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Neural Networks in Molecular and Cellular Neurobiology
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Neural Networks in Molecular and Cellular Neurobiology

A Special Issue of Current Issues in Molecular Biology (ISSN 1467-3045) belonging to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: 30 April 2027 | Viewed by 8220

Editor

Dr. Paschalis Theotokis

E-Mail Website
Guest Editor
Department of Histology-Embryology, School of Medicine, Aristotle University of Thessaloniki, 54655 Thessaloniki, Greece
Interests: neuroscience; multiple sclerosis; experimental autoimmune encephalomyelitis; intrathecal transplantation; stem cell differentiation; immunohistopathology; in situ hybridization; electron microscopy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuronal networks are fundamental components of the nervous system, comprising tightly regulated molecular and cellular processes such as synaptic signaling, ion channel dynamics, and intracellular signaling cascades. Neural networks link gene expression, protein interactions, and intercellular communication to higher-order neural functions. Unraveling these mechanisms is a central challenge in molecular biology. Recent advances in molecular biology techniques, coupled with new tools such as machine learning and AI tools, are accelerating progress in this field.

This Special Issue will focus on cutting-edge research at the intersection of molecular neurobiology and neural networks, specifically examining the impact of molecular and cellular interactions on neural networks in health and disease. We welcome original research, reviews, case reports, and perspectives that provide new molecular insights into the organization, regulation, and dysfunction of neural networks.

Dr. Paschalis Theotokis
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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology 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 2400 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

  • neural networks
  • neuroplasticity
  • intracellular signaling
  • computational neuroscience
  • artificial intelligence
  • neuromorphic computing

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Published Papers (3 papers)

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Research

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21 pages, 167029 KB  
Article
TGF-β1 Promotes the Recovery of Dorsal Root Ganglion Neurons from Cisplatin-Induced Injury Through Smad4-Dependent Mechanism
by Pan Wu, Yiling Wei, Xiang Chen, Qingmei Mo and Ming Zhuo
Curr. Issues Mol. Biol. 2026, 48(4), 344; https://doi.org/10.3390/cimb48040344 - 25 Mar 2026
Viewed by 1458
Abstract
Chemotherapy-induced peripheral (CIPN) neuropathy is a common dose-limiting side effect affecting roughly 30–40% patients. Dorsal root ganglia (DRG) neurons are one of the main targets of CIPN as chemotherapy drugs may accumulate in DRG neurons. Chemotherapy drugs may induce direct damages on DRG [...] Read more.
Chemotherapy-induced peripheral (CIPN) neuropathy is a common dose-limiting side effect affecting roughly 30–40% patients. Dorsal root ganglia (DRG) neurons are one of the main targets of CIPN as chemotherapy drugs may accumulate in DRG neurons. Chemotherapy drugs may induce direct damages on DRG neurons while also activating immune pathways, which results in the releasing of pro-inflammatory cytokines. This cascade may also damage neurons and amplify pain signaling. Transforming growth factor-β1 (TGF-β1) is a multifunctional cytokine with prominent immunomodulatory roles. Here, we report that TGF-β1 can promote axonal regeneration on DRG neurons injured by cisplatin via a suppressor of mothers against decapentaplegic (Smad) signaling pathway. To confirm the involvement of canonical TGF-β signaling, we applied the selective TGF-β type I receptor antagonist SB-431542 and performed a gene knockdown of Smad3 and Smad4, assessing their impacts on TGF-β1’s effects. Our results demonstrate that TGF-β1 could significantly enhance axonal regeneration in DRG, largely through a Smad4-dependent pathway, and we propose TGF-β1/Smad4 as a promising molecular target for treating CIPN. Full article
(This article belongs to the Special Issue Neural Networks in Molecular and Cellular Neurobiology)
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Review

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19 pages, 1744 KB  
Review
A Review of the Effect of Peripheral Amyloid β on the Central Nervous System
by Zulaikha Elia Zamzuri, Mohd Amir Kamaruzzaman, Seong Lin Teoh and Mohamad Fairuz Yahaya
Curr. Issues Mol. Biol. 2026, 48(5), 438; https://doi.org/10.3390/cimb48050438 - 23 Apr 2026
Viewed by 938
Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder classically defined by cerebral amyloid β (Aβ) plaque deposition and tau pathology. In recent years, AD has increasingly been recognized as a multisystem disorder rather than a purely brain-restricted condition, as mounting evidence indicates that [...] Read more.
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder classically defined by cerebral amyloid β (Aβ) plaque deposition and tau pathology. In recent years, AD has increasingly been recognized as a multisystem disorder rather than a purely brain-restricted condition, as mounting evidence indicates that Aβ metabolism is a dynamic, bidirectional process involving both central and peripheral compartments. Peripheral tissues, particularly platelets, liver, kidneys, and the gastrointestinal tract, contribute substantially to circulating Aβ levels and influence cerebral amyloid burden. Platelets are now considered the predominant source of peripheral Aβ, accounting for the majority of plasma Aβ under physiological and pathological conditions, while the liver and kidneys play critical roles in Aβ clearance through receptor-mediated uptake, enzymatic degradation and excretion. Disruption of these peripheral clearance pathways elevates circulating Aβ, increasing its transport into the brain via blood–brain barrier (BBB) mechanisms by enhanced RAGE-mediated influx and impaired LRP1-dependent efflux in AD. Peripheral Aβ entry into the central nervous system exacerbates neuroinflammation, mitochondrial dysfunction, and oxidative stress, thereby accelerating neuronal damage and disease progression. This review synthesizes updated evidence on peripheral sources of Aβ, differences between central and peripheral Aβ pools, mechanisms of Aβ transport across the BBB, pathological consequences of peripheral Aβ on the brain and emerging therapeutic strategies targeting peripheral Aβ metabolism, highlighting the importance of a systemic perspective in AD pathogenesis and treatment. Full article
(This article belongs to the Special Issue Neural Networks in Molecular and Cellular Neurobiology)
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30 pages, 10570 KB  
Review
Molecular Physiology of the Neuronal Synapse
by María Jesús Ramírez-Expósito, Cristina Cueto-Ureña and José Manuel Martínez-Martos
Curr. Issues Mol. Biol. 2026, 48(1), 88; https://doi.org/10.3390/cimb48010088 - 15 Jan 2026
Cited by 5 | Viewed by 5203
Abstract
Neuronal synapses are the functional units of communication in the central nervous system. This review describes the molecular mechanisms regulating synaptic transmission, plasticity, and circuit refinement. At the presynaptic active zone, scaffolding proteins including bassoon, piccolo, RIMs, and munc13 organize vesicle priming and [...] Read more.
Neuronal synapses are the functional units of communication in the central nervous system. This review describes the molecular mechanisms regulating synaptic transmission, plasticity, and circuit refinement. At the presynaptic active zone, scaffolding proteins including bassoon, piccolo, RIMs, and munc13 organize vesicle priming and the localization of voltage-gated calcium channels. Neurotransmitter release is mediated by the SNARE complex, comprising syntaxin-1, SNAP25, and synaptobrevin, and triggered by the calcium sensor synaptotagmin-1. Following exocytosis, synaptic vesicles are recovered through clathrin-mediated, ultrafast, bulk, or kiss-and-run endocytic pathways. Postsynaptically, the postsynaptic density (PSD) serves as a protein hub where scaffolds such as PSD-95, shank, homer, and gephyrin anchor excitatory (AMPA, NMDA) and inhibitory (GABA-A, Glycine) receptors are observed. Synaptic strength is modified during long-term potentiation (LTP) and depression (LTD) through signaling cascades involving kinases like CaMKII, PKA, and PKC, or phosphatases such as PP1 and calcineurin. These pathways regulate receptor trafficking, Arc-mediated endocytosis, and actin-dependent remodeling of dendritic spines. Additionally, synapse formation and elimination are guided by cell adhesion molecules, including neurexins and neuroligins, and by microglial pruning via the complement cascade (C1q, C3) and “don’t eat me” signals like CD47. Molecular diversity is further expanded by alternative splicing and post-translational modifications. A unified model of synaptic homeostasis is required to understand the basis of neuropsychiatric and neurological disorders. Full article
(This article belongs to the Special Issue Neural Networks in Molecular and Cellular Neurobiology)
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