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Biomedicines
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Neuroinflammation: From Molecular Mechanism to Therapeutic Perspectives
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Neuroinflammation: From Molecular Mechanism to Therapeutic Perspectives

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 8640

Special Issue Editor

Dr. Adriano Lama

E-Mail Website
Guest Editor
Department of Pharmacy, University of Naples Federico II, Naples, Italy
Interests: mood disorders; obesity; neuroendocrinology; neuroinflammation; gut-brain axis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuroinflammation is traditionally defined as the complex innate immune response to brain injuries. As an essential component of the innate immune system of the central nervous system (CNS), neuroinflammation initially plays a critical role in neural tissue repair and restoration. The process of neuroinflammation involves multiple types of cells and factors, which play different roles depending upon the context of the inflammation, duration, experimental models, or diseases.

Neuroinflammation is mediated by signaling molecules known as cytokines, which are proteins produced and secreted by different cell types that mediate the immune and inflammatory responses. Some of the ‘neuroinflammatory components’ are also involved in physiological function. For example, cytokines considered to be neuroinflammatory markers (IL-1, IL-18, IL-6 and TNF-α) have already been described as key players in physiological mechanisms involved in memory consolidation.

The identification of specific targets related to inflammation in the CNS represents a pivotal tool for the management of central disorders, including neurodegenerative and neuropsychiatric diseases.

Dr. Adriano Lama
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 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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • neurodegenerative disorders
  • mood disorders
  • gut–brain axis
  • neuroendocrine system
  • neuropharmacology
  • inflammation
  • cytokines

Published Papers (2 papers)

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Review

21 pages, 1999 KiB  
Review
Probenecid, an Old Drug with Potential New Uses for Central Nervous System Disorders and Neuroinflammation
by Claudia García-Rodríguez, Paula Mujica, Javiera Illanes-González, Araceli López, Camilo Vargas, Juan C. Sáez, Arlek González-Jamett and Álvaro O. Ardiles
Biomedicines 2023, 11(6), 1516; https://doi.org/10.3390/biomedicines11061516 - 24 May 2023
Cited by 7 | Viewed by 3907
Abstract
Probenecid is an old uricosuric agent used in clinics to treat gout and reduce the renal excretion of antibiotics. In recent years, probenecid has gained attention due to its ability to interact with membrane proteins such as TRPV2 channels, organic anion transporters, and [...] Read more.
Probenecid is an old uricosuric agent used in clinics to treat gout and reduce the renal excretion of antibiotics. In recent years, probenecid has gained attention due to its ability to interact with membrane proteins such as TRPV2 channels, organic anion transporters, and pannexin 1 hemichannels, which suggests new potential therapeutic utilities in medicine. Some current functions of probenecid include their use as an adjuvant to increase the bioavailability of several drugs in the Central Nervous System (CNS). Numerous studies also suggest that this drug has important neuroprotective, antiepileptic, and anti-inflammatory properties, as evidenced by their effect against neurological and neurodegenerative diseases. In these studies, the use of probenecid as a Panx1 hemichannel blocker to reduce neuroinflammation is highlighted since neuroinflammation is a major trigger for diverse CNS alterations. Although the clinical use of probenecid has declined over the years, advances in its use in preclinical research indicate that it may be useful to improve conventional therapies in the psychiatric field where the drugs used have a low bioavailability, either because of a deficient passage through the blood–brain barrier or a high efflux from the CNS or also a high urinary clearance. This review summarizes the history, pharmacological properties, and recent research uses of probenecid and discusses its future projections as a potential pharmacological strategy to intervene in neurodegeneration as an outcome of neuroinflammation. Full article
(This article belongs to the Special Issue Neuroinflammation: From Molecular Mechanism to Therapeutic Perspectives)
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Graphical abstract

17 pages, 2271 KiB  
Review
Pathophysiological Role of Microglial Activation Induced by Blood-Borne Proteins in Alzheimer’s Disease
by Sehwan Kim, Chanchal Sharma, Un Ju Jung and Sang Ryong Kim
Biomedicines 2023, 11(5), 1383; https://doi.org/10.3390/biomedicines11051383 - 7 May 2023
Cited by 5 | Viewed by 4355
Abstract
The blood–brain barrier (BBB) restricts entry of neurotoxic plasma components, blood cells, and pathogens into the brain, leading to proper neuronal functioning. BBB impairment leads to blood-borne protein infiltration such as prothrombin, thrombin, prothrombin kringle-2, fibrinogen, fibrin, and other harmful substances. Thus, microglial [...] Read more.
The blood–brain barrier (BBB) restricts entry of neurotoxic plasma components, blood cells, and pathogens into the brain, leading to proper neuronal functioning. BBB impairment leads to blood-borne protein infiltration such as prothrombin, thrombin, prothrombin kringle-2, fibrinogen, fibrin, and other harmful substances. Thus, microglial activation and release of pro-inflammatory mediators commence, resulting in neuronal damage and leading to impaired cognition via neuroinflammatory responses, which are important features observed in the brain of Alzheimer’s disease (AD) patients. Moreover, these blood-borne proteins cluster with the amyloid beta plaque in the brain, exacerbating microglial activation, neuroinflammation, tau phosphorylation, and oxidative stress. These mechanisms work in concert and reinforce each other, contributing to the typical pathological changes in AD in the brain. Therefore, the identification of blood-borne proteins and the mechanisms involved in microglial activation and neuroinflammatory damage can be a promising therapeutic strategy for AD prevention. In this article, we review the current knowledge regarding the mechanisms of microglial activation-mediated neuroinflammation caused by the influx of blood-borne proteins into the brain via BBB disruption. Subsequently, the mechanisms of drugs that inhibit blood-borne proteins, as a potential therapeutic approach for AD, along with the limitations and potential challenges of these approaches, are also summarized. Full article
(This article belongs to the Special Issue Neuroinflammation: From Molecular Mechanism to Therapeutic Perspectives)
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