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Applied Sciences
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Diagnosis and Pharmacological Treatment of Neurological Diseases
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Diagnosis and Pharmacological Treatment of Neurological Diseases

A special issue of Applied Sciences (ISSN 2076-3417). This special issue belongs to the section "Applied Biosciences and Bioengineering".

Deadline for manuscript submissions: 20 September 2026 | Viewed by 1883

Editors

Dr. Amalia Cornea

E-Mail Website
Guest Editor
Department of Neuroscience, “Victor Babes” University of Medicine and Pharmacy, 300041 Timisoara, Romania
Interests: demyelinating and autoimmune disease; polyneuropathies
Special Issues, Collections and Topics in MDPI journals
Dr. Alina Florina Serb

E-Mail Website
Guest Editor
Department of Biochemistry and Pharmacology, “Victor Babes” University of Medicine and Pharmacy, 300041 Timisoara, Romania
Interests: neurosciences; neuro-oncology; omics; neurodegenerative diseases; autoimmune neuropathies; biomedical mass spectrometry; biochemistry
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurological disorders represent a significant global health challenge that impacted nearly 3.4 billion people in 2021 and contribute significantly to disability and mortality. They encompass a wide range of conditions—including neurodegenerative, demyelinating, autoimmune, infectious, vascular, neuromuscular, and developmental disorders—that often present with overlapping symptoms, making timely and accurate diagnosis essential.

Neurological diagnosis is often complex and challenging due to the wide variety of symptoms and overlapping clinical presentations, which require assessments of anatomical and physiological functions and functional capacity.

This Special Issue welcomes original research, reviews, and case studies focusing on but not limited to the following topics:

  • Diagnostic precision: The integration of new and advanced assessment tools, such as imaging modalities and biomarkers, into clinical routine;
  • Differential diagnosis: Methods to distinguish between overlapping syndromes and to improve clinical decision-making;
  • Therapeutic approaches: Pharmacological, immunomodulatory, interventional, and multidisciplinary strategies tailored to address patient-specific needs, including innovative techniques, such as gene and RNA therapies, neuro and immunomodulation.

We welcome articles that aim to improve patients' outcomes through strategies that promote personalised and innovative care models.

Dr. Amalia Cornea
Dr. Alina Florina Serb
Guest Editors

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. Applied Sciences is an international peer-reviewed open access semimonthly 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

  • neurodegenerative disorders
  • demyelinating disorders
  • epilepsy
  • neuromuscular disorders
  • neuroinfectious diseases
  • brain and spinal cord tumours
  • pharmacological therapies
  • immunomodulation
  • immunosuppression
  • interventional therapies
  • biomarkers
  • MRI
  • cerebrospinal fluid

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Published Papers (3 papers)

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Research

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11 pages, 420 KB  
Article
Exploring the Potential Role of CYP2C19 Genetic Variability in Cenobamate Treatment
by Giovanni Falcicchio, Valeria Delmonte, Teresa Francavilla, Alessandro Introna, Maria Addolorata Mariggiò, Mariella Pafundi, Mirko Perrone, Angela Vinella and Emilio Russo
Appl. Sci. 2026, 16(11), 5679; https://doi.org/10.3390/app16115679 - 5 Jun 2026
Viewed by 386
Abstract
Background: Cenobamate is a novel antiseizure medication with potential interactions involving cytochrome P450 enzymes, including CYP2C19. Genetic variability in CYP2C19 may influence drug metabolism and tolerability, although its clinical relevance in cenobamate-treated patients remains unclear. Methods: We conducted a single-center retrospective study including [...] Read more.
Background: Cenobamate is a novel antiseizure medication with potential interactions involving cytochrome P450 enzymes, including CYP2C19. Genetic variability in CYP2C19 may influence drug metabolism and tolerability, although its clinical relevance in cenobamate-treated patients remains unclear. Methods: We conducted a single-center retrospective study including 48 adults with drug-resistant epilepsy treated with cenobamate. Patients were stratified by concomitant use of CYP2C19-substrate ASMs (patients with CYP2C19 substrates vs. patients without CYP2C19 substrates). CYP2C19 genotype was classified into metabolizer phenotypes. Adverse events (AEs) were categorized as potentially CYP-mediated or likely unrelated to CYP-mediated pharmacokinetic mechanisms based on clinical assessment, temporal association, and known pharmacological interaction profiles. Associations were explored using descriptive statistics and regression models. Results: Overall, 58.3% of patients received CYP2C19-substrate ASMs. AEs were more frequent among patients with CYP2C19 substrates (71.4% vs. 20.0%; p = 0.001), with potentially CYP-mediated AEs observed only in this group (32.1% vs. 0%; p < 0.001). Intermediate metabolizers showed a higher proportion of potentially CYP-mediated AEs (87.5%; p < 0.001). This pattern was not observed in patients without CYP2C19 substrates. Regression analyses suggested increased risk in intermediate metabolizers, although estimates were imprecise and should be considered exploratory. Conclusions: An exploratory association between CYP2C19 variability and AE occurrence was observed in patients treated with cenobamate combined mainly with clobazam and other CYP2C19-substrate ASMs. Intermediate metabolizers may represent a higher-risk subgroup, but these preliminary findings require prospective confirmation with pharmacokinetic monitoring. Full article
(This article belongs to the Special Issue Diagnosis and Pharmacological Treatment of Neurological Diseases)
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12 pages, 533 KB  
Article
Peripheral Blood Cell Ratios: Promising Predictive Biomarkers for the Diagnosis of Pediatric Autoimmune Encephalitis
by Andreea Bianca Dabu, Dana Craiu, Cristina Pomeran, Diana Gabriela Barca, Carmen Sandu, Cristina Motoescu, Alice Dica, Catrinel Mihaela Iliescu and Alexandru Ștefan Niculae
Appl. Sci. 2026, 16(9), 4522; https://doi.org/10.3390/app16094522 - 4 May 2026
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Abstract
Background: Autoimmune encephalitis (AE) is an increasingly well recognized disorder in the past decade both in adults and in children, yet pediatric data are still limited. A full peripheral blood cell count is a routine examination that provides valuable information regarding the immune [...] Read more.
Background: Autoimmune encephalitis (AE) is an increasingly well recognized disorder in the past decade both in adults and in children, yet pediatric data are still limited. A full peripheral blood cell count is a routine examination that provides valuable information regarding the immune system. Thus, there are peripheral blood cell count (PBCC)-derived ratios that reflect systemic inflammatory activity and they have been associated with disease severity in adults: the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR), systemic immune–inflammation index (SII), systemic inflammation response index (SIRI), and aggregate index of systemic inflammation (AISI). Methods: This study is a retrospective chart review of children under 18 years diagnosed with definite or probable AE and treated in our institution from 1 January 2018 until 1 December 2025. Only patients with available PBCC results at the time of the first hospital admission after neurological/psychiatric symptom onset were included. An age-matched control group was created by selecting the results of PBCC of patients presenting for routine pediatric follow-ups with normal inflammatory and hematologic parameters. The group means were compared using an independent-samples t-test or the Mann–Whitney U test for non-normally distributed data. Analysis of the receiver operating characteristics curve (ROC curve) was conducted, followed by the area under the curve ROC curve (AUC). Results: A total of 45 children with AE and 150 controls were included in the study. Of these, 22 patients (49%) had probable AE and 23 patients (51%) had definite AE. The NLR, PLR, SII, SIRI and AISI values were significantly higher in AE patients compared with the controls, but the AUC values (~0.58–0.66) indicate poor-to-fair discriminative ability. Youden’s index-based cut-off values were associated with high specificity and modest sensitivity. The likelihood ratios in the range of 2–3 (LR+) and 0.6–0.7 (LR−) suggest weak rule-in capacity and limited rule-out utility. Conclusions: Our results suggest that at the time of the initial hospitalization, children with AE already show altered peripheral immune cell profiles compared to their age-matched peers. The high specificity and the low sensitivity of the inflammatory indices make them more suitable for supporting the AE diagnosis in suggestive clinical circumstances, but not for screening. These results represent a foundation for further investigation of the roles that these indices have both as diagnostic and prognostic factors for these children. Full article
(This article belongs to the Special Issue Diagnosis and Pharmacological Treatment of Neurological Diseases)

Review

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26 pages, 1281 KB  
Review
Relationship Between the Risk of Cardiovascular Disease and Mitochondrial Dysfunction
by Ida Manna, Annamaria Cerantonio, Federico Rocca, Antonio Cerasa, Luigi Citrigno and Domenico Bosco
Appl. Sci. 2026, 16(10), 4669; https://doi.org/10.3390/app16104669 - 8 May 2026
Viewed by 561
Abstract
Cardiovascular diseases (CVDs) remain a leading cause of death worldwide. Mitochondria, essential organelles within cells, play a crucial role in maintaining cardiovascular health by producing energy through ATP synthesis. The heart’s high energy demand makes it particularly sensitive to mitochondrial function. In CVDs, [...] Read more.
Cardiovascular diseases (CVDs) remain a leading cause of death worldwide. Mitochondria, essential organelles within cells, play a crucial role in maintaining cardiovascular health by producing energy through ATP synthesis. The heart’s high energy demand makes it particularly sensitive to mitochondrial function. In CVDs, mitochondrial adaptability is compromised, resulting in dysfunction characterized by impaired respiratory chain activity, decreased ATP production, oxidative stress, and structural damage. This review consolidates current research on mitochondrial roles in CVD development, focusing on mitochondrial respiration, ATP synthesis, and the processes involved in maintaining mitochondrial quality, such as mitophagy. It discusses the challenges in developing therapies aimed at restoring mitochondrial function, including drug delivery issues and targeting specificity. The assessment includes analysis of mitochondrial anomalies associated with cardiac disease progression and potential therapeutic strategies. Mitochondrial dysfunction contributes to the progression of various CVDs by reducing energy output and increasing oxidative stress, leading to cardiomyocyte injury and death. Damaged mitochondria produce excessive reactive oxygen species (ROS), exacerbating cellular damage. Repairing mitochondrial components, especially the respiratory chain and ATP synthesis pathways, has shown potential in mitigating cellular injury and improving cardiac function. Restoring mitochondrial function is vital for preventing and treating CVDs. Targeted therapies that repair mitochondrial respiratory activity and enhance ATP production may reduce cellular damage, promote cardiomyocyte survival, and improve clinical outcomes. Understanding mitochondrial dynamics offers promising avenues for innovative interventions in cardiovascular health management. Full article
(This article belongs to the Special Issue Diagnosis and Pharmacological Treatment of Neurological Diseases)
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