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

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: 30 June 2026 | Viewed by 444

Special Issue Editors


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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

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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
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

  1. Mechanistic advances in disease pathology;
  2. Progress and challenges in diagnostics and early detection;
  3. 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-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
  • Alzheimer’s disease
  • Parkinson’s disease
  • dementia with Lewy bodies
  • motor neuron diseases
  • molecular pathobiology
  • diagnosis
  • treatment

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Published Papers (1 paper)

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Research

19 pages, 4674 KB  
Article
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 [...] Read more.
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
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