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Biomolecules
Special Issues
Alcohol-Related Nervous System Damage and Disease: From Mechanisms to Therapies
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Alcohol-Related Nervous System Damage and Disease: From Mechanisms to Therapies

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 16 October 2026 | Viewed by 1851

Special Issue Editor

Dr. Suzanne M. De La Monte

E-Mail Website
Guest Editor
Departments of Pathology and Laboratory Medicine, Neurology, and Neurosurgery, Rhode Island Hospital, Women & Infants Hospital, Brown University Health, Alpert Medical School of Brown University, Providence, RI 02912, USA
Interests: alcohol-related brain degeneration; Alzheimer's disease; diabetes; ethanol; fetal alcohol syndrome; insulin; neurodegeneration; oxidative stress; signal transduction; white matter
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is my pleasure to announce that I will serve as the Guest Editor for a Special Issue on alcohol-related neurodegeneration for publication in Biomolecules. For this Special Issue, we hope to focus on human research and include supportive experimental studies that could provide guidance for future human investigations. The articles may employ a range of methodological approaches to address problems related to disease characteristics, pathology, mechanisms, diagnostics, or therapeutics.

Dr. Suzanne M. De La Monte
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 250 words) can be sent to the Editorial Office for assessment.

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. Biomolecules 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 2700 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
  • brain
  • neurodegeneration
  • diagnostics
  • treatment
  • disease mechanisms
  • prevention
  • pathology
  • imaging
  • molecular and cellular studies
  • co-factor effects

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Published Papers (2 papers)

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Research

26 pages, 5154 KB  
Article
Systemic Interplay of BDNF and Serotonin Pathways Defines Behavioral and Molecular Responses to Midbrain 5-HT7 Overexpression and Chronic Ethanol Consumption
by Alexander Rodnyy, Alina Oreshko, Dmitry Eremin, Vladimir Naumenko and Darya Bazovkina
Biomolecules 2026, 16(1), 106; https://doi.org/10.3390/biom16010106 - 8 Jan 2026
Viewed by 754
Abstract
Chronic ethanol exposure and genetic factors interact to drive neuroadaptations in alcohol use disorders (AUD). However, the system-level coordination of molecular responses across brain regions remains unclear. The 5-HT system and BDNF are key regulators of neuroplasticity in alcoholism. The 5-HT7 receptor [...] Read more.
Chronic ethanol exposure and genetic factors interact to drive neuroadaptations in alcohol use disorders (AUD). However, the system-level coordination of molecular responses across brain regions remains unclear. The 5-HT system and BDNF are key regulators of neuroplasticity in alcoholism. The 5-HT7 receptor modulates both behavior and serotonin signaling. We investigated midbrain 5-HT7 overexpression in C57BL/6 mice given 5-week ethanol access. Our results showed complex, region-specific changes in 5-HT and BDNF signaling, as well as selective behavioral alterations. Ethanol abolished the antidepressant-like effect of 5-HT7 overexpression and increased anxiety-like behavior, without affecting baseline locomotion or novel object recognition. At the molecular level, ethanol suppressed 5-HT7-mediated CREB/BDNF signaling and differentially regulated 5-HT1A and 5-HT2A expression across regions. To extract general principles, we used integrative systems analysis based on population-averaged generalized estimating equations (GEE), and mapped effects in the (t1, t2) plane. We identified two regularities: first, regional specificity of responses, and second, divergence across regulatory levels, with opposing effects more frequent at the mRNA level and concordant effects more common at the protein level. These findings suggest that neuroadaptation to combined 5-HT7 and ethanol factors follows region- and level-specific rules, rather than a single global program, underscoring the value of integrative analysis. Full article
(This article belongs to the Special Issue Alcohol-Related Nervous System Damage and Disease: From Mechanisms to Therapies)
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14 pages, 1513 KB  
Article
Incretin-Related Pathology and Serum Exosome Detection in Experimental Alcohol-Related Brain Damage
by Suzanne M. de la Monte, Ming Tong and Yiwen Yang
Biomolecules 2025, 15(12), 1670; https://doi.org/10.3390/biom15121670 - 30 Nov 2025
Cited by 1 | Viewed by 707
Abstract
Alcohol’s chronic neurotoxic and degenerative effects mediate alcohol-related brain damage (ARBD), which is marked by neurobehavioral, cognitive, and motor deficits. Major underlying abnormalities include impairments in signaling through the insulin and insulin-like growth factor (IGF) pathways, which regulate energy metabolism. This study examined [...] Read more.
Alcohol’s chronic neurotoxic and degenerative effects mediate alcohol-related brain damage (ARBD), which is marked by neurobehavioral, cognitive, and motor deficits. Major underlying abnormalities include impairments in signaling through the insulin and insulin-like growth factor (IGF) pathways, which regulate energy metabolism. This study examined the potential role of dysregulated incretin network-related mechanisms as mediators of ARBD and evaluated a non-invasive serum exosome (S-EV)-based approach for detecting brain abnormalities. Frontal lobe tissue and S-EVs isolated from Long–Evans adolescent rats maintained for 2 weeks on control or 24% ethanol (caloric) containing liquid diets (n = 8/group) were analyzed using multiplex magnetic bead-based enzyme-linked immunosorbent assays (ELISAs). ARBD was associated with significantly reduced insulin, C-peptide, glucagon, ghrelin, leptin, GIP, and amylin levels in the frontal lobe and/or S-EV samples. In contrast, chronic ethanol exposure had no significant effects on PP, PYY, or GLP-1, and it did not increase proinflammatory cytokine expression. Chronic ethanol feeding broadly affected (primarily inhibiting) the expression of metabolic hormones linked to insulin/IGF signaling. The reductions in GIP and amylin suggest potential targets for therapeutic intervention to enhance brain energy metabolism via insulin networks. On the other hand, the findings suggest that GLP-1 receptor agonists may have limited efficacy in remediating the effects of ARBD. Finally, the results support the use of non-invasive S-EV assays to detect and guide treatment for metabolic brain dysfunction in ARBD. Full article
(This article belongs to the Special Issue Alcohol-Related Nervous System Damage and Disease: From Mechanisms to Therapies)
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