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New Advances in Neuroscience: Molecular Biological Insights
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New Advances in Neuroscience: Molecular Biological Insights

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 February 2026) | Viewed by 5881

Special Issue Editor

Dr. Palsamy Periyasamy

E-Mail Website
Guest Editor
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198, USA
Interests: epigenetics (including miRNA and lncRNAs); autophagy; mitochondrial dysfunction (mitophagy); neuroinflammation; HIV and drug abuse; inflammasomes; Nrf2/Keap1 signaling; inflammaging; glial activation

Special Issue Information

Dear Colleagues,

This Special Issue, titled “New Advances in Neuroscience: Molecular Biological Insights”, is dedicated to presenting the most recent breakthroughs and emerging trends in the field of neuroscience, with a particular focus on molecular-level discoveries. This issue features contributions from leading researchers around the globe, covering a broad spectrum of topics, including neurobiology, neuroimaging, and neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease. Additionally, it delves into neurodevelopmental disorders such as autism spectrum disorder, attention-deficit/hyperactivity disorder, and dyslexia, emphasizing the complex interplay of biological, genetic, and environmental factors that contribute to these conditions.

A central theme of this issue is the in-depth exploration of the molecular mechanisms underlying neurological disorders. This includes a focus on identifying genetic risk factors, disease biomarkers, and potential therapeutic targets. This issue also highlights significant advances in neuropharmacology and therapeutics, featuring research on novel medications, innovative drug delivery systems, and cutting-edge therapeutic approaches such as gene therapy, stem cell therapy, and deep brain stimulation.

Furthermore, this Special Issue addresses crucial intersections between neuroscience and public health, particularly in areas such as NeuroHIV, drug abuse, and the epigenetic factors influencing neurodegenerative diseases. It includes research on the molecular pathways disrupted by HIV in the brain, the neurobiological consequences of substance abuse, and the role of epigenetics in the progression and treatment of neurological disorders.

In addition, this issue presents pioneering studies on the role of exosomes in neural communication and disease progression, as well as the potential of targeting inflammasomes as a novel therapeutic approach in neuroinflammatory conditions. By integrating these diverse yet interconnected areas of research, this Special Issue aims to foster collaboration, inspire future research, and deepen our understanding of the intricate molecular processes that govern brain function and dysfunction. We invite contributions from researchers working in these critical areas of neuroscience.

Dr. Palsamy Periyasamy
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. 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

  • neurodegenerative diseases
  • neurodevelopmental disorders
  • neurohiv
  • drug abuse
  • neuropharmacology
  • epigenetics
  • exosomes
  • inflammasomes
  • biomarkers
  • gene therapy
  • stem cell therapy
  • deep brain stimulation
  • Alzheimer’s disease
  • Parkinson’s disease
  • Huntington’s disease
  • autism spectrum disorder
  • ADHD
  • dyslexia
  • neuroinflammation

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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24 pages, 6809 KB  
Article
DPP6 Loss Causes Age-Dependent Sleep Dysregulation and Depression-like Phenotypes Linked to Neurodegeneration
by Lin Lin, Ashley E. Pratt and Dax A. Hoffman
Int. J. Mol. Sci. 2026, 27(7), 3224; https://doi.org/10.3390/ijms27073224 - 2 Apr 2026
Viewed by 511
Abstract
Sleep disturbances are early hallmarks of Alzheimer’s disease (AD) and other dementias, yet the molecular mechanisms remain poorly understood. We previously showed that dipeptidyl aminopeptidase-like protein 6-knockout (DPP6-KO) mice exhibit accelerated neurodegeneration with synaptic loss, neuronal death, and circadian dysfunction resembling AD pathology. [...] Read more.
Sleep disturbances are early hallmarks of Alzheimer’s disease (AD) and other dementias, yet the molecular mechanisms remain poorly understood. We previously showed that dipeptidyl aminopeptidase-like protein 6-knockout (DPP6-KO) mice exhibit accelerated neurodegeneration with synaptic loss, neuronal death, and circadian dysfunction resembling AD pathology. Here, we investigate whether DPP6 deficiency directly causes sleep dysregulation and assess age-dependent effects using wireless EEG/EMG telemetry, behavioral monitoring, and body temperature recordings. We found striking age-dependent sleep phenotypes in DPP6-KO mice. Adult (3-month) DPP6-KO mice showed hyperactivity-driven REM sleep increases, while aged (12-month) DPP6-KO mice developed insomnia with fragmented sleep architecture. Critically, aged DPP6-KO mice exhibited decreased REM latency, a biomarker of depression, which we confirmed by behavioral assays. Conversely, DPP6 overexpression in aged wild-type mice increased NREM duration and reduced sleep fragmentation, demonstrating a protective effect. Throughout aging, DPP6-KO mice showed dysregulated locomotor activity and body temperature rhythms, suggesting broader disruption of circadian and metabolic homeostasis. These findings establish DPP6 as a critical regulator of sleep architecture whose loss recapitulates key sleep disturbances observed in AD/dementia. The progressive nature of sleep dysfunction in DPP6-KO mice, from REM abnormalities to insomnia, parallels human disease progression and positions DPP6 as a potential therapeutic target for sleep-related symptoms in neurodegenerative disorders. Full article
(This article belongs to the Special Issue New Advances in Neuroscience: Molecular Biological Insights)
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22 pages, 4726 KB  
Article
Single-Cell RNA-Seq Uncovers Robust Glial Cell Transcriptional Changes in Methamphetamine-Administered Mice
by Abiola Oladapo, Uma Maheswari Deshetty, Shannon Callen, Shilpa Buch and Palsamy Periyasamy
Int. J. Mol. Sci. 2025, 26(2), 649; https://doi.org/10.3390/ijms26020649 - 14 Jan 2025
Cited by 5 | Viewed by 3801
Abstract
Methamphetamine is a highly addictive stimulant known to cause neurotoxicity, cognitive deficits, and immune dysregulation in the brain. Despite significant research, the molecular mechanisms driving methamphetamine-induced neurotoxicity and glial cell dysfunction remain poorly understood. This study investigates how methamphetamine disrupts glial cell function [...] Read more.
Methamphetamine is a highly addictive stimulant known to cause neurotoxicity, cognitive deficits, and immune dysregulation in the brain. Despite significant research, the molecular mechanisms driving methamphetamine-induced neurotoxicity and glial cell dysfunction remain poorly understood. This study investigates how methamphetamine disrupts glial cell function and contributes to neurodevelopmental and neurodegenerative processes. Using single-cell RNA sequencing (scRNA-seq), we analyzed the transcriptomes of 4000 glial cell-associated genes from the cortical regions of mice chronically administered methamphetamine. Methamphetamine exposure altered the key pathways in astrocytes, including the circadian rhythm and cAMP signaling; in microglia, affecting autophagy, ubiquitin-mediated proteolysis, and mitophagy; and in oligodendrocytes, disrupting lysosomal function, cytoskeletal regulation, and protein processing. Notably, several transcription factors, such as Zbtb16, Hif3a, Foxo1, and Klf9, were significantly dysregulated in the glial cells. These findings reveal profound methamphetamine-induced changes in the glial transcriptomes, particularly in the cortical regions, highlighting potential molecular pathways and transcription factors as targets for therapeutic intervention. This study provides novel insights into the glial-mediated mechanisms of methamphetamine toxicity, contributing to our understanding of its effects on the central nervous system and laying the groundwork for future strategies to mitigate its neurotoxic consequences. Full article
(This article belongs to the Special Issue New Advances in Neuroscience: Molecular Biological Insights)
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Review

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29 pages, 1393 KB  
Review
The Electromechanical Connectome: Integrating Voltage, Mechanical Nano-Forces, and Subcellular Fluid Phase Dynamics in Human Neural Computation
by Florin Mihail Filipoiu, Catalina-Ioana Tataru, Nicolaie Dobrin, Matei Șerban, Răzvan-Adrian Covache-Busuioc, Corneliu Toader, Mugurel Petrinel Radoi, Octavian Munteanu and Mihaly Enyedi
Int. J. Mol. Sci. 2026, 27(4), 2074; https://doi.org/10.3390/ijms27042074 - 23 Feb 2026
Viewed by 746
Abstract
Electrophysiology, mechanobiology, and the study of soft matter within cells demonstrate increasing amounts of evidence that neuronal signaling arises from interactions between membrane potential, force, and phase. Herein, we have attempted to collect and organize the evidence for each of these areas of [...] Read more.
Electrophysiology, mechanobiology, and the study of soft matter within cells demonstrate increasing amounts of evidence that neuronal signaling arises from interactions between membrane potential, force, and phase. Herein, we have attempted to collect and organize the evidence for each of these areas of study into an approximate structure called the electromechanical connectome: a three-way state–space (membrane potentials, nanoscale mechanical forces, and cytoplasmic rheology, including phase-separated liquid–liquid droplets) where membrane potentials, nanoscale mechanical forces, and cytoplasmic rheology, and phase-separated liquid–liquid droplets are likely to influence one another, influencing synaptic processing, plasticity and network stability. We will also attempt to illustrate the following: how changes in electrostatic fields can be used to alter the arrangement of lipids, hydration, and dielectric microdomains, and the contact geometry between organelles and activity dependent transcription; how mechanical dynamics associated with spines, axons, and the active zone of synapses may be used to modify the energy landscape of channels, the docking and priming of vesicles, and the transport of cytoskeletons; and how viscosity corridors, along with phase-separated micro-reactors, can be used to regulate the kinetics of signaling, molecular trafficking and metabolic processes in local environments. With these connections in mind, we will propose a multiphysical attractor model in which cognition is the result of navigating through metastable manifolds, while neurodegenerative disease may be a result of the progressive loss of electromechanical coherence, phase boundary control and energetic flexibility. Finally, we will present testable hypotheses and use AI-enabled digital twin methods to potentially quantify the early deformation of manifolds and provide precision biomarkers and therapeutic options. Full article
(This article belongs to the Special Issue New Advances in Neuroscience: Molecular Biological Insights)
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