using Western blot analyses and immunohistochemistry. In addition, by applying zymography, expression of pro-metalloproteinase-9 (pro-MMP-9) was analyzed. No differences were found regarding infarct size and BBB dysfunction between stimulated and unstimulated animals 24 h after induction of stroke. Our results indicate that MLR-HFS neither improves nor worsens the damaged BBB after stroke. Attenuating cytokines/chemokines in the perilesional area, as mediated by MLR-HFS, tend to play a less significant role in preventing the BBB integrity. Full article
(This article belongs to the Special Issue Neuroinflammation and Cell Death)
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Open AccessArticle
Electrical Stimulation of the Mesencephalic Locomotor Region Attenuates Neuronal Loss and Cytokine Expression in the Perifocal Region of Photothrombotic Stroke in Rats
Int. J. Mol. Sci. 2019, 20(9), 2341; https://doi.org/10.3390/ijms20092341 - 11 May 2019
Cited by 2
Abstract
Deep brain stimulation of the mesencephalic locomotor region (MLR) improves the motor symptoms in Parkinson’s disease and experimental stroke by intervening in the motor cerebral network. Whether high-frequency stimulation (HFS) of the MLR is involved in non-motor processes, such as neuroprotection and inflammation [...] Read more.
Deep brain stimulation of the mesencephalic locomotor region (MLR) improves the motor symptoms in Parkinson’s disease and experimental stroke by intervening in the motor cerebral network. Whether high-frequency stimulation (HFS) of the MLR is involved in non-motor processes, such as neuroprotection and inflammation in the area surrounding the photothrombotic lesion, has not been elucidated. This study evaluates whether MLR-HFS exerts an anti-apoptotic and anti-inflammatory effect on the border zone of cerebral photothrombotic stroke. Rats underwent photothrombotic stroke of the right sensorimotor cortex and the implantation of a microelectrode into the ipsilesional MLR. After intervention, either HFS or sham stimulation of the MLR was applied for 24 h. The infarct volumes were calculated from consecutive brain sections. Neuronal apoptosis was analyzed by TUNEL staining. Flow cytometry and immunohistochemistry determined the perilesional inflammatory response. Neuronal apoptosis was significantly reduced in the ischemic penumbra after MLR-HFS, whereas the infarct volumes did not differ between the groups. MLR-HFS significantly reduced the release of cytokines and chemokines within the ischemic penumbra. MLR-HFS is neuroprotective and it reduces pro-inflammatory mediators in the area that surrounds the photothrombotic stroke without changing the number of immune cells, which indicates that MLR-HFS enables the function of inflammatory cells to be altered on a molecular level. Full article
(This article belongs to the Special Issue Neuroinflammation and Cell Death)
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Open AccessArticle
Protective Effect of N-Arachidonoyl Glycine-GPR18 Signaling after Excitotoxical Lesion in Murine Organotypic Hippocampal Slice Cultures
Int. J. Mol. Sci. 2019, 20(6), 1266; https://doi.org/10.3390/ijms20061266 - 13 Mar 2019
Cited by 2
Abstract
N-arachidonoyl glycine (NAGly) is an endocannabinoid involved in the regulation of different immune cells. It was shown to activate the GPR18 receptor, which was postulated to switch macrophages from cytotoxic to reparative. To study GPR18 expression and neuroprotection after NAGly treatment we used [...] Read more.
N-arachidonoyl glycine (NAGly) is an endocannabinoid involved in the regulation of different immune cells. It was shown to activate the GPR18 receptor, which was postulated to switch macrophages from cytotoxic to reparative. To study GPR18 expression and neuroprotection after NAGly treatment we used excitotoxically lesioned organotypic hippocampal slice cultures (OHSC). The effect of NAGly was also tested in isolated microglia and astrocytes as these cells play a crucial role during neuronal injury. In the present study, the GPR18 receptor was found in OHSC at mRNA level and was downregulated after N-Methyl-D-aspartate (NMDA) treatment at a single time point. Furthermore, treatment with NAGly reduced neuronal damage and this effect was abolished by GPR18 and cannabinoid receptor (CB)2 receptor antagonists. The activation but not motility of primary microglia and astrocytes was influenced when incubated with NAGly. However, NAGly alone reduced the phosphorylation of Akt but no changes in activation of the p44/42 and p38 MAPK and CREB pathways in BV2 cells could be observed. Given NAGly mediated actions we speculate that GPR18 and its ligand NAGly are modulators of glial and neuronal cells during neuronal damage. Full article
(This article belongs to the Special Issue Neuroinflammation and Cell Death)
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Open AccessArticle
Anti-Inflammatory Activity of A Polyphenolic Extract from Arabidopsis thaliana in In Vitro and In Vivo Models of Alzheimer’s Disease
Int. J. Mol. Sci. 2019, 20(3), 708; https://doi.org/10.3390/ijms20030708 - 07 Feb 2019
Cited by 8
Abstract
Alzheimer’s disease (AD) is the most common neurodegenerative disorder and the primary form of dementia in the elderly. One of the main features of AD is the increase in amyloid-beta (Aβ) peptide production and aggregation, leading to oxidative stress, neuroinflammation and neurodegeneration. Polyphenols [...] Read more.
Alzheimer’s disease (AD) is the most common neurodegenerative disorder and the primary form of dementia in the elderly. One of the main features of AD is the increase in amyloid-beta (Aβ) peptide production and aggregation, leading to oxidative stress, neuroinflammation and neurodegeneration. Polyphenols are well known for their antioxidant, anti-inflammatory and neuroprotective effects and have been proposed as possible therapeutic agents against AD. Here, we investigated the effects of a polyphenolic extract of Arabidopsis thaliana (a plant belonging to the Brassicaceae family) on inflammatory response induced by Aβ. BV2 murine microglia cells treated with both Aβ25–35 peptide and extract showed a lower pro-inflammatory (IL-6, IL-1β, TNF-α) and a higher anti-inflammatory (IL-4, IL-10, IL-13) cytokine production compared to cells treated with Aβ only. The activation of the Nrf2-antioxidant response element signaling pathway in treated cells resulted in the upregulation of heme oxygenase-1 mRNA and in an increase of NAD(P)H:quinone oxidoreductase 1 activity. To establish whether the extract is also effective against Aβ-induced neurotoxicity in vivo, we evaluated its effect on the impaired climbing ability of AD Drosophila flies expressing human Aβ1–42. Arabidopsis extract significantly restored the locomotor activity of these flies, thus confirming its neuroprotective effects also in vivo. These results point to a protective effect of the Arabidopsis extract in AD, and prompt its use as a model in studying the impact of complex mixtures derived from plant-based food on neurodegenerative diseases. Full article
(This article belongs to the Special Issue Neuroinflammation and Cell Death)
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