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Neuroinflammation and Cell Death: What Is New?
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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: closed (31 December 2021) | Viewed by 12845

Special Issue Editors

Dr. Antonella Scorziello

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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, Collections and Topics in MDPI journals
Dr. Maria José Sisalli

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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 submissions that pass pre-check are 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

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Published Papers (3 papers)

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Research

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20 pages, 6045 KiB  
Article
Impact of Two Neuronal Sigma-1 Receptor Modulators, PRE084 and DMT, on Neurogenesis and Neuroinflammation in an Aβ1–42-Injected, Wild-Type Mouse Model of AD
by Emőke Borbély, Viktória Varga, Titanilla Szögi, Ildikó Schuster, Zsolt Bozsó, Botond Penke and Lívia Fülöp
Int. J. Mol. Sci. 2022, 23(5), 2514; https://doi.org/10.3390/ijms23052514 - 24 Feb 2022
Cited by 12 | Viewed by 3792
Abstract
Alzheimer’s disease (AD) is the most common form of dementia characterized by cognitive dysfunctions. Pharmacological interventions to slow the progression of AD are intensively studied. A potential direction targets neuronal sigma-1 receptors (S1Rs). S1R ligands are recognized as promising therapeutic agents that may [...] Read more.
Alzheimer’s disease (AD) is the most common form of dementia characterized by cognitive dysfunctions. Pharmacological interventions to slow the progression of AD are intensively studied. A potential direction targets neuronal sigma-1 receptors (S1Rs). S1R ligands are recognized as promising therapeutic agents that may alleviate symptom severity of AD, possibly via preventing amyloid-β-(Aβ-) induced neurotoxicity on the endoplasmic reticulum stress-associated pathways. Furthermore, S1Rs may also modulate adult neurogenesis, and the impairment of this process is reported to be associated with AD. We aimed to investigate the effects of two S1R agonists, dimethyltryptamine (DMT) and PRE084, in an Aβ-induced in vivo mouse model characterizing neurogenic and anti-neuroinflammatory symptoms of AD, and the modulatory effects of S1R agonists were analyzed by immunohistochemical methods and western blotting. DMT, binding moderately to S1R but with high affinity to 5-HT receptors, negatively influenced neurogenesis, possibly as a result of activating both receptors differently. In contrast, the highly selective S1R agonist PRE084 stimulated hippocampal cell proliferation and differentiation. Regarding neuroinflammation, DMT and PRE084 significantly reduced Aβ1–42-induced astrogliosis, but neither had remarkable effects on microglial activation. In summary, the highly selective S1R agonist PRE084 may be a promising therapeutic agent for AD. Further studies are required to clarify the multifaceted neurogenic and anti-neuroinflammatory roles of these agonists. Full article
(This article belongs to the Special Issue Neuroinflammation and Cell Death: What Is New?)
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12 pages, 2072 KiB  
Article
MitoQ Is Able to Modulate Apoptosis and Inflammation
by Elisa Piscianz, Alessandra Tesser, Erika Rimondi, Elisabetta Melloni, Claudio Celeghini and Annalisa Marcuzzi
Int. J. Mol. Sci. 2021, 22(9), 4753; https://doi.org/10.3390/ijms22094753 - 30 Apr 2021
Cited by 11 | Viewed by 2991
Abstract
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?)
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Review

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19 pages, 2848 KiB  
Review
Possible Link between SARS-CoV-2 Infection and Parkinson’s Disease: The Role of Toll-Like Receptor 4
by Carmela Conte
Int. J. Mol. Sci. 2021, 22(13), 7135; https://doi.org/10.3390/ijms22137135 - 1 Jul 2021
Cited by 27 | Viewed by 5129
Abstract
Parkinson’s disease (PD) is the most common neurodegenerative motor disorder characterized by selective degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) of the midbrain, depletion of dopamine (DA), and impaired nigrostriatal pathway. The pathological hallmark of PD includes [...] Read more.
Parkinson’s disease (PD) is the most common neurodegenerative motor disorder characterized by selective degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) of the midbrain, depletion of dopamine (DA), and impaired nigrostriatal pathway. The pathological hallmark of PD includes the aggregation and accumulation α-synuclein (α-SYN). Although the precise mechanisms underlying the pathogenesis of PD are still unknown, the activation of toll-like receptors (TLRs), mainly TLR4 and subsequent neuroinflammatory immune response, seem to play a significant role. Mounting evidence suggests that viral infection can concur with the precipitation of PD or parkinsonism. The recently identified coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of ongoing pandemic coronavirus disease 2019 (COVID-19), responsible for 160 million cases that led to the death of more than three million individuals worldwide. Studies have reported that many patients with COVID-19 display several neurological manifestations, including acute cerebrovascular diseases, conscious disturbance, and typical motor and non-motor symptoms accompanying PD. In this review, the neurotropic potential of SARS-CoV-2 and its possible involvement in the pathogenesis of PD are discussed. Specifically, the involvement of the TLR4 signaling pathway in mediating the virus entry, as well as the massive immune and inflammatory response in COVID-19 patients is explored. The binding of SARS-CoV-2 spike (S) protein to TLR4 and the possible interaction between SARS-CoV-2 and α-SYN as contributing factors to neuronal death are also considered. Full article
(This article belongs to the Special Issue Neuroinflammation and Cell Death: What Is New?)
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