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Molecular Research of Neurodegenerative and Psychiatric Diseases, 2nd Edition
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Molecular Research of Neurodegenerative and Psychiatric Diseases, 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 January 2026 | Viewed by 7502

Special Issue Editor

Dr. Dubravka Švob Štrac

E-Mail Website
Guest Editor
Laboratory for Molecular Neuropsychiatry, Division of Molecular Medicine, Rudjer Boskovic Institute, Bijenicka cesta 54, 10 000 Zagreb, Croatia
Interests: molecular basis; genetics; psychiatric disorders; neurodegenerative diseases; pharmacogenetics; neurobiology; neuropharmacology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis and Huntington’s disease, as well as psychiatric diseases, such as schizophrenia, anxiety, depression and addictions, are multifactorial and heterogeneous disorders, which pose significant health, social and economic problems. Despite many studies, their complex etiology is still poorly understood, and therapeutic strategies are often limited to relieving their symptoms. The elucidation of their molecular background may contain keys for identifying risk factors, offering novel diagnostic or prognostic biomarkers, as well as providing novel and specific targets for their prevention and treatment. This Special Issue aims to present the most up-to-date findings regarding research targeting molecular mechanisms underlying different neurodegenerative and psychiatric diseases. It aims to provide a broad overview of novel advances in the field, including studies at the molecular, epi/genetic and cellular levels, but will also cover integrative, imaging and psychopharmacology research areas, as well as comprehensive omics approaches. We welcome the submission of studies using various preclinical in vitro and in vivo models, as well as clinical studies involving human subjects.

Dr. Dubravka Švob Štrac
Guest Editor

Manuscript Submission Information

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Keywords

  • neurodegenerative disorders
  • psychiatric diseases
  • biomarkers
  • therapeutic targets
  • omics approaches
  • molecular pathways
  • cell biology
  • animal models
  • clinical studies

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Published Papers (6 papers)

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13 pages, 2753 KiB  
Article
Evaluating the Causal Role of Genetically Inferred Immune Cells and Inflammatory Cytokines on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
by Lincheng Duan, Jingyi Yang, Junxin Zhao, Zhuoyang Chen, Hong Yang and Dingjun Cai
Biomedicines 2025, 13(5), 1200; https://doi.org/10.3390/biomedicines13051200 - 15 May 2025
Viewed by 1260
Abstract
Background/Objectives: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a multifaceted and diverse disorder with an ambiguous etiology. Recent evidence indicates that immune system impairment and inflammatory mechanisms are pivotal to the initiation and advancement of ME/CFS. Nonetheless, the causal relationships among these factors [...] Read more.
Background/Objectives: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a multifaceted and diverse disorder with an ambiguous etiology. Recent evidence indicates that immune system impairment and inflammatory mechanisms are pivotal to the initiation and advancement of ME/CFS. Nonetheless, the causal relationships among these factors remain inadequately comprehended. Methods: This study investigated the causative contributions of immunological dysfunction and inflammatory variables in ME/CFS utilizing genome-wide association study (GWAS) data. We employed Mendelian randomization (MR) to investigate associations between 91 inflammatory cytokines, 731 immune cell characteristics, and the risk of ME/CFS. Summary statistics for immune cell traits and inflammatory cytokines were sourced from European GWAS cohorts (n = 3757 and n = 14,824, respectively), while ME/CFS data were obtained from the UK Biobank (n = 462,933, including 2076 cases). We predominantly employed the inverse variance weighted (IVW) approach, complemented by MR-Egger, weighted median, BWMR, and MR-RAPS tests to guarantee robust and precise outcomes. Results: The study revealed significant causal links between various inflammatory factors, immune cell characteristics, and the risk of ME/CFS. Increased CXCL5 and CCL20 levels were significantly linked to a higher risk of ME/CFS, while elevated TNF levels were inversely related to ME/CFS risk. Furthermore, 13 immune cell characteristics were identified as having substantial causal associations with the likelihood of ME/CFS. These data are supportive of the causality that immune system dysfunction and inflammatory variables play a pivotal role in the development of ME/CFS. Conclusions: This study provides new insights into the causal role of immune system dysfunction in the development of ME/CFS, contributing to a deeper understanding of its underlying mechanisms. These results offer a foundation for identifying diagnostic biomarkers and developing targeted therapeutic strategies. Future research should validate these findings using multi-center cohort studies and further investigate the mechanisms behind key factors to enable the development of personalized treatment approaches. Full article
(This article belongs to the Special Issue Molecular Research of Neurodegenerative and Psychiatric Diseases, 2nd Edition)
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14 pages, 2269 KiB  
Article
Gene Polymorphisms of Parkinson’s Disease Risk Locus and Idiopathic REM Sleep Behavior Disorder
by Min Zhong, Yang Jiao, Aonan Zhao, Mengyue Niu, Jinjun Ran, Jun Liu and Yuanyuan Li
Biomedicines 2025, 13(4), 788; https://doi.org/10.3390/biomedicines13040788 - 24 Mar 2025
Viewed by 562
Abstract
Background/Objectives: Genetic factors play an important role in idiopathic rapid eye movement sleep behavior disorder (iRBD) but have not been fully studied. This study aimed to analyze the Parkinson’s disease (PD)-related genetic loci in iRBD in the southern Chinese population. Methods: [...] Read more.
Background/Objectives: Genetic factors play an important role in idiopathic rapid eye movement sleep behavior disorder (iRBD) but have not been fully studied. This study aimed to analyze the Parkinson’s disease (PD)-related genetic loci in iRBD in the southern Chinese population. Methods: In this study, we recruited 292 individuals with PD, 62 with iRBD, and 189 healthy controls (HC). Candidate genes were identified primarily from the Parkinson’s Progression Markers Initiative (PPMI) database. Genotypic and allele frequency analyses were conducted to compare the distribution across HC, iRBD, and PD groups. The effects of significant single-nucleotide polymorphisms (SNPs) on gene expression were examined. Clinical manifestations associated with different genotypes were also analyzed. The receiver operating characteristic (ROC) curve and Kaplan–Meier plots were utilized to further verify the diagnostic and predictive value of these SNPs. Results: We identified two significant SNPs associated with iRBD: rs13294100 of SH3GL2 and rs165599 of COMT. Clinical scale and polysomnography data analysis indicated that iRBD patients with the GA or AA genotype at the COMT rs165599 locus have lower RBDSQ scores and higher sleep efficiency. Moreover, we identified that COMT rs165599 and MCCC1 rs12637471 may play an important role in both PD and iRBD, while SNCA rs356181 was different between iRBD and PD. Conclusions: Our research revealed that in the southern Chinese demographic, genetic loci in SH3GL2 and COMT were linked to iRBD and may act as potential biomarkers for iRBD risk. Additionally, there is evidence suggesting a partial genetic overlap between iRBD and PD, indicating a shared genetic predisposition. Full article
(This article belongs to the Special Issue Molecular Research of Neurodegenerative and Psychiatric Diseases, 2nd Edition)
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17 pages, 1999 KiB  
Article
Understanding Causal Relationships Between Imaging-Derived Phenotypes and Parkinson’s Disease: A Mendelian Randomization and Observational Study
by Yichi Zhang, Min Zhong, Zhao Yang, Xiaojin Wang, Zhongxun Dong, Liche Zhou, Qianyi Yin, Bingshun Wang, Jun Liu, Yuanyuan Li and Mengyue Niu
Biomedicines 2025, 13(3), 747; https://doi.org/10.3390/biomedicines13030747 - 18 Mar 2025
Viewed by 644
Abstract
Background/Objectives: Observational studies have suggested a correlation between brain imaging alterations and Parkinson’s disease (PD). However, data on causal relationships are still lacking. This study aimed to examine the causal relationship between brain imaging-derived phenotypes (IDPs) and PD. Methods: A bidirectional two-sample Mendelian [...] Read more.
Background/Objectives: Observational studies have suggested a correlation between brain imaging alterations and Parkinson’s disease (PD). However, data on causal relationships are still lacking. This study aimed to examine the causal relationship between brain imaging-derived phenotypes (IDPs) and PD. Methods: A bidirectional two-sample Mendelian randomization analysis was conducted to explore the causal association between IDPs and PD. Summary-level data for IDPs (n = 39,691), PD (n = 482,730), and PD symptoms (n = 4093) were obtained from genome-wide association studies of European ancestry. Clinical validation was performed in an Asian cohort, which involved healthy controls (n = 81), patients with idiopathic rapid-eye-movement sleep behavior disorder (iRBD) (n = 47), and patients with PD (n = 85). Results: We found 13 IDPs with significant causal effects on PD and seven reciprocal effects of PD on IDPs. For instance, increased median T2star in the right caudate (odds ratio = 1.23, 95% confidence interval 1.08–1.40, p = 0.0057) and bilateral putamen (left: odds ratio = 1.25, 95% confidence interval 1.09–1.43, p = 0.0056; right: odds ratio = 1.25, 95% confidence interval 1.10–1.43, p = 0.0056) were associated with PD. Enlargement of the left thalamus (odds ratio = 1.50, 95% confidence interval 1.14–1.96, p = 0.016) demonstrated causal links with PD. No reverse causal effects were detected. Observational analyses results in the Asian cohort (healthy controls, iRBD, PD) aligned with the Mendelian randomization results. Conclusions: Our results suggest bidirectional causal links between IDPs and PD, offering insights into disease mechanisms and potential imaging biomarkers for PD. Full article
(This article belongs to the Special Issue Molecular Research of Neurodegenerative and Psychiatric Diseases, 2nd Edition)
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25 pages, 2329 KiB  
Article
Genomic Characterisation of the Relationship and Causal Links Between Vascular Calcification, Alzheimer’s Disease, and Cognitive Traits
by Emmanuel O. Adewuyi and Simon M. Laws
Biomedicines 2025, 13(3), 618; https://doi.org/10.3390/biomedicines13030618 - 3 Mar 2025
Viewed by 996
Abstract
Background/Objectives: Observational studies suggest a link between vascular calcification and dementia or cognitive decline, but the evidence is conflicting, and the underlying mechanisms are unclear. Here, we investigate the shared genetic and causal relationships of vascular calcification—coronary artery calcification (CAC) and abdominal aortic [...] Read more.
Background/Objectives: Observational studies suggest a link between vascular calcification and dementia or cognitive decline, but the evidence is conflicting, and the underlying mechanisms are unclear. Here, we investigate the shared genetic and causal relationships of vascular calcification—coronary artery calcification (CAC) and abdominal aortic calcification (AAC)—with Alzheimer’s disease (AD), and five cognitive traits. Methods: We analyse large-scale genome-wide association studies (GWAS) summary statistics, using well-regarded methods, including linkage disequilibrium score regression (LDSC), Mendelian randomisation (MR), pairwise GWAS (GWAS-PW), and gene-based association analysis. Results: Our findings reveal a nominally significant positive genome-wide genetic correlation between CAC and AD, which becomes non-significant after excluding the APOE region. CAC and AAC demonstrate significant negative correlations with cognitive performance and educational attainment. MR found no causal association between CAC or AAC and AD or cognitive traits, except for a bidirectional borderline-significant association between AAC and fluid intelligence scores. Pairwise-GWAS analysis identifies no shared causal SNPs (posterior probability of association [PPA]3 < 0.5). However, we find pleiotropic loci (PPA4 > 0.9), particularly on chromosome 19, with gene association analyses revealing significant genes in shared regions, including APOE, TOMM40, NECTIN2, and APOC1. Moreover, we identify suggestively significant loci (PPA4 > 0.5) on chromosomes 1, 6, 7, 9 and 19, implicating pleiotropic genes, including NAV1, IPO9, PHACTR1, UFL1, FHL5, and FOCAD. Conclusions: Current findings reveal limited genetic correlation and no significant causal associations of CAC and AAC with AD or cognitive traits. However, significant pleiotropic loci, particularly at the APOE region, highlight the complex interplay between vascular calcification and neurodegenerative processes. Given APOE’s roles in lipid metabolism, neuroinflammation, and vascular integrity, its involvement may link vascular and neurodegenerative disorders, pointing to potential targets for further investigation. Full article
(This article belongs to the Special Issue Molecular Research of Neurodegenerative and Psychiatric Diseases, 2nd Edition)
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19 pages, 3121 KiB  
Article
Neuroprotective Effects of Dehydroepiandrosterone Sulphate Against Aβ Toxicity and Accumulation in Cellular and Animal Model of Alzheimer’s Disease
by Barbara Vuic, Tina Milos, Erika Kvak, Marcela Konjevod, Lucija Tudor, Szidónia Farkas, Gordana Nedic Erjavec, Matea Nikolac Perkovic, Dora Zelena and Dubravka Svob Strac
Biomedicines 2025, 13(2), 432; https://doi.org/10.3390/biomedicines13020432 - 11 Feb 2025
Cited by 1 | Viewed by 1084
Abstract
Background/Objectives: Beneficial effects of neurosteroid dehydroepiandrosterone sulphate (DHEAS) on cognition, emotions and behavior have been previously reported, suggesting its potential in the prevention and treatment of various neuropsychiatric and neurodegenerative disorders, including Alzheimer’s disease (AD). This study aimed to investigate the potential neuroprotective [...] Read more.
Background/Objectives: Beneficial effects of neurosteroid dehydroepiandrosterone sulphate (DHEAS) on cognition, emotions and behavior have been previously reported, suggesting its potential in the prevention and treatment of various neuropsychiatric and neurodegenerative disorders, including Alzheimer’s disease (AD). This study aimed to investigate the potential neuroprotective actions of DHEAS against Aβ toxicity in both cellular and animal models of AD. Methods: After optimizing the AD model in vitro, we investigated the DHEAS effects on the viability and death of primary mouse neurons exposed to toxic Aβ42 oligomers for 24 h. In order to extend our research to an in vivo study, we further tested the acute effects of intraperitoneal DHEAS administration on the Aβ plaque density in different brain regions of 3xTg-AD mice, an animal model of AD. Results: In cell culture, DHEAS hampered the decrease in the neuronal viability caused by toxic Aβ oligomers, primarily by influencing mitochondrial function and apoptosis. DHEAS also counteracted the increase in the mRNA expression of selected genes (PI3K, Akt, Bcl2, Bax), induced in neuronal culture by treatment with Aβ42 oligomers. Obtained data suggested the involvement of mitochondria, caspases 3 and 7, as well as the PI3K/Akt and Bcl2 signaling network in the antiapoptotic properties of DHEAS in neurons. Forty-eight hours after DHEAS treatment, a significantly lower number of Aβ plaques was observed in the motor cortex but not in other brain areas of 3xTg-AD mice. Conclusions: Results indicated potential neuroprotective effects of DHEAS against Aβ toxicity and accumulation, suggesting that DHEAS supplementation should be further studied as a novel option for AD prevention and/or treatment. Full article
(This article belongs to the Special Issue Molecular Research of Neurodegenerative and Psychiatric Diseases, 2nd Edition)
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14 pages, 692 KiB  
Systematic Review
Fibromyalgia, Depression, and Autoimmune Disorders: An Interconnected Web of Inflammation
by Stefania Sedda, Maria Piera L. Cadoni, Serenella Medici, Elena Aiello, Gian Luca Erre, Alessandra Matilde Nivoli, Ciriaco Carru and Donatella Coradduzza
Biomedicines 2025, 13(2), 503; https://doi.org/10.3390/biomedicines13020503 - 18 Feb 2025
Cited by 1 | Viewed by 2103
Abstract
Background: Fibromyalgia, depression, and autoimmune diseases represent a triad of interconnected conditions characterized by overlapping biological pathways, including chronic inflammation, immune dysregulation, and neurochemical imbalances. Understanding their shared mechanisms offers opportunities for innovative therapeutic approaches. Objective: This systematic review explores the common inflammatory- [...] Read more.
Background: Fibromyalgia, depression, and autoimmune diseases represent a triad of interconnected conditions characterized by overlapping biological pathways, including chronic inflammation, immune dysregulation, and neurochemical imbalances. Understanding their shared mechanisms offers opportunities for innovative therapeutic approaches. Objective: This systematic review explores the common inflammatory- and immune-related pathways among these conditions, emphasizing their implications for biomarker development and novel therapeutic strategies. Methods: Following PRISMA guidelines, a comprehensive literature search was conducted in databases including PubMed, Scopus, Web of Science, and the Cochrane Library. Studies examining the relationship between fibromyalgia, depression, and autoimmune diseases with a focus on immune responses, inflammatory biomarkers, and therapeutic interventions were included. The quality of the selected studies was assessed using the Cochrane Risk of Bias tool. Results: From the 255 identified studies, 12 met the inclusion criteria. Evidence supports the role of pro-inflammatory cytokines (e.g., IL-6, TNF-α) and neurochemical dysregulation (e.g., serotonin, dopamine) as key factors in the pathophysiology of these conditions. Pilot studies highlight the potential of immune-modulating therapies, including low-dose IL-2 and anti-inflammatory agents such as N-acetylcysteine and minocycline, in alleviating both physical and psychological symptoms. Emerging biomarkers, including cytokine profiles and platelet serotonin activity, show promise for personalized treatment approaches. Conclusions: The shared inflammatory pathways linking fibromyalgia, depression, and autoimmune diseases underscore the need for integrated therapeutic strategies. Although pilot studies provide preliminary insights, validation through large-scale, multicenter trials is essential. Future research should focus on standardizing methodologies and leveraging biomarker-driven precision medicine to improve outcomes for patients with these complex, multifactorial conditions. Full article
(This article belongs to the Special Issue Molecular Research of Neurodegenerative and Psychiatric Diseases, 2nd Edition)
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