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New Insights into the Mechanisms of Neurodegeneration and Regeneration: From Bench to Bedside

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: 20 August 2026 | Viewed by 5959

Special Issue Editor

Dr. Irina Ivanova Stoyanova

E-Mail Website
Guest Editor
School of Medicine, European University of Cyprus, Frankfurt Branch, Frankfurt am Main, Germany
Interests: neuronal network; neuron; neuroplasticity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to shed greater light on the mechanisms of the degeneration and regeneration of nervous system components across the multidisciplinary field of neuroscience. Both processes, neurodegeneration and regeneration, involve complex and interconnected pathways, associated with changes in the internal microenvironment and cellular metabolism. Neurodegeneration is multifaceted, encompassing protein misfolding and aggregation, oxidative stress, mitochondrial dysfunction, neuroinflammation, and disorders of calcium homeostasis. On the contrary, nervous system regeneration implicates events observed during embryonal development: axonal regrowth, neurogenesis, and synaptogenesis, and alterations in synaptic plasticity. Contributions highlighting these aspects of the nervous system under normal and pathological conditions, as well as variations in brain development, are welcome. We encourage neuroscientists from many subfields to share their ideas, reviews, and original studies, with the hope that this Issue will provide a platform for debate on the etiology of neurodegenerative diseases, thus giving impetus to further identify and validate new therapeutic approaches to the plethora of neuropathological entities.

Dr. Irina Ivanova Stoyanova
Guest Editor

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Keywords

  • neurodegeneration
  • neuroregeneration
  • molecular neurobiology
  • brain development
  • developmental brain disorders
  • synaptogenesis
  • synaptic plasticity
  • cognitive neuroscience
  • neurotrauma

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Published Papers (4 papers)

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Research

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16 pages, 911 KB  
Article
Evaluation of the Telomere Length in Patients with Spinal Muscular Atrophy
by Betül Okur Altındaş, Sedat Öktem, Kürşat Bora Çarman and Mahmut Selman Yıldırım
Int. J. Mol. Sci. 2025, 26(22), 11223; https://doi.org/10.3390/ijms262211223 - 20 Nov 2025
Viewed by 967
Abstract
Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disorder caused by biallelic SMN1 gene loss, leading to motor neuron degeneration and progressive muscle weakness. The SMN protein is also implicated in telomerase biogenesis, suggesting a possible link between SMA and telomere regulation. [...] Read more.
Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disorder caused by biallelic SMN1 gene loss, leading to motor neuron degeneration and progressive muscle weakness. The SMN protein is also implicated in telomerase biogenesis, suggesting a possible link between SMA and telomere regulation. This study aimed to investigate relative telomere length in pediatric SMA patients and evaluate, for the first time, the potential effects of gene replacement therapy with onasemnogene abeparvovec. Relative telomere length was measured in peripheral blood lymphocytes using quantitative real-time PCR in 58 patients and 58 age- and sex-matched healthy controls. Of the patients, 19 had received gene replacement therapy. SMA patients without this treatment exhibited significantly shorter telomeres compared with controls (p = 0.029), whereas no significant difference was observed between gene-treated patients and controls (p = 0.108). Direct comparison revealed longer telomeres in treated patients than in untreated ones (p = 0.012). These findings indicate that telomere attrition is present in SMA and may be mitigated by gene replacement. While the exact contribution of telomere biology to SMA pathogenesis remains to be clarified, telomere length may represent a biomarker for disease severity and treatment response, as well as a potential therapeutic target in this disorder. Full article
(This article belongs to the Special Issue New Insights into the Mechanisms of Neurodegeneration and Regeneration: From Bench to Bedside)
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16 pages, 1915 KB  
Article
Correlation of DJ-1, GDF15, and MFGE8 Gene Expression with Clinicopathological Findings in Gliomas and Meningiomas
by Ayla Solmaz Avcikurt, Huseyin Utku Adilay, Omur Gunaldi, Sinem Gultekin Tosun and Salim Katar
Int. J. Mol. Sci. 2025, 26(18), 9194; https://doi.org/10.3390/ijms26189194 - 20 Sep 2025
Viewed by 1173
Abstract
In light of the growing significance of molecular biomarkers in central nervous system tumours, in this study, we aimed to comprehensively and quantitatively analyze the mRNA expression levels of DJ-1 (Parkinsonism-associated deglycase 7, PARK7), GDF15 (Growth Differentiation Factor 15), and MFGE8 (Milk [...] Read more.
In light of the growing significance of molecular biomarkers in central nervous system tumours, in this study, we aimed to comprehensively and quantitatively analyze the mRNA expression levels of DJ-1 (Parkinsonism-associated deglycase 7, PARK7), GDF15 (Growth Differentiation Factor 15), and MFGE8 (Milk Fat Globule-EGF Factor 8 Protein) in glioma and meningioma tissues and to thoroughly evaluate the associations between these gene expression profiles and clinicopathological parameters. Real-time PCR (qRT-PCR) analyses performed on tumour tissues obtained from a total of 27 glioma and 18 meningioma patients revealed that these three genes exhibited significantly elevated expression compared to control samples. Despite their different cellular origins, statistically significant positive correlations were observed between the expression levels of DJ-1, GDF15, and MFGE8 and both tumour grade and the Ki-67 proliferation index (Ki-67 Pi) in both glioma and meningioma cases, indicating that higher gene expression is associated with increased tumour aggressiveness in both tumour types. Receiver operating characteristic (ROC) curve analyses further confirmed the diagnostic and prognostic potential of these genes. Additionally, protein–protein interaction networks involving the target genes were characterised, providing valuable insights into their molecular mechanisms. These findings suggest that DJ-1, GDF15, and MFGE8 may play a role in the aggressiveness, invasion, and proliferation of gliomas and meningiomas. Moreover, integrating these genes as molecular biomarkers into tumour classification systems may provide a foundation for the development of personalised and targeted therapeutic strategies, although further studies are needed to support this. Full article
(This article belongs to the Special Issue New Insights into the Mechanisms of Neurodegeneration and Regeneration: From Bench to Bedside)
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Review

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21 pages, 1014 KB  
Review
Insights into the Impact of Low-Dose Ionizing Radiation on Neurodegenerative Disease Progression in In Vivo Models
by Valeria V. Goloborshcheva, Yana S. Kostikova, Valerian G. Kucheryanu, Sergei G. Morozov and Viktor S. Kokhan
Int. J. Mol. Sci. 2026, 27(8), 3368; https://doi.org/10.3390/ijms27083368 - 9 Apr 2026
Viewed by 524
Abstract
The effective treatment of neurodegenerative diseases (NDDs), such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis, remains a critical challenge in modern medicine. Given the limitations of current therapies, alternative strategies to slow neurodegeneration are urgently needed. This study presents a critical [...] Read more.
The effective treatment of neurodegenerative diseases (NDDs), such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis, remains a critical challenge in modern medicine. Given the limitations of current therapies, alternative strategies to slow neurodegeneration are urgently needed. This study presents a critical review of the current evidence regarding low-dose ionizing radiation (IR) as a promising modality for modulating neurodegenerative processes. This study examines current experimental data on the effects of low-dose IR (LDIR) on cellular protective and compensatory mechanisms, including evidence from in vivo models of NDDs. Our analysis demonstrates that LDIR enhances antioxidant activity and DNA repair, stimulates autophagy and neuroplasticity, and modulates neuroinflammatory signaling. Collectively, these findings support the hypothesis of the neuroprotective potential of LDIR, underscoring its translational viability provided that strict dosimetric guidelines are followed and individual biological responses are rigorously monitored. Full article
(This article belongs to the Special Issue New Insights into the Mechanisms of Neurodegeneration and Regeneration: From Bench to Bedside)
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18 pages, 5597 KB  
Review
The Determinant of Tau Spreading in Alzheimer’s Disease: Dependent on Senile Plaque, Neural Circuits, or Spatial Proximity?
by Yuichi Riku, Jean-Pierre Brion, Kunie Ando, Toshiki Uchihara and Yasushi Iwasaki
Int. J. Mol. Sci. 2025, 26(24), 12088; https://doi.org/10.3390/ijms262412088 - 16 Dec 2025
Viewed by 1679
Abstract
Alzheimer’s disease (AD) is neuropathologically characterized by tau-immunopositive neurofibrillary tangles (NFTs) and amyloid-β (Aβ)-immunopositive senile plaques. According to the widely accepted amyloid cascade hypothesis, Aβ pathology represents the upstream event in AD pathophysiology and induces tau aggregation. However, numerous studies have suggested that [...] Read more.
Alzheimer’s disease (AD) is neuropathologically characterized by tau-immunopositive neurofibrillary tangles (NFTs) and amyloid-β (Aβ)-immunopositive senile plaques. According to the widely accepted amyloid cascade hypothesis, Aβ pathology represents the upstream event in AD pathophysiology and induces tau aggregation. However, numerous studies have suggested that tau aggregates correlate more closely with neuronal loss and regional brain atrophy than with Aβ depositions. Tau aggregation in AD demonstrates a hierarchical spreading pattern beginning in the transentorhinal cortex, but the mechanisms underlying this spreading manner of lesions remain to be elucidated. This review aims to address current controversies regarding tau pathology in AD from the perspectives of both the ‘amyloid cascade’ and ‘tauopathy’ hypotheses. From the ‘amyloid cascade’ viewpoint, Aβ deposition prominently involves distal axon and axon terminals, and in some regions, there are anatomical correspondences between axonal Aβ pathology and cytoplasmic tau aggregations (e.g., a close relationship between senile plaques in the molecular layer of the hippocampal dentate gyrus and NFTs in the transentorhinal cortex). Nevertheless, this model cannot explain the whole body of hierarchical spreading of tau aggregation because notable spaciotemporal discrepancies also exist in many regions. From the ‘tauopathy’ perspective, the distribution of tau aggregates in AD involves key nodes within the memory circuits. Also, experimental studies have suggested that patient-derived tau exhibits seeding and neuron-to-neuron propagation properties. Interestingly, tau aggregation in AD appears to spread laterally in a proximity-dependent, cortico-cortical fashion rather than along long-range memory circuits. This contrasts with the system-selective, poly-nodal degenerations seen in four-repeat tauopathies, amyotrophic lateral sclerosis, or spinocerebellar degenerations. Moreover, the proportions of three-repeat and four-repeat isoforms shift during the maturation of NFTs in AD. Overall, spreading patterns of tau-pathology in AD cannot be fully explained by Aβ pathology and also differ from the system degeneration seen in other tauopathies. Full article
(This article belongs to the Special Issue New Insights into the Mechanisms of Neurodegeneration and Regeneration: From Bench to Bedside)
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