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Molecular Research on the Neurodegenerative Diseases
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Molecular Research on the 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: 20 February 2025 | Viewed by 6334

Special Issue Editors

Dr. Laszlo Bodai

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, Faculty of Science and Informatics, University of Szeged, Szeged, Hungary
Interests: molecular pathogenesis of neurodegeneration; Huntington’s disease; Alzheimer’s disease; transcriptomics; miRNAs; epigenetic regulation of transcription; histone variants and histone modifications; animal models
Special Issues, Collections and Topics in MDPI journals
Dr. Nora Zsindely

E-Mail Website
Guest Editor
Department of Genetics, Faculty of Science and Informatics, University of Szeged, Szeged, Hungary
Interests: genetics; gene expression regulation; chromatin biology; histone modifications; transcriptomics

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are severe conditions that cause cognitive decline, psychiatric symptoms, and/or movement disturbances, potentially culminating in fatality. Considering that age is a pivotal risk factor in the prevalent types of these disorders, their occurrence is expected to rise with the increasing life expectancy of today’s aging populations. Projections suggest that the global number of individuals affected by dementia will surpass 60 million by 2030 and exceed 110 million by 2050. Consequently, these disorders pose a substantial and growing health and economic burden.

The most common neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease, typically occur sporadically, while others follow an inherited Mendelian pattern. However, it can generally be stated that the pathomechanisms of neurodegenerative disorders are complex, encompassing numerous fundamental biological processes at the molecular and cellular levels. These affected processes include, among others, proteostasis, transcription, mitochondrial function, and intra- and intercellular signalling. An enhanced understanding of the roles played by these molecular mechanisms in pathology is crucial when aiming to develop much-needed causative therapies.

The objective of this Special Issue is to spotlight recent advances in investigating the molecular basis of neurodegenerative disorders’ pathology and explore the potential therapeutic applications of these mechanisms. We welcome the submission of original scientific research and review articles for this Special Issue.

Dr. Laszlo Bodai
Dr. Nora Zsindely
Guest Editors

Manuscript Submission Information

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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.

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Keywords

  • neurodegeneration
  • neurodegenerative disorders
  • Alzheimer’s disease
  • Parkinson’s disease
  • polyglutamine diseases
  • amyotrophic lateral sclerosis
  • multiple sclerosis
  • molecular pathomechanisms
  • pathogenesis

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Published Papers (4 papers)

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Research

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22 pages, 27347 KiB  
Article
Chronic Oxidative Stress and Stress Granule Formation in UBQLN2 ALS Neurons: Insights into Neuronal Degeneration and Potential Therapeutic Targets
by Ao Gu, Yiti Zhang, Jianfeng He, Mingri Zhao, Lingjie Ding, Wanxi Liu, Jianing Xiao, Jiali Huang, Mujun Liu and Xionghao Liu
Int. J. Mol. Sci. 2024, 25(24), 13448; https://doi.org/10.3390/ijms252413448 - 15 Dec 2024
Viewed by 963
Abstract
The pathogenesis of neurodegenerative diseases results from the interplay between genetic and environmental factors. Aging and chronic oxidative stress are critical contributors to neurodegeneration. UBQLN2, a ubiquitin-related protein, aids in protein degradation and protects against oxidative stress. In ALS neurons harboring UBQLN2 mutations, [...] Read more.
The pathogenesis of neurodegenerative diseases results from the interplay between genetic and environmental factors. Aging and chronic oxidative stress are critical contributors to neurodegeneration. UBQLN2, a ubiquitin-related protein, aids in protein degradation and protects against oxidative stress. In ALS neurons harboring UBQLN2 mutations, oxidative stress accelerates pathological changes, yet the precise mechanisms remain unclear. Using induced motor neurons (iMNs) derived from UBQLN2 P497H iPSCs, we observed ALS-like phenotypes, including TDP-43 mislocalization, increased cell death, and reduced viability. Sodium arsenite (SA)-induced oxidative stress triggered stress granule formation, while autophagy dysfunction exacerbated neuronal degeneration. CHX and bosutinib treatments reduced ubiquitinated protein accumulation and alleviated degeneration, highlighting potential therapeutic pathways. These findings emphasize the role of chronic oxidative stress and stress granule formation in UBQLN2 ALS, offering insights into novel therapeutic targets. Full article
(This article belongs to the Special Issue Molecular Research on the Neurodegenerative Diseases)
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22 pages, 3679 KiB  
Article
IRE1/JNK Is the Leading UPR Pathway in 6-OHDA-Induced Degeneration of Differentiated SH-SY5Y Cells
by Natalia Siwecka, Grzegorz Galita, Zuzanna Granek, Wojciech Wiese, Ireneusz Majsterek and Wioletta Rozpędek-Kamińska
Int. J. Mol. Sci. 2024, 25(14), 7679; https://doi.org/10.3390/ijms25147679 - 12 Jul 2024
Cited by 2 | Viewed by 1506
Abstract
Parkinson’s disease (PD) is a neurodegenerative disorder which affects dopaminergic neurons of the midbrain. Accumulation of α-synuclein or exposure to neurotoxins like 6-hydroxydopamine (6-OHDA) induces endoplasmic reticulum (ER) stress along with the unfolded protein response (UPR), which executes apoptosis via activation of PERK/CHOP [...] Read more.
Parkinson’s disease (PD) is a neurodegenerative disorder which affects dopaminergic neurons of the midbrain. Accumulation of α-synuclein or exposure to neurotoxins like 6-hydroxydopamine (6-OHDA) induces endoplasmic reticulum (ER) stress along with the unfolded protein response (UPR), which executes apoptosis via activation of PERK/CHOP or IRE1/JNK signaling. The present study aimed to determine which of these pathways is a major contributor to neurodegeneration in an 6-OHDA-induced in vitro model of PD. For this purpose, we have applied pharmacological PERK and JNK inhibitors (AMG44 and JNK V) in differentiated SH-SY5Y cells exposed to 6-OHDA. Inhibition of PERK and JNK significantly decreased genotoxicity and improved mitochondrial respiration, but only JNK inhibition significantly increased cell viability. Gene expression analysis revealed that the effect of JNK inhibition was dependent on a decrease in MAPK10 and XBP1 mRNA levels, whereas inhibition of either PERK or JNK significantly reduced the expression of DDIT3 mRNA. Western blot has shown that JNK inhibition strongly induced the XBP1s protein, and inhibition of each pathway attenuated the phosphorylation of eIF2α and JNK, as well as the expression of CHOP. Collectively, our data suggests that targeting the IRE1/JNK pathway of the UPR is a more effective option for PD treatment as it simultaneously affects more than one pro-apoptotic pathway. Full article
(This article belongs to the Special Issue Molecular Research on the Neurodegenerative Diseases)
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Review

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17 pages, 2485 KiB  
Review
Small Molecules, α-Synuclein Pathology, and the Search for Effective Treatments in Parkinson’s Disease
by Gian Pietro Sechi and M. Margherita Sechi
Int. J. Mol. Sci. 2024, 25(20), 11198; https://doi.org/10.3390/ijms252011198 - 18 Oct 2024
Cited by 1 | Viewed by 1401
Abstract
Parkinson’s disease (PD) is a progressive age-related neurodegenerative disorder affecting millions of people worldwide. Essentially, it is characterised by selective degeneration of dopamine neurons of the nigro-striatal pathway and intraneuronal aggregation of misfolded α-synuclein with formation of Lewy bodies and Lewy neurites. Moreover, [...] Read more.
Parkinson’s disease (PD) is a progressive age-related neurodegenerative disorder affecting millions of people worldwide. Essentially, it is characterised by selective degeneration of dopamine neurons of the nigro-striatal pathway and intraneuronal aggregation of misfolded α-synuclein with formation of Lewy bodies and Lewy neurites. Moreover, specific small molecules of intermediary metabolism may have a definite pathophysiological role in PD. These include dopamine, levodopa, reduced glutathione, glutathione disulfide/oxidised glutathione, and the micronutrients thiamine and ß-Hydroxybutyrate. Recent research indicates that these small molecules can interact with α-synuclein and regulate its folding and potential aggregation. In this review, we discuss the current knowledge on interactions between α-synuclein and both the small molecules of intermediary metabolism in the brain relevant to PD, and many other natural and synthetic small molecules that regulate α-synuclein aggregation. Additionally, we analyse some of the relevant molecular mechanisms potentially involved. A better understanding of these interactions may have relevance for the development of rational future therapies. In particular, our observations suggest that the micronutrients ß-Hydroxybutyrate and thiamine might have a synergistic therapeutic role in halting or reversing the progression of PD and other neuronal α-synuclein disorders. Full article
(This article belongs to the Special Issue Molecular Research on the Neurodegenerative Diseases)
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16 pages, 2327 KiB  
Review
The Role of miR-137 in Neurodegenerative Disorders
by László Bodai, Roberta Borosta, Ágnes Ferencz, Mercédesz Kovács and Nóra Zsindely
Int. J. Mol. Sci. 2024, 25(13), 7229; https://doi.org/10.3390/ijms25137229 - 30 Jun 2024
Viewed by 1820
Abstract
Neurodegenerative diseases affect an increasing part of the population of modern societies, burdening healthcare systems and causing immense suffering at the personal level. The pathogenesis of several of these disorders involves dysregulation of gene expression, which depends on several molecular processes ranging from [...] Read more.
Neurodegenerative diseases affect an increasing part of the population of modern societies, burdening healthcare systems and causing immense suffering at the personal level. The pathogenesis of several of these disorders involves dysregulation of gene expression, which depends on several molecular processes ranging from transcription to protein stability. microRNAs (miRNAs) are short non-coding RNA molecules that modulate gene expression by suppressing the translation of partially complementary mRNAs. miR-137 is a conserved, neuronally enriched miRNA that is implicated in neurodegeneration. Here, we review the current body of knowledge about the role that miR-137 plays in five prominent neurodegenerative disorders, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and multiple sclerosis. The presented data indicate that, rather than having a general neuroprotective role, miR-137 modulates the pathology of distinct disorders differently. Full article
(This article belongs to the Special Issue Molecular Research on the Neurodegenerative Diseases)
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