Neuroregeneration in Neurodegenerative Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 May 2020) | Viewed by 12289

Special Issue Editor


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Guest Editor
1. Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Campus de Gualtar, 4710-057 Braga, Portugal
2. ICVS/3B's–PT Government Associate Laboratory, Braga/Guimarães, Portugal
Interests: regenerative medicine; stem cells; secretome; biomaterials; spinal cord injury; Parkinson's disease
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Special Issue Information

Dear Colleagues,

Neurodegeneration induced by disease and/or trauma commonly leads to drastic alterations in patients’ life, imposing severe limitations to their daily lives, as well as those of their relatives. Indeed, neurodegenerative diseases, epilepsy, neuromuscular disorders, spinal cord, and traumatic brain injuries, or stroke, just to mention a few, often pose unique challenges for treatment. The latter are mainly due to the low regenerative potential of the central nervous system. The nervous system, unlike many other tissues, has a limited capacity for self-repair. Therefore, there is a great interest in the possibility of repairing the nervous system using strategies that can replace the lost cell population or, alternatively, induce local neuronal proliferation, differentiation, and modulation of the local inflammatory environment. Routes such as stem cell transplantation and cell secretome administration have been shown to improve the conditions of several animal models of injury and disease of the CNS. On the other hand, bioengineering approaches, in which the brain–spinal cord or brain machine interface with each other, and biomaterials in the forms of hydrogels and nanoparticles, with or without combination with stem cells, have also achieved positive results. Finally, with the advent of new biomolecular tools, such as CRIPR-Cas9, other avenues have been opened for the possible regeneration/repair of the CNS. Having this in consideration, the present Special Issue aims to address the most recent developments in this field, particularly targeting those that lead to neurogeneration and with it induce functional repair.

Prof. Dr. António Salgado
Guest Editor

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Keywords

Dear Colleagues,

Neurodegeneration induced by disease and/or trauma commonly leads to drastic alterations in patients’ life, imposing severe limitations to their daily lives, as well as those of their relatives. Indeed, neurodegenerative diseases, epilepsy, neuromuscular disorders, spinal cord, and traumatic brain injuries, or stroke, just to mention a few, often pose unique challenges for treatment. The latter are mainly due to the low regenerative potential of the central nervous system. The nervous system, unlike many other tissues, has a limited capacity for self-repair. Therefore, there is a great interest in the possibility of repairing the nervous system using strategies that can replace the lost cell population or, alternatively, induce local neuronal proliferation, differentiation, and modulation of the local inflammatory environment. Routes such as stem cell transplantation and cell secretome administration have been shown to improve the conditions of several animal models of injury and disease of the CNS. On the other hand, bioengineering approaches, in which the brain–spinal cord or brain machine interface with each other, and biomaterials in the forms of hydrogels and nanoparticles, with or without combination with stem cells, have also achieved positive results. Finally, with the advent of new biomolecular tools, such as CRIPR-Cas9, other avenues have been opened for the possible regeneration/repair of the CNS. Having this in consideration, the present Special Issue aims to address the most recent developments in this field, particularly targeting those that lead to neurogeneration and with it induce functional repair.

Published Papers (3 papers)

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Research

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16 pages, 2304 KiB  
Article
Identification of Prion Disease-Related Somatic Mutations in the Prion Protein Gene (PRNP) in Cancer Patients
by Yong-Chan Kim, Sae-Young Won and Byung-Hoon Jeong
Cells 2020, 9(6), 1480; https://doi.org/10.3390/cells9061480 - 17 Jun 2020
Cited by 19 | Viewed by 3360
Abstract
Prion diseases are caused by misfolded prion protein (PrPSc) and are accompanied by spongiform vacuolation of brain lesions. Approximately three centuries have passed since prion diseases were first discovered around the world; however, the exact role of certain factors affecting the [...] Read more.
Prion diseases are caused by misfolded prion protein (PrPSc) and are accompanied by spongiform vacuolation of brain lesions. Approximately three centuries have passed since prion diseases were first discovered around the world; however, the exact role of certain factors affecting the causative agent of prion diseases is still debatable. In recent studies, somatic mutations were assumed to be cause of several diseases. Thus, we postulated that genetically unstable cancer tissue may cause somatic mutations in the prion protein gene (PRNP), which could trigger the onset of prion diseases. To identify somatic mutations in the PRNP gene in cancer tissues, we analyzed somatic mutations in the PRNP gene in cancer patients using the Cancer Genome Atlas (TCGA) database. In addition, to evaluate whether the somatic mutations in the PRNP gene in cancer patients had a damaging effect, we performed in silico analysis using PolyPhen-2, PANTHER, PROVEAN, and AMYCO. We identified a total of 48 somatic mutations in the PRNP gene, including 8 somatic mutations that are known pathogenic mutations of prion diseases. We identified significantly different distributions among the types of cancer, the mutation counts, and the ages of diagnosis between the total cancer patient population and cancer patients carrying somatic mutations in the PRNP gene. Strikingly, although invasive breast carcinoma and glioblastoma accounted for a high percentage of the total cancer patient population (9.9% and 5.4%, respectively), somatic mutations in the PRNP gene have not been identified in these two cancer types. We suggested the possibility that somatic mutations of the PRNP gene in glioblastoma can be masked by a diagnosis of prion disease. In addition, we found four aggregation-prone somatic mutations, these being L125F, E146Q, R151C, and K204N. To the best of our knowledge, this is the first specific analysis of the somatic mutations in the PRNP gene in cancer patients. Full article
(This article belongs to the Special Issue Neuroregeneration in Neurodegenerative Disease)
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21 pages, 6759 KiB  
Article
Lactulose and Melibiose Inhibit α-Synuclein Aggregation and Up-Regulate Autophagy to Reduce Neuronal Vulnerability
by Chiung Mei Chen, Chih-Hsin Lin, Yih-Ru Wu, Chien-Yu Yen, Yu-Ting Huang, Jia-Lan Lin, Chung-Yin Lin, Wan-Ling Chen, Chih-Ying Chao, Guey-Jen Lee-Chen, Ming-Tsan Su and Kuo-Hsuan Chang
Cells 2020, 9(5), 1230; https://doi.org/10.3390/cells9051230 - 16 May 2020
Cited by 11 | Viewed by 4101
Abstract
Parkinson’s disease (PD) is a neurodegenerative disease characterized by selective dopaminergic (DAergic) neuronal degeneration in the substantia nigra (SN) and proteinaceous α-synuclein-positive Lewy bodies and Lewy neuritis. As a chemical chaperone to promote protein stability and an autophagy inducer to clear aggregate-prone proteins, [...] Read more.
Parkinson’s disease (PD) is a neurodegenerative disease characterized by selective dopaminergic (DAergic) neuronal degeneration in the substantia nigra (SN) and proteinaceous α-synuclein-positive Lewy bodies and Lewy neuritis. As a chemical chaperone to promote protein stability and an autophagy inducer to clear aggregate-prone proteins, a disaccharide trehalose has been reported to alleviate neurodegeneration in PD cells and mouse models. Its trehalase-indigestible analogs, lactulose and melibiose, also demonstrated potentials to reduce abnormal protein aggregation in spinocerebellar ataxia cell models. In this study, we showed the potential of lactulose and melibiose to inhibit α-synuclein aggregation using biochemical thioflavin T fluorescence, cryogenic transmission electron microscopy (cryo-TEM) and prokaryotic split Venus complementation assays. Lactulose and melibiose further reduced α-synuclein aggregation and associated oxidative stress, as well as protected cells against α-synuclein-induced neurotoxicity by up-regulating autophagy and nuclear factor, erythroid 2 like 2 (NRF2) pathway in DAergic neurons derived from SH-SY5Y cells over-expressing α-synuclein. Our findings strongly indicate the potential of lactulose and melibiose for mitigating PD neurodegeneration, offering new drug candidates for PD treatment. Full article
(This article belongs to the Special Issue Neuroregeneration in Neurodegenerative Disease)
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Review

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16 pages, 2737 KiB  
Review
Ongoing Research on the Role of Gintonin in the Management of Neurodegenerative Disorders
by Muhammad Ikram, Rahat Ullah, Amjad Khan and Myeong Ok Kim
Cells 2020, 9(6), 1464; https://doi.org/10.3390/cells9061464 - 15 Jun 2020
Cited by 24 | Viewed by 4328
Abstract
Neurodegenerative disorders, namely Parkinson’s disease (PD), Huntington’s disease (HD), Alzheimer’s disease (AD), and multiple sclerosis (MS), are increasingly major health concerns due to the increasingly aged population worldwide. These conditions often share the same underlying pathological mechanisms, including elevated oxidative stress, neuroinflammation, and [...] Read more.
Neurodegenerative disorders, namely Parkinson’s disease (PD), Huntington’s disease (HD), Alzheimer’s disease (AD), and multiple sclerosis (MS), are increasingly major health concerns due to the increasingly aged population worldwide. These conditions often share the same underlying pathological mechanisms, including elevated oxidative stress, neuroinflammation, and the aggregation of proteins. Several studies have highlighted the potential to diminish the clinical outcomes of these disorders via the administration of herbal compounds, among which gintonin, a derivative of ginseng, has shown promising results. Gintonin is a noncarbohydrate/saponin that has been characterized as a lysophosphatidic acid receptor (LPA Receptor) ligand. Gintonin may cause a significant elevation in calcium levels [Ca2+]i intracellularly, which promotes calcium-mediated cellular effects via the modulation of ion channels and cell surface receptors, regulating the inflammatory effects. Years of research have suggested that gintonin has antioxidant and anti-inflammatory effects against different models of neurodegeneration, and these effects may be employed to tackle the neurological changes. Therefore, we collected the main scientific findings and comprehensively presented them, covering preparation, absorption, and receptor-mediated functions, including effects against Alzheimer’s disease models, Parkinson’s disease models, anxiety and depression-like models, and other neurological disorders, aiming to provide some insights for the possible usage of gintonin in the management of neurodegenerative conditions. Full article
(This article belongs to the Special Issue Neuroregeneration in Neurodegenerative Disease)
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