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Advances in Molecular Pathobiology, Diagnosis, and Treatment of Neurodegenerative Diseases

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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 (30 June 2026) | Viewed by 2247

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Editors

Prof. Dr. Saak V. Ovsepian

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Guest Editor

1. Faculty of Engineering and Science, University of Greenwich, Chatham Maritime, London ME4 4TB, UK
2. Faculty of Medicine, Tbilisi State University, 0177 Tbilisi, Georgia
Interests: synaptic physiology; transmitter release; beta amyloid; neuroimaging; calcium imaging; optogenetics; neurodegenerative disease; depression; dendritic spine; synaptic plasticity
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Stergios Boussios

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Guest Editor

1. Department of Medical Oncology, Ioannina University Hospital, Ioannina, Greece
2. Faculty of Medicine, School of Health Sciences, University of Ioannina, Ioannina, Greece
3. AELIA Organization, 9th Km Thessaloniki-Thermi, 57001 Thessaloniki, Greece
4. Faculty of Medicine, Health and Social Care, Canterbury Christ Church University, Canterbury, UK
5. School of Cancer and Pharmaceutical Sciences, Faculty of Life Sciences and Medicine, King's College London, London, UK
6. Kent and Medway Medical School, University of Kent, Canterbury, UK
7. Department of Research and Innovation, Medway NHS Foundation Trust, Gillingham, UK
Interests: prostate cancer; renal cancer; ovarian cancer; homologous recombination of DNA; PARP inhibitors; cervical cancer; carcinoma of unknown primary; colorectal cancer; cancer and autoimmune diseases; biomarkers
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Dr. Jaison Jeevanandam

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Guest Editor

Experimental Neurobiology Group, National Institute of Mental Health, Klecany, Czech Republic
Interests: metal oxide nanoparticles; phytochemistry; diabetes treatment; nanochemistry; bionanomaterials
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue will highlight recent advances in molecular studies of the pathobiology, diagnosis, and treatment of neurodegenerative diseases. The focus is on the most prevalent conditions, including Alzheimer’s disease and related dementias, Parkinson’s disease and dementia with Lewy bodies, and motor neuron diseases.

The Issue will bring together reviews, hypotheses, and perspectives that address

Mechanistic advances in disease pathology;
Progress and challenges in diagnostics and early detection;
Developments in molecular therapies, including outstanding questions and challenges.

We invite comprehensive, balanced, and up to date contributions from experts working across these domains.

Prof. Dr. Saak V. Ovsepian
Prof. Dr. Stergios Boussios
Dr. Jaison Jeevanandam
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. 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
Alzheimer’s disease
Parkinson’s disease
dementia with Lewy bodies
motor neuron diseases
molecular pathobiology
diagnosis
treatment

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Published Papers (3 papers)

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Research

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20 pages, 519 KB

Open AccessArticle

A Multi-Locus and Machine Learning-Based Assessment of SNCA Variants in Alzheimer’s Disease

by Hatice Segmen and Mustafa Yildiz

Int. J. Mol. Sci. 2026, 27(11), 5143; https://doi.org/10.3390/ijms27115143 - 5 Jun 2026

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Abstract

This study investigates the role of single nucleotide polymorphisms (SNPs) in the SNCA gene, encoding alpha-synuclein, in Alzheimer’s disease (AD). A case–control study was conducted including 95 AD patients and 97 healthy controls. Four SNCA polymorphisms (rs2583988, rs2619363, rs2619364, rs10005233) were analyzed using logistic regression, haplotype estimation, genotype combination analysis, and Random Forest modeling. Significant associations were identified for rs2583988, rs2619364, and rs2619363, while rs10005233 showed no association. The rs2583988 C allele and rs2619364 G allele were more frequent in patients, suggesting increased disease risk. Linkage disequilibrium analysis revealed weak correlations (low r²), indicating largely independent genetic effects. Multivariate logistic regression showed that clinical parameters, rather than genetic variants, were independently associated with AD. Multi-locus genotype analysis demonstrated that specific SNP combinations were linked to increased disease risk. Firth regression confirmed associations in low-frequency genotypes. The outcomes derived from the Random Forest methodology were classified as exploratory and not as proof of clinical predictive utility, attributed to the limited sample size, the absence of external validation, and the educational imbalance. Ordinal logistic regression indicated no association between SNCA variants and cognitive severity, while education had a protective effect. The selected SNCA variants showed exploratory associations with AD in this cohort; however, they failed to maintain their validity as independent predictors in multivariate logistic regression analysis. Before drawing any conclusions regarding screening or risk stratification, these findings require independent replication, correction for multiple testing and functional validation. Full article

(This article belongs to the Special Issue Advances in Molecular Pathobiology, Diagnosis, and Treatment of Neurodegenerative Diseases)

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19 pages, 4674 KB

Open AccessArticle

Fluoxetine Repurposing Mitigates Alzheimer’s Disease Pathology via the GSK3β–CREB–ADAM10 Axis

by Soo-Ho Lee, Yeonghoon Son, Hyosun Jang, Hyun-Yong Kim, Kwang Seok Kim, Hyun-Shik Lee and Hae-June Lee

Int. J. Mol. Sci. 2026, 27(6), 2676; https://doi.org/10.3390/ijms27062676 - 14 Mar 2026

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Abstract

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder in the aging population. Drug repurposing provides a cost-effective strategy to identify novel therapeutics that may mitigate age-associated pathologies. Here, we report the therapeutic potential of fluoxetine, a selective serotonin reuptake inhibitor commonly used as an antidepressant, in alleviating cognitive impairment and AD-like pathology in 5xFAD mice, a transgenic model of familial AD. Chronic fluoxetine administration significantly ameliorated anxiety-like behavior and cognitive deficits in 5xFAD mice, as assessed by open field, Y-maze, and novel object recognition tests. Fluoxetine treatment was associated with reduced amyloid plaque deposition in the hippocampus and cortex, attenuation of microglial activation, and decreased expression of inflammatory cytokines. At the molecular level, fluoxetine increased phosphorylation of GSK3β at Ser9, which was associated with enhanced CREB phosphorylation and upregulation of the α-secretase ADAM10. These effects were further examined in SH-SY5Y neuronal cells, where CREB phosphorylation and ADAM10 expression were significantly modulated by GSK3β inhibition, whereas CaMKII inhibition had no detectable effect under our experimental conditions. Our findings suggest that fluoxetine modulates amyloid-associated signaling pathways in the 5xFAD model, in part through regulation of the GSK3β-CREB signaling framework. These results provide mechanistic insight into how fluoxetine may influence APP processing in an amyloid-driven pathological context, although further studies are required to clarify its translational implications in human AD. Full article

(This article belongs to the Special Issue Advances in Molecular Pathobiology, Diagnosis, and Treatment of Neurodegenerative Diseases)

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Review

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32 pages, 1482 KB

Open AccessReview

The Role of the Ketogenic Diet in Modulating Biochemical Pathophysiology in Psychiatric and Neurodegenerative Disorders

by Yoo Been Chang and James D. Baleja

Int. J. Mol. Sci. 2026, 27(11), 4932; https://doi.org/10.3390/ijms27114932 - 29 May 2026

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Abstract

The ketogenic diet, a high-fat and low-carbohydrate diet, has potential therapeutic effects on various neurological and psychiatric disorders. The diet shifts the body’s energy production in the form of adenosine triphosphate from using glucose to fats. The increased fatty acid β-oxidation results in the production of ketone bodies. This metabolic adaptation changes cellular bioenergetics, especially in the brain, which is highly reliant on energy metabolism. Schizophrenia, a psychotic disorder, and bipolar disorder, a mood disorder, are distinct psychiatric illnesses that can both involve disturbances in mood, cognition, and perception. These disturbances differ in prominence and clinical significance between the two conditions. Although the underlying mechanisms behind each disorder vary, they share some common pathophysiology, such as imbalances in the neurotransmitter system, mitochondrial dysfunction, and oxidative stress. Alzheimer’s disease, a neurodegenerative disorder marked by progressive cognitive decline, shares similar cellular disruptions, along with additional pathological features such as neuroinflammation and neuronal death. Recent studies suggest that the ketogenic diet may exert therapeutic effects by modulating underlying biochemical pathways. Its ability to reduce oxidative stress, improve mitochondrial function, and stabilize neurotransmitter balance may help alleviate symptoms and potentially slow disease progression. Full article

(This article belongs to the Special Issue Advances in Molecular Pathobiology, Diagnosis, and Treatment of Neurodegenerative Diseases)

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