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Induced Impairment of Neurogenesis and Brain Diseases
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Induced Impairment of Neurogenesis and Brain Diseases

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

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 54846

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special Issue Editor

Dr. Feng Ru Tang

E-Mail Website
Guest Editor
Radiobiology Research Laboratory, Singapore Nuclear Research and Safety Initiative, National University of Singapore, Singapore 138602, Singapore
Interests: radiobiology; neurogenesis; neurodegeneration; neurological and neuropsychological disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Impairment of neurogenesis can be induced after pre-and post-natal chemical and biological toxin, alcohol and radiation exposure, drug treatment, hormone imbalances, stress, pain, hypoxia, brain trauma, malnutrition, aging. It also occurs in genetic disorder such as Down syndrome (DS), autism, fragile X syndrome (FXS), neurological disorders including Alzheimer's disease (AD), Parkinson's disease (PD) epilepsy, Huntington's disease (HD) and neuropsychological disorders including depression, schizophrenia although the causal relationship between impairment of neurogenesis and neurological and neuropsychological disorders remains unknown.  In this special issue of “Cells” entitled “Induced Impairment of Neurogenesis and Brain Diseases”, I invite you to submit animal or cell experimental research work and review papers to discuss different causes of the impairment of neurogenesis, relevant neurobehavioral changes, molecular mechanisms and therapeutic approaches. It is aimed to update researchers and clinicians about the complexity of the development of impairment of neurogenesis, the importance of the involvement of impairment of neurogenesis in neurological and neuropsychological disorders and to provide some clues for design novel therapeutic approaches by targeting impairment of neurogenesis to effectively prevent or treat different genetic, neurological and neuropsychological disorders.

Dr. FengRu Tang
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurogenesis
  • impairment
  • chemical and biological toxin
  • stress
  • radiation
  • hormone
  • aging
  • genetic disorder, brain trauma
  • neurological and neuropsychological disorders

Published Papers (13 papers)

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Research

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14 pages, 4381 KiB  
Article
The Central Domain of MCPH1 Controls Development of the Cerebral Cortex and Gonads in Mice
by Yaru Wang, Wen Zong, Wenli Sun, Chengyan Chen, Zhao-Qi Wang and Tangliang Li
Cells 2022, 11(17), 2715; https://doi.org/10.3390/cells11172715 - 31 Aug 2022
Cited by 3 | Viewed by 1801
Abstract
MCPH1 is the first gene identified to be responsible for the human autosomal recessive disorder primary microcephaly (MCPH). Mutations in the N-terminal and central domains of MCPH1 are strongly associated with microcephaly in human patients. A recent study showed that the central domain [...] Read more.
MCPH1 is the first gene identified to be responsible for the human autosomal recessive disorder primary microcephaly (MCPH). Mutations in the N-terminal and central domains of MCPH1 are strongly associated with microcephaly in human patients. A recent study showed that the central domain of MCPH1, which is mainly encoded by exon 8, interacts with E3 ligase βTrCP2 and regulates the G2/M transition of the cell cycle. In order to investigate the biological functions of MCPH1’s central domain, we constructed a mouse model that lacked the central domain of MCPH1 by deleting its exon 8 (designated as Mcph1-Δe8). Mcph1-Δe8 mice exhibited a reduced brain size and thinner cortex, likely caused by a compromised self-renewal capacity and premature differentiation of Mcph1-Δe8 neuroprogenitors during corticogenesis. Furthermore, Mcph1-Δe8 mice were sterile because of a loss of germ cells in the testis and ovary. The embryonic fibroblasts of Mcph1-Δe8 mice exhibited premature chromosome condensation (PCC). All of these findings indicate that Mcph1-Δe8 mice are reminiscent of MCPH1 complete knockout mice and Mcph1-ΔBR1 mice. Our study demonstrates that the central domain of MCPH1 represses microcephaly, and is essential for gonad development in mammals. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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23 pages, 3386 KiB  
Article
Enhanced Cognition and Neurogenesis in miR-146b Deficient Mice
by Keerthana Chithanathan, Kelli Somelar, Monika Jürgenson, Tamara Žarkovskaja, Kapilraj Periyasamy, Ling Yan, Nathaniel Magilnick, Mark P. Boldin, Ana Rebane, Li Tian and Alexander Zharkovsky
Cells 2022, 11(13), 2002; https://doi.org/10.3390/cells11132002 - 22 Jun 2022
Cited by 6 | Viewed by 2237
Abstract
The miR-146 family consists of two microRNAs (miRNAs), miR-146a and miR-146b, which are both known to suppress a variety of immune responses. Here in this study, we show that miR-146b is abundantly expressed in neuronal cells, while miR-146a is mainly expressed in microglia [...] Read more.
The miR-146 family consists of two microRNAs (miRNAs), miR-146a and miR-146b, which are both known to suppress a variety of immune responses. Here in this study, we show that miR-146b is abundantly expressed in neuronal cells, while miR-146a is mainly expressed in microglia and astroglia of adult mice. Accordingly, miR-146b deficient (Mir146b-/-) mice exhibited anxiety-like behaviors and enhanced cognition. Characterization of cellular composition of Mir146b-/- mice using flow cytometry revealed an increased number of neurons and a decreased abundancy of astroglia in the hippocampus and frontal cortex, whereas microglia abundancy remained unchanged. Immunohistochemistry showed a higher density of neurons in the frontal cortex of Mir146b-/- mice, enhanced hippocampal neurogenesis as evidenced by an increased proliferation, and survival of newly generated cells with enhanced maturation into neuronal phenotype. No microglial activation or signs of neuroinflammation were observed in Mir146b-/- mice. Further analysis demonstrated that miR-146b deficiency is associated with elevated expression of glial cell line-derived neurotrophic factor (Gdnf) mRNA in the hippocampus, which might be at least in part responsible for the observed neuronal expansion and the behavioral phenotype. This hypothesis is partially supported by the positive correlation between performance of mice in the object recognition test and Gdnf mRNA expression in Mir146b-/- mice. Together, these results show the distinct function of miR-146b in controlling behaviors and provide new insights in understanding cell-specific function of miR-146b in the neuronal and astroglial organization of the mouse brain. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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21 pages, 6671 KiB  
Article
NXN Gene Epigenetic Changes in an Adult Neurogenesis Model of Alzheimer’s Disease
by Idoia Blanco-Luquin, Blanca Acha, Amaya Urdánoz-Casado, Eva Gómez-Orte, Miren Roldan, Diego R. Pérez-Rodríguez, Juan Cabello and Maite Mendioroz
Cells 2022, 11(7), 1069; https://doi.org/10.3390/cells11071069 - 22 Mar 2022
Cited by 3 | Viewed by 2627
Abstract
In view of the proven link between adult hippocampal neurogenesis (AHN) and learning and memory impairment, we generated a straightforward adult neurogenesis in vitro model to recapitulate DNA methylation marks in the context of Alzheimer’s disease (AD). Neural progenitor cells (NPCs) were differentiated [...] Read more.
In view of the proven link between adult hippocampal neurogenesis (AHN) and learning and memory impairment, we generated a straightforward adult neurogenesis in vitro model to recapitulate DNA methylation marks in the context of Alzheimer’s disease (AD). Neural progenitor cells (NPCs) were differentiated for 29 days and Aβ peptide 1–42 was added. mRNA expression of Neuronal Differentiation 1 (NEUROD1), Neural Cell Adhesion Molecule 1 (NCAM1), Tubulin Beta 3 Class III (TUBB3), RNA Binding Fox-1 Homolog 3 (RBFOX3), Calbindin 1 (CALB1), and Glial Fibrillary Acidic Protein (GFAP) was determined by RT-qPCR to characterize the culture and framed within the multistep process of AHN. Hippocampal DNA methylation marks previously identified in Contactin-Associated Protein 1 (CNTNAP1), SEPT5-GP1BB Readthrough (SEPT5-GP1BB), T-Box Transcription Factor 5 (TBX5), and Nucleoredoxin (NXN) genes were profiled by bisulfite pyrosequencing or bisulfite cloning sequencing; mRNA expression was also measured. NXN outlined a peak of DNA methylation overlapping type 3 neuroblasts. Aβ-treated NPCs showed transient decreases of mRNA expression for SEPT5-GP1BB and NXN on day 9 or 19 and an increase in DNA methylation on day 29 for NXN. NXN and SEPT5-GP1BB may reflect alterations detected in the brain of AD human patients, broadening our understanding of this disease. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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24 pages, 7863 KiB  
Article
Ghrelin Regulates Expression of the Transcription Factor Pax6 in Hypoxic Brain Progenitor Cells and Neurons
by Irina I. Stoyanova, Andrii Klymenko, Jeannette Willms, Thorsten R. Doeppner, Anton B. Tonchev and David Lutz
Cells 2022, 11(5), 782; https://doi.org/10.3390/cells11050782 - 23 Feb 2022
Cited by 3 | Viewed by 2459
Abstract
The nature of brain impairment after hypoxia is complex and recovery harnesses different mechanisms, including neuroprotection and neurogenesis. Experimental evidence suggests that hypoxia may trigger neurogenesis postnatally by influencing the expression of a variety of transcription factors. However, the existing data are controversial. [...] Read more.
The nature of brain impairment after hypoxia is complex and recovery harnesses different mechanisms, including neuroprotection and neurogenesis. Experimental evidence suggests that hypoxia may trigger neurogenesis postnatally by influencing the expression of a variety of transcription factors. However, the existing data are controversial. As a proof-of-principle, we subjected cultured cerebral cortex neurons, cerebellar granule neurons and organotypic cerebral cortex slices from rat brains to hypoxia and treated these cultures with the hormone ghrelin, which is well-known for its neuroprotective functions. We found that hypoxia elevated the expression levels and stimulated nuclear translocation of ghrelin’s receptor GHSR1 in the cultured neurons and the acute organotypic slices, whereas ghrelin treatment reduced the receptor expression to normoxic levels. GHSR1 expression was also increased in cerebral cortex neurons of mice with induced experimental stroke. Additional quantitative analyses of immunostainings for neuronal proliferation and differentiation markers revealed that hypoxia stimulated the proliferation of neuronal progenitors, whereas ghrelin application during the phase of recovery from hypoxia counteracted these effects. At the mechanistic level, we provide a link between the described post-ischemic phenomena and the expression of the transcription factor Pax6, an important regulator of neural progenitor cell fate. In contrast to the neurogenic niches in the brain where hypoxia is known to increase Pax6 expression, the levels of the transcription factor in cultured hypoxic cerebral cortex cells were downregulated. Moreover, the application of ghrelin to hypoxic neurons normalised the expression levels of these factors. Our findings suggest that ghrelin stimulates neurogenic factors for the protection of neurons in a GHSR1-dependent manner in non-neurogenic brain areas such as the cerebral cortex after exposure to hypoxia. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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16 pages, 3917 KiB  
Article
TRIM32 Deficiency Impairs the Generation of Pyramidal Neurons in Developing Cerebral Cortex
by Yan-Yun Sun, Wen-Jin Chen, Ze-Ping Huang, Gang Yang, Ming-Lei Wu, De-En Xu, Wu-Lin Yang, Yong-Chun Luo, Zhi-Cheng Xiao, Ru-Xiang Xu and Quan-Hong Ma
Cells 2022, 11(3), 449; https://doi.org/10.3390/cells11030449 - 28 Jan 2022
Cited by 5 | Viewed by 2948
Abstract
Excitatory-inhibitory imbalance (E/I) is a fundamental mechanism underlying autism spectrum disorders (ASD). TRIM32 is a risk gene genetically associated with ASD. The absence of TRIM32 causes impaired generation of inhibitory GABAergic interneurons, neural network hyperexcitability, and autism-like behavior in mice, emphasizing the role [...] Read more.
Excitatory-inhibitory imbalance (E/I) is a fundamental mechanism underlying autism spectrum disorders (ASD). TRIM32 is a risk gene genetically associated with ASD. The absence of TRIM32 causes impaired generation of inhibitory GABAergic interneurons, neural network hyperexcitability, and autism-like behavior in mice, emphasizing the role of TRIM32 in maintaining E/I balance, but despite the description of TRIM32 in regulating proliferation and differentiation of cultured mouse neural progenitor cells (NPCs), the role of TRIM32 in cerebral cortical development, particularly in the production of excitatory pyramidal neurons, remains unknown. The present study observed that TRIM32 deficiency resulted in decreased numbers of distinct layer-specific cortical neurons and decreased radial glial cell (RGC) and intermediate progenitor cell (IPC) pool size. We further demonstrated that TRIM32 deficiency impairs self-renewal of RGCs and IPCs as indicated by decreased proliferation and mitosis. A TRIM32 deficiency also affects or influences the formation of cortical neurons. As a result, TRIM32-deficient mice showed smaller brain size. At the molecular level, RNAseq analysis indicated reduced Notch signalling in TRIM32-deficient mice. Therefore, the present study indicates a role for TRIM32 in pyramidal neuron generation. Impaired generation of excitatory pyramidal neurons may explain the hyperexcitability observed in TRIM32-deficient mice. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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19 pages, 3943 KiB  
Article
Cell Type-Specific Role of RNA Nuclease SMG6 in Neurogenesis
by Gabriela Maria Guerra, Doreen May, Torsten Kroll, Philipp Koch, Marco Groth, Zhao-Qi Wang, Tang-Liang Li and Paulius Grigaravičius
Cells 2021, 10(12), 3365; https://doi.org/10.3390/cells10123365 - 30 Nov 2021
Cited by 5 | Viewed by 3053
Abstract
SMG6 is an endonuclease, which cleaves mRNAs during nonsense-mediated mRNA decay (NMD), thereby regulating gene expression and controling mRNA quality. SMG6 has been shown as a differentiation license factor of totipotent embryonic stem cells. To investigate whether it controls the differentiation of lineage-specific [...] Read more.
SMG6 is an endonuclease, which cleaves mRNAs during nonsense-mediated mRNA decay (NMD), thereby regulating gene expression and controling mRNA quality. SMG6 has been shown as a differentiation license factor of totipotent embryonic stem cells. To investigate whether it controls the differentiation of lineage-specific pluripotent progenitor cells, we inactivated Smg6 in murine embryonic neural stem cells. Nestin-Cre-mediated deletion of Smg6 in mouse neuroprogenitor cells (NPCs) caused perinatal lethality. Mutant mice brains showed normal structure at E14.5 but great reduction of the cortical NPCs and late-born cortical neurons during later stages of neurogenesis (i.e., E18.5). Smg6 inactivation led to dramatic cell death in ganglionic eminence (GE) and a reduction of interneurons at E14.5. Interestingly, neurosphere assays showed self-renewal defects specifically in interneuron progenitors but not in cortical NPCs. RT-qPCR analysis revealed that the interneuron differentiation regulators Dlx1 and Dlx2 were reduced after Smg6 deletion. Intriguingly, when Smg6 was deleted specifically in cortical and hippocampal progenitors, the mutant mice were viable and showed normal size and architecture of the cortex at E18.5. Thus, SMG6 regulates cell fate in a cell type-specific manner and is more important for neuroprogenitors originating from the GE than for progenitors from the cortex. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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19 pages, 2687 KiB  
Article
Early Life Irradiation-Induced Hypoplasia and Impairment of Neurogenesis in the Dentate Gyrus and Adult Depression Are Mediated by MicroRNA- 34a-5p/T-Cell Intracytoplasmic Antigen-1 Pathway
by Hong Wang, Zhaowu Ma, Hongyuan Shen, Zijun Wu, Lian Liu, Boxu Ren, Peiyan Wong, Gautam Sethi and Fengru Tang
Cells 2021, 10(9), 2476; https://doi.org/10.3390/cells10092476 - 18 Sep 2021
Cited by 7 | Viewed by 2488
Abstract
Early life radiation exposure causes abnormal brain development, leading to adult depression. However, few studies have been conducted to explore pre- or post-natal irradiation-induced depression-related neuropathological changes. Relevant molecular mechanisms are also poorly understood. We induced adult depression by irradiation of mice at [...] Read more.
Early life radiation exposure causes abnormal brain development, leading to adult depression. However, few studies have been conducted to explore pre- or post-natal irradiation-induced depression-related neuropathological changes. Relevant molecular mechanisms are also poorly understood. We induced adult depression by irradiation of mice at postnatal day 3 (P3) to reveal hippocampal neuropathological changes and investigate their molecular mechanism, focusing on MicroRNA (miR) and its target mRNA and protein. P3 mice were irradiated by γ-rays with 5Gy, and euthanized at 1, 7 and 120 days after irradiation. A behavioral test was conducted before the animals were euthanized at 120 days after irradiation. The animal brains were used for different studies including immunohistochemistry, CAP-miRSeq, Real-Time Quantitative Reverse Transcription PCR (qRT-PCR) and western blotting. The interaction of miR-34a-5p and its target T-cell intracytoplasmic antigen-1 (Tia1) was confirmed by luciferase reporter assay. Overexpression of Tia1 in a neural stem cell (NSC) model was used to further validate findings from the mouse model. Irradiation with 5 Gy at P3 induced depression in adult mice. Animal hippocampal pathological changes included hypoplasia of the infrapyramidal blade of the stratum granulosum, aberrant and impaired cell division, and neurogenesis in the dentate gyrus. At the molecular level, upregulation of miR-34a-5p and downregulation of Tia1 mRNA were observed in both animal and neural stem cell models. The luciferase reporter assay and gene transfection studies further confirmed a direct interaction between miR-43a-5p and Tia1. Our results indicate that the early life γ-radiation-activated miR-43a-5p/Tia1 pathway is involved in the pathogenesis of adult depression. This novel finding may provide a new therapeutic target by inhibiting the miR-43a-5p/Tia1 pathway to prevent radiation-induced pathogenesis of depression. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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Review

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21 pages, 1298 KiB  
Review
The Influence of Gut Microbiota on Neurogenesis: Evidence and Hopes
by Fiorella Sarubbo, Virve Cavallucci and Giovambattista Pani
Cells 2022, 11(3), 382; https://doi.org/10.3390/cells11030382 - 23 Jan 2022
Cited by 24 | Viewed by 6078
Abstract
Adult neurogenesis (i.e., the life-long generation of new neurons from undifferentiated neuronal precursors in the adult brain) may contribute to brain repair after damage, and participates in plasticity-related processes including memory, cognition, mood and sensory functions. Among the many intrinsic (oxidative stress, inflammation, [...] Read more.
Adult neurogenesis (i.e., the life-long generation of new neurons from undifferentiated neuronal precursors in the adult brain) may contribute to brain repair after damage, and participates in plasticity-related processes including memory, cognition, mood and sensory functions. Among the many intrinsic (oxidative stress, inflammation, and ageing), and extrinsic (environmental pollution, lifestyle, and diet) factors deemed to impact neurogenesis, significant attention has been recently attracted by the myriad of saprophytic microorganismal communities inhabiting the intestinal ecosystem and collectively referred to as the gut microbiota. A growing body of evidence, mainly from animal studies, reveal the influence of microbiota and its disease-associated imbalances on neural stem cell proliferative and differentiative activities in brain neurogenic niches. On the other hand, the long-claimed pro-neurogenic activity of natural dietary compounds endowed with antioxidants and anti-inflammatory properties (such as polyphenols, polyunsaturated fatty acids, or pro/prebiotics) may be mediated, at least in part, by their action on the intestinal microflora. The purpose of this review is to summarise the available information regarding the influence of the gut microbiota on neurogenesis, analyse the possible underlying mechanisms, and discuss the potential implications of this emerging knowledge for the fight against neurodegeneration and brain ageing. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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23 pages, 8299 KiB  
Review
Ionizing Radiation-Induced Brain Cell Aging and the Potential Underlying Molecular Mechanisms
by Qin-Qi Wang, Gang Yin, Jiang-Rong Huang, Shi-Jun Xi, Feng Qian, Rui-Xue Lee, Xiao-Chun Peng and Feng-Ru Tang
Cells 2021, 10(12), 3570; https://doi.org/10.3390/cells10123570 - 17 Dec 2021
Cited by 20 | Viewed by 5936
Abstract
Population aging is occurring rapidly worldwide, challenging the global economy and healthcare services. Brain aging is a significant contributor to various age-related neurological and neuropsychological disorders, including Alzheimer’s disease and Parkinson’s disease. Several extrinsic factors, such as exposure to ionizing radiation, can accelerate [...] Read more.
Population aging is occurring rapidly worldwide, challenging the global economy and healthcare services. Brain aging is a significant contributor to various age-related neurological and neuropsychological disorders, including Alzheimer’s disease and Parkinson’s disease. Several extrinsic factors, such as exposure to ionizing radiation, can accelerate senescence. Multiple human and animal studies have reported that exposure to ionizing radiation can have varied effects on organ aging and lead to the prolongation or shortening of life span depending on the radiation dose or dose rate. This paper reviews the effects of radiation on the aging of different types of brain cells, including neurons, microglia, astrocytes, and cerebral endothelial cells. Further, the relevant molecular mechanisms are discussed. Overall, this review highlights how radiation-induced senescence in different cell types may lead to brain aging, which could result in the development of various neurological and neuropsychological disorders. Therefore, treatment targeting radiation-induced oxidative stress and neuroinflammation may prevent radiation-induced brain aging and the neurological and neuropsychological disorders it may cause. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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10 pages, 961 KiB  
Review
Emerging Roles of N6-Methyladenosine Modification in Neurodevelopment and Neurodegeneration
by Liqi Shu, Xiaoli Huang, Xuejun Cheng and Xuekun Li
Cells 2021, 10(10), 2694; https://doi.org/10.3390/cells10102694 - 9 Oct 2021
Cited by 22 | Viewed by 4111
Abstract
N6-methyladenosine (m6A), the most abundant modification in messenger RNAs (mRNAs), is deposited by methyltransferases (“writers”) Mettl3 and Mettl14 and erased by demethylases (“erasers”) Fto and Alkbh5. m6A can be recognized by m6A-binding proteins (“readers”), such as Yth [...] Read more.
N6-methyladenosine (m6A), the most abundant modification in messenger RNAs (mRNAs), is deposited by methyltransferases (“writers”) Mettl3 and Mettl14 and erased by demethylases (“erasers”) Fto and Alkbh5. m6A can be recognized by m6A-binding proteins (“readers”), such as Yth domain family proteins (Ythdfs) and Yth domain-containing protein 1 (Ythdc1). Previous studies have indicated that m6A plays an essential function in various fundamental biological processes, including neurogenesis and neuronal development. Dysregulated m6A modification contributes to neurological disorders, including neurodegenerative diseases. In this review, we summarize the current knowledge about the roles of m6A machinery, including writers, erasers, and readers, in regulating gene expression and the function of m6A in neurodevelopment and neurodegeneration. We also discuss the perspectives for studying m6A methylation. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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21 pages, 894 KiB  
Review
Control of Neuroinflammation through Radiation-Induced Microglial Changes
by Alexandra Boyd, Sarah Byrne, Ryan J. Middleton, Richard B. Banati and Guo-Jun Liu
Cells 2021, 10(9), 2381; https://doi.org/10.3390/cells10092381 - 10 Sep 2021
Cited by 25 | Viewed by 4965
Abstract
Microglia, the innate immune cells of the central nervous system, play a pivotal role in the modulation of neuroinflammation. Neuroinflammation has been implicated in many diseases of the CNS, including Alzheimer’s disease and Parkinson’s disease. It is well documented that microglial activation, initiated [...] Read more.
Microglia, the innate immune cells of the central nervous system, play a pivotal role in the modulation of neuroinflammation. Neuroinflammation has been implicated in many diseases of the CNS, including Alzheimer’s disease and Parkinson’s disease. It is well documented that microglial activation, initiated by a variety of stressors, can trigger a potentially destructive neuroinflammatory response via the release of pro-inflammatory molecules, and reactive oxygen and nitrogen species. However, the potential anti-inflammatory and neuroprotective effects that microglia are also thought to exhibit have been under-investigated. The application of ionising radiation at different doses and dose schedules may reveal novel methods for the control of microglial response to stressors, potentially highlighting avenues for treatment of neuroinflammation associated CNS disorders, such as Alzheimer’s disease and Parkinson’s disease. There remains a need to characterise the response of microglia to radiation, particularly low dose ionising radiation. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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35 pages, 5543 KiB  
Review
Therapeutic Potential of Complementary and Alternative Medicines in Peripheral Nerve Regeneration: A Systematic Review
by Yoon-Yen Yow, Tiong-Keat Goh, Ke-Ying Nyiew, Lee-Wei Lim, Siew-Moi Phang, Siew-Huah Lim, Shyamala Ratnayeke and Kah-Hui Wong
Cells 2021, 10(9), 2194; https://doi.org/10.3390/cells10092194 - 25 Aug 2021
Cited by 11 | Viewed by 5304
Abstract
Despite the progressive advances, current standards of treatments for peripheral nerve injury do not guarantee complete recovery. Thus, alternative therapeutic interventions should be considered. Complementary and alternative medicines (CAMs) are widely explored for their therapeutic value, but their potential use in peripheral nerve [...] Read more.
Despite the progressive advances, current standards of treatments for peripheral nerve injury do not guarantee complete recovery. Thus, alternative therapeutic interventions should be considered. Complementary and alternative medicines (CAMs) are widely explored for their therapeutic value, but their potential use in peripheral nerve regeneration is underappreciated. The present systematic review, designed according to guidelines of Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols, aims to present and discuss the current literature on the neuroregenerative potential of CAMs, focusing on plants or herbs, mushrooms, decoctions, and their respective natural products. The available literature on CAMs associated with peripheral nerve regeneration published up to 2020 were retrieved from PubMed, Scopus, and Web of Science. According to current literature, the neuroregenerative potential of Achyranthes bidentata, Astragalus membranaceus, Curcuma longa, Panax ginseng, and Hericium erinaceus are the most widely studied. Various CAMs enhanced proliferation and migration of Schwann cells in vitro, primarily through activation of MAPK pathway and FGF-2 signaling, respectively. Animal studies demonstrated the ability of CAMs to promote peripheral nerve regeneration and functional recovery, which are partially associated with modulations of neurotrophic factors, pro-inflammatory cytokines, and anti-apoptotic signaling. This systematic review provides evidence for the potential use of CAMs in the management of peripheral nerve injury. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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17 pages, 761 KiB  
Review
TGF-β/Smad Signalling in Neurogenesis: Implications for Neuropsychiatric Diseases
by Lih-Fhung Hiew, Chi-Him Poon, Heng-Ze You and Lee-Wei Lim
Cells 2021, 10(6), 1382; https://doi.org/10.3390/cells10061382 - 3 Jun 2021
Cited by 33 | Viewed by 8334
Abstract
TGF-β/Smad signalling has been the subject of extensive research due to its role in the cell cycle and carcinogenesis. Modifications to the TGF-β/Smad signalling pathway have been found to produce disparate effects on neurogenesis. We review the current research on canonical and non-canonical [...] Read more.
TGF-β/Smad signalling has been the subject of extensive research due to its role in the cell cycle and carcinogenesis. Modifications to the TGF-β/Smad signalling pathway have been found to produce disparate effects on neurogenesis. We review the current research on canonical and non-canonical TGF-β/Smad signalling pathways and their functions in neurogenesis. We also examine the observed role of neurogenesis in neuropsychiatric disorders and the relationship between TGF-β/Smad signalling and neurogenesis in response to stressors. Overlapping mechanisms of cell proliferation, neurogenesis, and the development of mood disorders in response to stressors suggest that TGF-β/Smad signalling is an important regulator of stress response and is implicated in the behavioural outcomes of mood disorders. Full article
(This article belongs to the Special Issue Induced Impairment of Neurogenesis and Brain Diseases)
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