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Brain Sciences
Special Issues
Addiction and Neuroinflammation
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Addiction and Neuroinflammation

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (25 March 2024) | Viewed by 3903

Special Issue Editors

Dr. Nasim Maleki

E-Mail Website
Guest Editor
Department of Psychiatry, Harvard Medical School, Massachusetts General Hospital, Boston 02114, USA
Interests: allostasis; arterial spin labeling; brain aging; migraine disorders; pain threshold; pul-vinar; retinal vessels; sex dimorphism; sex dimorphism in alcoholism; thalamocortical network
Special Issues, Collections and Topics in MDPI journals
Dr. Benjamin Thompson

E-Mail Website
Guest Editor Assistant
Department of Psychiatry, Harvard Medical School, Massachusetts General Hospital, Boston, MA 02114, USA
Interests: addiction; addiction recovery; allostasis; emotional regulation; salience network

Special Issue Information

Dear Colleagues,

Chronic and heavy alcohol consumption can significantly impact multiple organs in the body, particularly the brain, resulting in both acute and chronic inflammation. Alcohol-induced inflammation in brain cells can arise through various mechanisms, triggering an exaggerated immune response within the central nervous system. To gain a comprehensive understanding of these mechanisms, we encourage research papers that specifically explore the effects of long-term alcohol use on processes such as microglial activation, the release of pro-inflammatory cytokines, disruption of the blood–brain barrier, excessive oxidative stress, and neurodegeneration in the context of alcohol-related neuroinflammation. Additionally, we welcome studies that investigate the relationship between alcohol-related neuroinflammation and the heightened susceptibility to neurological disorders.

Dr. Nasim Maleki
Guest Editor

Dr. Benjamin Thompson
Guest Editor Assistant

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. Brain Sciences 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 2200 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

  • alcohol use disorder
  • alcoholism
  • alcohol abuse
  • alcohol dependence
  • inflammation
  • neuroinflammation
  • neurodegeneration
  • pro-inflammatory cytokines

Published Papers (3 papers)

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Research

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14 pages, 1856 KiB  
Article
Nicotine, THC, and Dolutegravir Modulate E-Cigarette-Induced Changes in Addiction- and Inflammation-Associated Genes in Rat Brains and Astrocytes
by Jacqueline Renee Kulbe, Lauren Nguyen, Alexandra Anh Le, Anna Elizabeth Laird, Michael A. Taffe, Jacques D. Nguyen and Jerel Adam Fields
Brain Sci. 2023, 13(11), 1556; https://doi.org/10.3390/brainsci13111556 - 7 Nov 2023
Cited by 1 | Viewed by 1585
Abstract
E-cigarette use has been marketed as a safer alternative to traditional cigarettes, as a means of smoking cessation, and are used at a higher rate than the general population in people with HIV (PWH). Early growth receptor 2 (EGR2) and Activity-Regulated Cytoskeleton-Associated Protein [...] Read more.
E-cigarette use has been marketed as a safer alternative to traditional cigarettes, as a means of smoking cessation, and are used at a higher rate than the general population in people with HIV (PWH). Early growth receptor 2 (EGR2) and Activity-Regulated Cytoskeleton-Associated Protein (ARC) have a role in addiction, synaptic plasticity, inflammation, and neurodegeneration. This study showed that 10 days of exposure to e-cigarette vapor altered gene expression in the brains of 6-month-old, male, Sprague Dawley rats. Specifically, the e-cigarette solvent vapor propylene glycol (PG) downregulated EGR2 and ARC mRNA expression in frontal cortex, an effect which was reversed by nicotine (NIC) and THC, suggesting that PG could have a protective role against NIC and cannabis dependence. However, in vitro, PG upregulated EGR2 and ARC mRNA expression at 18 h in cultured C6 rat astrocytes suggesting that PG may have neuroinflammatory effects. PG-induced upregulation of EGR2 and ARC mRNA was reversed by NIC but not THC. The HIV antiretroviral DTG reversed the effect NIC had on decreasing PG-induced upregulation of EGR2, which is concerning because EGR2 has been implicated in HIV latency reversal, T-cell apoptosis, and neuroinflammation, a process that underlies the development of HIV-associated neurocognitive disorders. Full article
(This article belongs to the Special Issue Addiction and Neuroinflammation)
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Review

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22 pages, 1802 KiB  
Review
Protein Kinase C (PKC) in Neurological Health: Implications for Alzheimer’s Disease and Chronic Alcohol Consumption
by Nishtha Singh, Shouvik Kumar Nandy, Anupam Jyoti, Juhi Saxena, Aditi Sharma, Arif Jamal Siddiqui and Lalit Sharma
Brain Sci. 2024, 14(6), 554; https://doi.org/10.3390/brainsci14060554 - 29 May 2024
Viewed by 682
Abstract
Protein kinase C (PKC) is a diverse enzyme family crucial for cell signalling in various organs. Its dysregulation is linked to numerous diseases, including cancer, cardiovascular disorders, and neurological problems. In the brain, PKC plays pivotal roles in synaptic plasticity, learning, memory, and [...] Read more.
Protein kinase C (PKC) is a diverse enzyme family crucial for cell signalling in various organs. Its dysregulation is linked to numerous diseases, including cancer, cardiovascular disorders, and neurological problems. In the brain, PKC plays pivotal roles in synaptic plasticity, learning, memory, and neuronal survival. Specifically, PKC’s involvement in Alzheimer’s Disease (AD) pathogenesis is of significant interest. The dysregulation of PKC signalling has been linked to neurological disorders, including AD. This review elucidates PKC’s pivotal role in neurological health, particularly its implications in AD pathogenesis and chronic alcohol addiction. AD, characterised by neurodegeneration, implicates PKC dysregulation in synaptic dysfunction and cognitive decline. Conversely, chronic alcohol consumption elicits neural adaptations intertwined with PKC signalling, exacerbating addictive behaviours. By unravelling PKC’s involvement in these afflictions, potential therapeutic avenues emerge, offering promise for ameliorating their debilitating effects. This review navigates the complex interplay between PKC, AD pathology, and alcohol addiction, illuminating pathways for future neurotherapeutic interventions. Full article
(This article belongs to the Special Issue Addiction and Neuroinflammation)
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11 pages, 599 KiB  
Review
Could Alcohol-Related Cognitive Decline Be the Result of Iron-Induced Neuroinflammation?
by Thomas D. W. Wilcockson and Sankanika Roy
Brain Sci. 2024, 14(6), 520; https://doi.org/10.3390/brainsci14060520 - 21 May 2024
Viewed by 1266
Abstract
Excessive and prolonged alcohol use can have long-term severe neurological consequences. The mechanisms involved may be complicated; however, new evidence seems to indicate the involvement of iron accumulation and neuroinflammation. Prolonged alcohol consumption has been linked to the accumulation of iron in specific [...] Read more.
Excessive and prolonged alcohol use can have long-term severe neurological consequences. The mechanisms involved may be complicated; however, new evidence seems to indicate the involvement of iron accumulation and neuroinflammation. Prolonged alcohol consumption has been linked to the accumulation of iron in specific regions of the brain. Evidence suggests that excess iron in the brain can trigger microglia activation in response. This activation leads to the release of pro-inflammatory cytokines and reactive oxygen species, which can cause damage to neurons and surrounding brain tissue. Additionally, iron-induced oxidative stress and inflammation can disrupt the blood–brain barrier, allowing immune cells from the periphery to infiltrate the brain. This infiltration can lead to further neuroinflammatory responses. Inflammation in the brain subsequently disrupts neuronal networks, impairs synaptic plasticity, and accelerates neuronal cell death. Consequently, cognitive functions such as memory, attention, and decision-making are compromised. Additionally, chronic neuroinflammation can hasten the development and progression of neurodegenerative diseases, further exacerbating cognitive impairment. Therefore, alcohol could act as a trigger for iron-induced neuroinflammation and cognitive decline. Overall, the mechanisms at play here seem to strongly link alcohol with cognitive decline, with neuroinflammation resulting from alcohol-induced iron accumulation playing a pivotal role. Full article
(This article belongs to the Special Issue Addiction and Neuroinflammation)
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