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Molecular Mechanisms of Neuropsychiatric Diseases
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Molecular Mechanisms of Neuropsychiatric Diseases

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

Deadline for manuscript submissions: closed (20 May 2024) | Viewed by 2399

Special Issue Editor

Dr. Dmitrii A. Pavlov

E-Mail Website
Guest Editor
Department of Psychology, University of Calgary, Calgary, AB T2N 1N4, Canada
Interests: neuropsychiatric diseases; emotional stress; epigenetics; inflammation; transcriptomics

Special Issue Information

Dear Colleagues,

Neuropsychiatric diseases are a group of disorders that affect the brain and its functions, often resulting in alterations of behavior, mood, and cognition. These disorders can have a significant impact on the quality of life of individuals affected by them, and they often have complex and multifactorial etiologies.

Molecular mechanisms of neuropsychiatric diseases refer to the underlying biological and biochemical processes that contribute to the development and progression of these disorders. These mechanisms involve a variety of factors, including genetic, environmental, and epigenetic factors, as well as alterations in cellular signaling pathways and neuronal circuits.

Some of the molecular mechanisms that have been implicated in neuropsychiatric diseases include alterations in neurotransmitter systems, changes in synaptic plasticity, inflammation, oxidative stress, and mitochondrial dysfunction. Understanding these molecular mechanisms is essential for developing new treatments for these disorders and improving the lives of affected individuals and we hope that our special issue significantly contributes to that.

Dr. Dmitrii A. Pavlov
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. 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

  • neurotransmitters
  • synaptic plasticity
  • epigenetics
  • genetic mutations
  • inflammation
  • oxidative stress
  • mitochondrial dysfunction
  • apoptosis
  • neuroinflammation
  • excitotoxicity
  • glutamate

Published Papers (2 papers)

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Research

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15 pages, 2588 KiB  
Article
Maternal Chronic Ultrasound Stress Provokes Immune Activation and Behavioral Deficits in the Offspring: A Mouse Model of Neurodevelopmental Pathology
by Dmitrii Pavlov, Anna Gorlova, Abrar Haque, Carlos Cavalcante, Evgeniy Svirin, Alisa Burova, Elizaveta Grigorieva, Elizaveta Sheveleva, Dmitry Malin, Sofia Efimochkina, Andrey Proshin, Aleksei Umriukhin, Sergey Morozov and Tatyana Strekalova
Int. J. Mol. Sci. 2023, 24(14), 11712; https://doi.org/10.3390/ijms241411712 - 20 Jul 2023
Cited by 2 | Viewed by 1479
Abstract
Neurodevelopmental disorders stemming from maternal immune activation can significantly affect a child’s life. A major limitation in pre-clinical studies is the scarcity of valid animal models that accurately mimic these challenges. Among the available models, administration of lipopolysaccharide (LPS) to pregnant females is [...] Read more.
Neurodevelopmental disorders stemming from maternal immune activation can significantly affect a child’s life. A major limitation in pre-clinical studies is the scarcity of valid animal models that accurately mimic these challenges. Among the available models, administration of lipopolysaccharide (LPS) to pregnant females is a widely used paradigm. Previous studies have reported that a model of ‘emotional stress’, involving chronic exposure of rodents to ultrasonic frequencies, induces neuroinflammation, aberrant neuroplasticity, and behavioral deficits. In this study, we explored whether this model is a suitable paradigm for maternal stress and promotes neurodevelopmental abnormalities in the offspring of stressed females. Pregnant dams were exposed to ultrasound stress for 21 days. A separate group was injected with LPS on embryonic days E11.5 and E12.5 to mimic prenatal infection. The behavior of the dams and their female offspring was assessed using the sucrose test, open field test, and elevated plus maze. Additionally, the three-chamber sociability test and Barnes maze were used in the offspring groups. ELISA and qPCR were used to examine pro-inflammatory changes in the blood and hippocampus of adult females. Ultrasound-exposed adult females developed a depressive-like syndrome, hippocampal overexpression of GSK-3β, IL-1β, and IL-6 and increased serum concentrations of IL-1β, IL-6, IL-17, RANTES, and TNFα. The female offspring also displayed depressive-like behavior, as well as cognitive deficits. These abnormalities were comparable to the behavioral changes induced by LPS. The ultrasound stress model can be a promising animal paradigm of neurodevelopmental pathology associated with prenatal ‘emotional stress’. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neuropsychiatric Diseases)
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Review

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12 pages, 470 KiB  
Review
Novel Leptin-Based Therapeutic Strategies to Limit Synaptic Dysfunction in Alzheimer’s Disease
by Jenni Harvey
Int. J. Mol. Sci. 2024, 25(13), 7352; https://doi.org/10.3390/ijms25137352 - 4 Jul 2024
Viewed by 536
Abstract
Accumulation of hyper-phosphorylated tau and amyloid beta (Aβ) are key pathological hallmarks of Alzheimer’s disease (AD). Increasing evidence indicates that in the early pre-clinical stages of AD, phosphorylation and build-up of tau drives impairments in hippocampal excitatory synaptic function, which ultimately leads to [...] Read more.
Accumulation of hyper-phosphorylated tau and amyloid beta (Aβ) are key pathological hallmarks of Alzheimer’s disease (AD). Increasing evidence indicates that in the early pre-clinical stages of AD, phosphorylation and build-up of tau drives impairments in hippocampal excitatory synaptic function, which ultimately leads to cognitive deficits. Consequently, limiting tau-related synaptic abnormalities may have beneficial effects in AD. There is now significant evidence that the hippocampus is an important brain target for the endocrine hormone leptin and that leptin has pro-cognitive properties, as activation of synaptic leptin receptors markedly influences higher cognitive processes including learning and memory. Clinical studies have identified a link between the circulating leptin levels and the risk of AD, such that AD risk is elevated when leptin levels fall outwith the physiological range. This has fuelled interest in targeting the leptin system therapeutically. Accumulating evidence supports this possibility, as numerous studies have shown that leptin has protective effects in a variety of models of AD. Recent findings have demonstrated that leptin has beneficial effects in the preclinical stages of AD, as leptin prevents the early synaptic impairments driven by tau protein and amyloid β. Here we review recent findings that implicate the leptin system as a potential novel therapeutic target in AD. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neuropsychiatric Diseases)
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