Journal Browser

Journal Browser

Special Issue "Neuroinflammation and Cell Death: What Is New?"

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

Deadline for manuscript submissions: 31 July 2021.

Special Issue Editors

Dr. Antonella Scorziello
E-Mail 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 Issues and Collections in MDPI journals
Dr. Maria José Sisalli
Guest Editor
Università degli Studi di Napoli Federico IIdisabled, Naples, Italy

Special Issue Information

Dear Colleagues,

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. Neuroinflammation is indeed emerging as an important clue in the pathophysiology of several neurodegenerative disorders for the development of disease-modifying treatments and therefore, potentially able to countreact this process. However, whether the neuroinflammatory processes are a cause or a consequence of neuronal degeneration still remains an unanswered question. The activation of brain glial cells, principally microglia and astrocytes represents a critical feature of neuroinflammation mainly related to the release various soluble factors that can accelerate the rate of neurodegeneration, the synaptic loss, and the synaptic dysfunction associated to neurological disorderd. On the other hand, there is evidence that activated microglia might also have neuroprotective effects in these pathological conditions.

This Special Issue of IJMS aims to provide a comprehensive synopsis of the state-of-the-art of neuroinflammation research from cellular to molecular mechanisms in order to delve deeper into the unresolved questions with a special focus on 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
Dr. Maria José Sisalli
Guest Editors

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.


  • 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 (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:


Open AccessArticle
MitoQ Is Able to Modulate Apoptosis and Inflammation
Int. J. Mol. Sci. 2021, 22(9), 4753; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094753 - 30 Apr 2021
Viewed by 200
Mitoquinone (MitoQ) is a mitochondrial reactive oxygen species scavenger that is characterized by high bioavailability. Prior studies have demonstrated its neuroprotective potential. Indeed, the release of reactive oxygen species due to damage to mitochondrial components plays a pivotal role in the pathogenesis of [...] Read more.
Mitoquinone (MitoQ) is a mitochondrial reactive oxygen species scavenger that is characterized by high bioavailability. Prior studies have demonstrated its neuroprotective potential. Indeed, the release of reactive oxygen species due to damage to mitochondrial components plays a pivotal role in the pathogenesis of several neurodegenerative diseases. The present study aimed to examine the impact of the inflammation platform activation on the neuronal cell line (DAOY) treated with specific inflammatory stimuli and whether MitoQ addition can modulate these deregulations. DAOY cells were pre-treated with MitoQ and then stimulated by a blockade of the cholesterol pathway, also called mevalonate pathway, using a statin, mimicking cholesterol deregulation, a common parameter present in some neurodegenerative and autoinflammatory diseases. To verify the role played by MitoQ, we examined the expression of genes involved in the inflammation mechanism and the mitochondrial activity at different time points. In this experimental design, MitoQ showed a protective effect against the blockade of the mevalonate pathway in a short period (12 h) but did not persist for a long time (24 and 48 h). The results obtained highlight the anti-inflammatory properties of MitoQ and open the question about its application as an effective adjuvant for the treatment of the autoinflammatory disease characterized by a cholesterol deregulation pathway that involves mitochondrial homeostasis. Full article
(This article belongs to the Special Issue Neuroinflammation and Cell Death: What Is New?)
Show Figures

Graphical abstract

Back to TopTop