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Neurological Diseases: From Pathogenesis to Molecular Diagnosis and Treatment
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Neurological Diseases: From Pathogenesis to Molecular Diagnosis and Treatment

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: 31 March 2026 | Viewed by 833

Special Issue Editors

Dr. Barbara Miziak

E-Mail Website
Guest Editor
Department of Pathophysiology, Medical University of Lublin, 20-090 Lublin, Poland
Interests: epilepsy; epileptogenesis; status epilepticus; neuroprotection; antiepileptic drugs; seizures
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Stanisław Jerzy Czuczwar

E-Mail Website
Guest Editor
Department of Pathophysiology, Medical University of Lublin, 20-090 Lublin, Poland
Interests: Alzheimer; epilepsy; stroke
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurological diseases constitute a large, heterogeneous group of disorders whose common feature is damage to the central nervous system. Their etiology includes mechanisms such as neurodegeneration, vascular changes, autoimmune processes, synaptic transmission disorders, and genetic defects. Frequently, the development of secondary chronic neuroglial inflammation, oxidative stress, and ion and energy homeostasis disorders can also be observed. In the pathogenesis of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease, the main role is played by the abnormal accumulation and aggregation of proteins and their toxic effect on nerve cells. In demyelinating diseases, such as multiple sclerosis, pathogenesis is mainly based on autoimmune damage to myelin sheaths. In the case of stroke, cerebral circulation disorders and cell death are observed. The etiology of epilepsy is multifactorial and includes neurotransmitter dysfunction and genetic mutations, as well as metabolic and electrolyte disorders, neurodegenerative processes, and inflammation in the brain.

Thorough knowledge and understanding of the above mechanisms also offer great opportunities for the development of therapies focusing on the pathomechanisms of neurological diseases. Currently, the most dominant form of therapy is pharmacotherapy, but newer strategies also include gene therapies, microRNA expression modulation, monoclonal antibodies, immunotherapies, and regenerative therapies.

Dr. Barbara Miziak
Prof. Dr. Stanisław Jerzy Czuczwar
Guest Editors

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Keywords

  • Alzheimer's disease
  • Parkinson's disease
  • Huntington's disease
  • epilepsy
  • stroke
  • neurological diseases
  • treatment of neurological diseases

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Published Papers (2 papers)

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Research

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15 pages, 4353 KB  
Article
The ErbB2–Dock7 Signaling Axis Mediates Excessive Cell Morphogenesis Induced by Autism Spectrum Disorder- and Intellectual Disability-Associated Sema5A p.Arg676Cys
by Mikito Takahashi, Hideji Yako, Ayaka Suzuki, Ryuma Isa, Yuki Miyamoto and Junji Yamauchi
Int. J. Mol. Sci. 2025, 26(21), 10656; https://doi.org/10.3390/ijms262110656 - 1 Nov 2025
Viewed by 438
Abstract
Characterized by social communication deficits and the presence of restricted and repetitive behaviors, autism spectrum disorder (ASD) is a significant neurodevelopmental condition. Genetic studies have revealed a strong association between ASD and numerous mutations that alter the function of key proteins, either through [...] Read more.
Characterized by social communication deficits and the presence of restricted and repetitive behaviors, autism spectrum disorder (ASD) is a significant neurodevelopmental condition. Genetic studies have revealed a strong association between ASD and numerous mutations that alter the function of key proteins, either through activation or inactivation. These alterations are widely hypothesized to affect neuronal morphogenesis; however, a comprehensive understanding of the specific molecular cascades driving these cellular and symptomatic changes remains lacking. In this study, we report for the first time that signaling through the atypical Rho family guanine-nucleotide exchange factor (GEF) Dock7 and ErbB2, an activator acting upstream of Dock7, drives the excessive elongation of neuronal processes observed in association with the ASD- and intellectual disability (ID)-linked semaphorin-5A (Sema5A) Arg676Cys variant (p.Arg676Cys). Knockdown of Dock7 using short hairpin RNA or inhibition of ErbB2 kinase signaling with a specific chemical inhibitor reduced this excessive process elongation in primary cortical neurons. Similar results were obtained in the N1E-115 cell line, a neuronal cell model that undergoes neuronal morphological differentiation. Moreover, inhibition of ErbB2-Dock7 signaling specifically decreased the overactivation of the downstream molecules Rac1 and Cdc42. These findings indicate that the ErbB2–Dock7 signaling axis plays a role in mediating the aberrant neuronal morphology associated with the ASD- and ID-linked Sema5A p.Arg676Cys. Targeting this pathway may therefore offer a potential approach to addressing the molecular and cellular developmental challenges observed in ASD. Full article
(This article belongs to the Special Issue Neurological Diseases: From Pathogenesis to Molecular Diagnosis and Treatment)
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Review

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22 pages, 4168 KB  
Review
Methamphetamine-Associated Cardiomyopathy and Cardioembolic Stroke: Brain–Heart–Gut Axis Crosstalk, Diagnostic Strategies, and Anticoagulation Challenges
by Pei-Jung Lin, Chia-Hui Wu, Jen-Hung Huang, Jakir Hossain Bhuiyan Masud, Chien-Tai Hong, Lung Chan and Chen-Chih Chung
Int. J. Mol. Sci. 2025, 26(24), 11908; https://doi.org/10.3390/ijms262411908 - 10 Dec 2025
Viewed by 216
Abstract
Methamphetamine (MA) abuse has emerged as a multisystem insult driving cardiovascular and neurovascular consequences. Methamphetamine-associated cardiomyopathy (MACM) remains an underrecognized cause of cardioembolic stroke through left ventricular thrombus (LVT) formation. MA-induced gut dysbiosis and enteric neural disruption exacerbate systemic inflammation and autonomic imbalance, [...] Read more.
Methamphetamine (MA) abuse has emerged as a multisystem insult driving cardiovascular and neurovascular consequences. Methamphetamine-associated cardiomyopathy (MACM) remains an underrecognized cause of cardioembolic stroke through left ventricular thrombus (LVT) formation. MA-induced gut dysbiosis and enteric neural disruption exacerbate systemic inflammation and autonomic imbalance, resulting in broader dysregulation of the brain–heart–gut axis. This study aimed to synthesize contemporary evidence on chronic MA exposure and its role in LVT formation, stroke pathogenesis, diagnostic approaches, and anticoagulation management. We conducted a focused narrative review of PubMed- and Scopus-indexed literature (1990–2025) addressing cardiovascular, neurovascular, and gut-mediated consequences of chronic MA exposure. Observational cohorts and case reports were integrated to characterize pathophysiology, imaging approaches, and therapeutic considerations, supplemented by a representative clinical case. Chronic MA exposure mediates persistent catecholamine excess, myocardial fibrosis, ventricular dysfunction, and a prothrombotic milieu. Gut dysbiosis-related inflammation and autonomic dysregulation further promote intracardiac stasis. Affected individuals are typically young men with severe systolic dysfunction (left ventricular ejection fraction 20–30%), with a substantial proportion demonstrating apical or mural LVT on systematic imaging. Case-level evidence highlights a broader systemic embolic burden, involving the limbs, kidneys, and aorta. Echocardiography remains the first-line screening method, while cardiac CT and MRI offer greater sensitivity for thrombus detection. Anticoagulation is challenged by bleeding risk, inconsistent adherence, and the absence of standardized protocols. MACM represents a critical and underrecognized etiology of cardioembolic stroke in young adults. Early recognition of brain–heart–gut axis disruption, systematic cardiac imaging, and individualized anticoagulation are crucial for preventing emboli. Prospective registries and standardized imaging-guided treatment strategies are needed to improve outcomes in this high-risk population. Full article
(This article belongs to the Special Issue Neurological Diseases: From Pathogenesis to Molecular Diagnosis and Treatment)
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