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Molecular Mechanisms of Neurodegeneration 2023
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Molecular Mechanisms of Neurodegeneration 2023

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 (31 October 2023) | Viewed by 20967

Special Issue Editor

Prof. Dr. Hideaki Matsui

E-Mail Website
Guest Editor
Department of Neuroscience of Disease, Brain Research Institute, Niigata University, Niigata 951-8585, Japan
Interests: neurodegeneration; Parkinson's disease; aging; zebrafish; medaka; neuroscience; autism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases are diseases in which neurons are gradually lost for unknown causes, and include Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, spinocerebellar ataxia, multiple-system atrophy, and so on. Researchers, to date, have identified a considerable number of genes that cause familial diseases in addition to risk genes for sporadic diseases, and have also identified abnormal proteins that accumulate in cells. However, the pathogenesis of these diseases is still largely a mystery, and a fundamental cure is far from certain.

It is essential to elucidate the molecular pathogenesis of these neurodegenerative diseases beyond the causative genes and accumulated proteins in order to elucidate the pathophysiology of the diseases in the future. We open the Special Issue “Molecular Mechanisms of Neurodegeneration 2023” in the International Journal of Molecular Sciences (https://www.mdpi.com/journal/ijms, ISSN 1422-0067, IF 6.208, JCR Category Q1). Original manuscripts and reviews dealing with the molecular pathogenesis of neurodegeneration from outstanding experts on the topic are very welcome.

Prof. Dr. Hideaki Matsui
Guest Editor

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Keywords

  • neurodegenerative disease
  • Alzheimer’s disease
  • Parkinson’s disease
  • amyotrophic lateral sclerosis
  • spinocerebellar ataxia
  • multiple-system atrophy

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Published Papers (7 papers)

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Research

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15 pages, 3814 KiB  
Article
Controlling Gut Microbiota by Twendee X® May Contribute to Dementia Prevention
by Fukka You, Yoshiaki Harakawa, Toshikazu Yoshikawa and Haruhiko Inufusa
Int. J. Mol. Sci. 2023, 24(23), 16642; https://doi.org/10.3390/ijms242316642 - 23 Nov 2023
Cited by 2 | Viewed by 1553
Abstract
The human gut microbiota (GM) is a complex and dynamic ecosystem that hosts trillions of commensal and potentially pathogenic microorganisms. It is crucial in protecting humans from pathogens and in maintaining immune and metabolic homeostasis. Numerous studies have demonstrated that GM has a [...] Read more.
The human gut microbiota (GM) is a complex and dynamic ecosystem that hosts trillions of commensal and potentially pathogenic microorganisms. It is crucial in protecting humans from pathogens and in maintaining immune and metabolic homeostasis. Numerous studies have demonstrated that GM has a significant impact on health and disease, including Alzheimer’s disease (AD). AD is a progressive neurodegenerative disorder characterized by impaired short-term memory and cognitive deficits. Patients with AD have been reported to exhibit abnormalities in GM density and species composition. Oxidative stress (OS) has been implicated in the onset and progression of AD; however, the relationship between OS and gut microbiota in AD onset and progression is not clear. Twendee X® (TwX), an oral supplement consisting of eight active ingredients, has been shown to prevent dementia in mild cognitive impairment (MCI) in humans and substantially improve cognitive impairment in mouse models of AD. This positive effect is achieved through the potency of the combined antioxidants that regulate OS; therefore, similar results cannot be achieved by a single antioxidant ingredient. To examine the impact of long-term OS elevation, as seen in AD on the body and GM, we examined GM alterations during the initial OS elevation using a two-week OS loading rat model, and examined the effects of TwX on OS and GM. Furthermore, using a questionnaire survey and fecal samples, we analyzed the impact of TwX on healthy individuals’ gut bacteria and the associated effect on their quality of life (QOL). TwX was found to increase the number of bacteria species and their diversity in GM, as well as butyrate-producing bacteria, which tend to be reduced in AD patients. Additionally, TwX improved defecation condition and QOL. The gut bacteria function as part of the homeostatic function during OS elevation, and the prophylactic administration of TwX strengthened this function. The results suggest that the preventative effect of TwX on dementia may involve the GM, in addition to the other previously demonstrated effects. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neurodegeneration 2023)
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15 pages, 3511 KiB  
Article
Ablation of Death-Associated Protein Kinase 1 Changes the Transcriptomic Profile and Alters Neural-Related Pathways in the Brain
by Ruomeng Li, Shuai Zhi, Guihua Lan, Xiaotong Chen, Xiuzhi Zheng, Li Hu, Long Wang, Tao Zhang, Tae Ho Lee, Shitao Rao and Dongmei Chen
Int. J. Mol. Sci. 2023, 24(7), 6542; https://doi.org/10.3390/ijms24076542 - 31 Mar 2023
Cited by 5 | Viewed by 2361
Abstract
Death-associated protein kinase 1 (DAPK1), a Ca2+/calmodulin-dependent serine/threonine kinase, mediates various neuronal functions, including cell death. Abnormal upregulation of DAPK1 is observed in human patients with neurological diseases, such as Alzheimer’s disease (AD) and epilepsy. Ablation of DAPK1 expression and suppression [...] Read more.
Death-associated protein kinase 1 (DAPK1), a Ca2+/calmodulin-dependent serine/threonine kinase, mediates various neuronal functions, including cell death. Abnormal upregulation of DAPK1 is observed in human patients with neurological diseases, such as Alzheimer’s disease (AD) and epilepsy. Ablation of DAPK1 expression and suppression of DAPK1 activity attenuates neuropathology and behavior impairments. However, whether DAPK1 regulates gene expression in the brain, and whether its gene profile is implicated in neuronal disorders, remains elusive. To reveal the function and pathogenic role of DAPK1 in neurological diseases in the brain, differential transcriptional profiling was performed in the brains of DAPK1 knockout (DAPK1-KO) mice compared with those of wild-type (WT) mice by RNA sequencing. We showed significantly altered genes in the cerebral cortex, hippocampus, brain stem, and cerebellum of both male and female DAPK1-KO mice compared to those in WT mice, respectively. The genes are implicated in multiple neural-related pathways, including: AD, Parkinson’s disease (PD), Huntington’s disease (HD), neurodegeneration, glutamatergic synapse, and GABAergic synapse pathways. Moreover, our findings imply that the potassium voltage-gated channel subfamily A member 1 (Kcna1) may be involved in the modulation of DAPK1 in epilepsy. Our study provides insight into the pathological role of DAPK1 in the regulatory networks in the brain and new therapeutic strategies for the treatment of neurological diseases. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neurodegeneration 2023)
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Review

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32 pages, 1310 KiB  
Review
From Recognition to Remedy: The Significance of Biomarkers in Neurodegenerative Disease Pathology
by Corneliu Toader, Nicolaie Dobrin, Felix-Mircea Brehar, Constantin Popa, Razvan-Adrian Covache-Busuioc, Luca Andrei Glavan, Horia Petre Costin, Bogdan-Gabriel Bratu, Antonio Daniel Corlatescu, Andrei Adrian Popa and Alexandru Vlad Ciurea
Int. J. Mol. Sci. 2023, 24(22), 16119; https://doi.org/10.3390/ijms242216119 - 9 Nov 2023
Cited by 10 | Viewed by 3016
Abstract
With the inexorable aging of the global populace, neurodegenerative diseases (NDs) like Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) pose escalating challenges, which are underscored by their socioeconomic repercussions. A pivotal aspect in addressing these challenges lies in the [...] Read more.
With the inexorable aging of the global populace, neurodegenerative diseases (NDs) like Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) pose escalating challenges, which are underscored by their socioeconomic repercussions. A pivotal aspect in addressing these challenges lies in the elucidation and application of biomarkers for timely diagnosis, vigilant monitoring, and effective treatment modalities. This review delineates the quintessence of biomarkers in the realm of NDs, elucidating various classifications and their indispensable roles. Particularly, the quest for novel biomarkers in AD, transcending traditional markers in PD, and the frontier of biomarker research in ALS are scrutinized. Emergent susceptibility and trait markers herald a new era of personalized medicine, promising enhanced treatment initiation especially in cases of SOD1-ALS. The discourse extends to diagnostic and state markers, revolutionizing early detection and monitoring, alongside progression markers that unveil the trajectory of NDs, propelling forward the potential for tailored interventions. The synergy between burgeoning technologies and innovative techniques like -omics, histologic assessments, and imaging is spotlighted, underscoring their pivotal roles in biomarker discovery. Reflecting on the progress hitherto, the review underscores the exigent need for multidisciplinary collaborations to surmount the challenges ahead, accelerate biomarker discovery, and herald a new epoch of understanding and managing NDs. Through a panoramic lens, this article endeavors to provide a comprehensive insight into the burgeoning field of biomarkers in NDs, spotlighting the promise they hold in transforming the diagnostic landscape, enhancing disease management, and illuminating the pathway toward efficacious therapeutic interventions. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neurodegeneration 2023)
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28 pages, 992 KiB  
Review
Recent Mechanisms of Neurodegeneration and Photobiomodulation in the Context of Alzheimer’s Disease
by Matthew Su, Damir Nizamutdinov, Hanli Liu and Jason H. Huang
Int. J. Mol. Sci. 2023, 24(11), 9272; https://doi.org/10.3390/ijms24119272 - 25 May 2023
Cited by 9 | Viewed by 4131
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disease and the world’s primary cause of dementia, a condition characterized by significant progressive declines in memory and intellectual capacities. While dementia is the main symptom of Alzheimer’s, the disease presents with many other debilitating symptoms, and [...] Read more.
Alzheimer’s disease (AD) is a neurodegenerative disease and the world’s primary cause of dementia, a condition characterized by significant progressive declines in memory and intellectual capacities. While dementia is the main symptom of Alzheimer’s, the disease presents with many other debilitating symptoms, and currently, there is no known treatment exists to stop its irreversible progression or cure the disease. Photobiomodulation has emerged as a very promising treatment for improving brain function, using light in the range from red to the near-infrared spectrum depending on the application, tissue penetration, and density of the target area. The goal of this comprehensive review is to discuss the most recent achievements in and mechanisms of AD pathogenesis with respect to neurodegeneration. It also provides an overview of the mechanisms of photobiomodulation associated with AD pathology and the benefits of transcranial near-infrared light treatment as a potential therapeutic solution. This review also discusses the older reports and hypotheses associated with the development of AD, as well as some other approved AD drugs. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neurodegeneration 2023)
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15 pages, 1086 KiB  
Review
The Role of Exercise in Maintaining Mitochondrial Proteostasis in Parkinson’s Disease
by Jingwen Li, Yanli Xu, Tingting Liu, Yuxiang Xu, Xiantao Zhao and Jianshe Wei
Int. J. Mol. Sci. 2023, 24(9), 7994; https://doi.org/10.3390/ijms24097994 - 28 Apr 2023
Cited by 5 | Viewed by 2555
Abstract
Parkinson’s disease (PD) is the second most common rapidly progressive neurodegenerative disease and has serious health and socio-economic consequences. Mitochondrial dysfunction is closely related to the onset and progression of PD, and the use of mitochondria as a target for PD therapy has [...] Read more.
Parkinson’s disease (PD) is the second most common rapidly progressive neurodegenerative disease and has serious health and socio-economic consequences. Mitochondrial dysfunction is closely related to the onset and progression of PD, and the use of mitochondria as a target for PD therapy has been gaining traction in terms of both recognition and application. The disruption of mitochondrial proteostasis in the brain tissue of PD patients leads to mitochondrial dysfunction, which manifests as mitochondrial unfolded protein response, mitophagy, and mitochondrial oxidative phosphorylation. Physical exercise is important for the maintenance of human health, and has the great advantage of being a non-pharmacological therapy that is non-toxic, low-cost, and universally applicable. In this review, we investigate the relationships between exercise, mitochondrial proteostasis, and PD and explore the role and mechanisms of mitochondrial proteostasis in delaying PD through exercise. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neurodegeneration 2023)
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17 pages, 982 KiB  
Review
Pathophysiology and Neuroimmune Interactions Underlying Parkinson’s Disease and Traumatic Brain Injury
by Alyssa Lillian, Wanhong Zuo, Linda Laham, Sabine Hilfiker and Jiang-Hong Ye
Int. J. Mol. Sci. 2023, 24(8), 7186; https://doi.org/10.3390/ijms24087186 - 13 Apr 2023
Cited by 3 | Viewed by 2988
Abstract
Parkinson’s disease (PD) is a progressive neurodegenerative disorder clinically defined by motor instability, bradykinesia, and resting tremors. The clinical symptomatology is seen alongside pathologic changes, most notably the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the accumulation of [...] Read more.
Parkinson’s disease (PD) is a progressive neurodegenerative disorder clinically defined by motor instability, bradykinesia, and resting tremors. The clinical symptomatology is seen alongside pathologic changes, most notably the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the accumulation of α-synuclein and neuromelanin aggregates throughout numerous neural circuits. Traumatic brain injury (TBI) has been implicated as a risk factor for developing various neurodegenerative diseases, with the most compelling argument for the development of PD. Dopaminergic abnormalities, the accumulation of α-synuclein, and disruptions in neural homeostatic mechanisms, including but not limited to the release of pro-inflammatory mediators and the production of reactive oxygen species (ROS), are all present following TBI and are closely related to the pathologic changes seen in PD. Neuronal iron accumulation is discernable in degenerative and injured brain states, as is aquaporin-4 (APQ4). APQ4 is an essential mediator of synaptic plasticity in PD and regulates edematous states in the brain after TBI. Whether the cellular and parenchymal changes seen post-TBI directly cause neurodegenerative diseases such as PD is a point of considerable interest and debate; this review explores the vast array of neuroimmunological interactions and subsequent analogous changes that occur in TBI and PD. There is significant interest in exploring the validity of the relationship between TBI and PD, which is a focus of this review. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neurodegeneration 2023)
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28 pages, 1260 KiB  
Review
Fish Models for Exploring Mitochondrial Dysfunction Affecting Neurodegenerative Disorders
by Takayoshi Otsuka and Hideaki Matsui
Int. J. Mol. Sci. 2023, 24(8), 7079; https://doi.org/10.3390/ijms24087079 - 11 Apr 2023
Cited by 4 | Viewed by 3314
Abstract
Neurodegenerative disorders are characterized by the progressive loss of neuronal structure or function, resulting in memory loss and movement disorders. Although the detailed pathogenic mechanism has not been elucidated, it is thought to be related to the loss of mitochondrial function in the [...] Read more.
Neurodegenerative disorders are characterized by the progressive loss of neuronal structure or function, resulting in memory loss and movement disorders. Although the detailed pathogenic mechanism has not been elucidated, it is thought to be related to the loss of mitochondrial function in the process of aging. Animal models that mimic the pathology of a disease are essential for understanding human diseases. In recent years, small fish have become ideal vertebrate models for human disease due to their high genetic and histological homology to humans, ease of in vivo imaging, and ease of genetic manipulation. In this review, we first outline the impact of mitochondrial dysfunction on the progression of neurodegenerative diseases. Then, we highlight the advantages of small fish as model organisms, and present examples of previous studies regarding mitochondria-related neuronal disorders. Lastly, we discuss the applicability of the turquoise killifish, a unique model for aging research, as a model for neurodegenerative diseases. Small fish models are expected to advance our understanding of the mitochondrial function in vivo, the pathogenesis of neurodegenerative diseases, and be important tools for developing therapies to treat diseases. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Neurodegeneration 2023)
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