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21 pages, 3459 KiB

Open AccessArticle

Failure to Thrive: Impaired BDNF Transport along the Cortical–Striatal Axis in Mouse Q140 Neurons of Huntington’s Disease

by Michael T. Maloney, Wei Wang, Sumana Bhowmick, Ivan Millan, Mridu Kapur, Nicolas Herrera, Everett Frost, Elena Y. Zhang, Scott Song, Melissa Wang, Amelia Bora Park, Annabelle Y. Yao and Yanmin Yang

Biology 2023, 12(2), 157; https://doi.org/10.3390/biology12020157 - 19 Jan 2023

Cited by 3 | Viewed by 2615

Abstract

Boosting trophic support to striatal neurons by increasing levels of brain-derived neurotrophic factor (BDNF) has been considered as a target for therapeutic intervention for several neurodegenerative diseases, including Huntington’s disease (HD). To aid in the implementation of such a strategy, a thorough understanding [...] Read more.

Boosting trophic support to striatal neurons by increasing levels of brain-derived neurotrophic factor (BDNF) has been considered as a target for therapeutic intervention for several neurodegenerative diseases, including Huntington’s disease (HD). To aid in the implementation of such a strategy, a thorough understanding of BDNF cortical–striatal transport is critical to help guide its strategic delivery. In this manuscript, we investigate the dynamic behavior of BDNF transport along the cortical–striatal axis in Q140 primary neurons, a mouse model for HD. We examine this by using single-molecule labeling of BDNF conjugated with quantum dots (QD-BDNF) to follow the transport along the cortical–striatal axis in a microfluidic chamber system specifically designed for the co-culture of cortical and striatal primary neurons. Using this approach, we observe a defect of QD-BDNF transport in Q140 neurons. Our study demonstrates that QD-BDNF transport along the cortical–striatal axis involves the impairment of anterograde transport within axons of cortical neurons, and of retrograde transport within dendrites of striatal neurons. One prominent feature we observe is the extended pause time of QD-BDNF retrograde transport within Q140 striatal dendrites. Taken together, these finding support the hypothesis that delinquent spatiotemporal trophic support of BDNF to striatal neurons, driven by impaired transport, may contribute to the pathogenesis of HD, providing us with insight into how a BDNF supplementation therapeutic strategy may best be applied for HD. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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23 pages, 7155 KiB

Open AccessArticle

Human Adipose-Derived Stem Cells Combined with Nano-Hydrogel Promote Functional Recovery after Spinal Cord Injury in Rats

by Jianping Li, Zhisheng Ji, Yu Wang, Tiantian Li, Jinghua Luo, Jun Li, Xueshuang Shi, Liming Li, Liumin He and Wutian Wu

Biology 2022, 11(5), 781; https://doi.org/10.3390/biology11050781 - 20 May 2022

Cited by 18 | Viewed by 3449

Abstract

The treatment of spinal cord injury aims to reconstruct the fiber connection and restore the interrupted neural pathways. Adipose mesenchymal stem cells (ADSCs) can promote the recovery of motor functions in spinal cord injury. However, poor survival of ADSCs and leakage outside of [...] Read more.

The treatment of spinal cord injury aims to reconstruct the fiber connection and restore the interrupted neural pathways. Adipose mesenchymal stem cells (ADSCs) can promote the recovery of motor functions in spinal cord injury. However, poor survival of ADSCs and leakage outside of the injury site after local transplantation reduce the number of cells, which seriously attenuates the cumulative effect. We performed heterotopic transplantation on rats with severe spinal cord injury using human ADSCs loaded within self-assembly hydrogel RADA16-RGD (R: arginine; A: alanine; D: aspartic acid; G: glycine). Our results indicate that the combined transplantation of human ADSCs with RADA16-RGD improved the survival of ADSCs at the injured site. The inflammatory reaction was inhibited, with improved survival of the neurons and increased residual area of nerve fibers and myelin protein. The functional behaviors were promoted, as determined by the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale score and electrophysiological measurements. ADSCs can promote the repair of spinal cord injury. This study provides new ideas for the treatment of spinal cord injury. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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17 pages, 3036 KiB

Open AccessArticle

Hydroxychloroquine Attenuates Acute Inflammation (LPS)-Induced Apoptosis via Inhibiting TRPV1 Channel/ROS Signaling Pathways in Human Monocytes

by Mustafa Güzel and Orhan Akpınar

Biology 2021, 10(10), 967; https://doi.org/10.3390/biology10100967 - 27 Sep 2021

Cited by 14 | Viewed by 2975

Abstract

Acute inflammation (INF) and apoptosis are induced in monocytes by the generation of several factors, including the products of cytosolic oxygen free radicals (cROS) and the excessive influx of Ca²⁺ via the stimulation of TRPV1. These are main factors in the etiology [...] Read more.

Acute inflammation (INF) and apoptosis are induced in monocytes by the generation of several factors, including the products of cytosolic oxygen free radicals (cROS) and the excessive influx of Ca²⁺ via the stimulation of TRPV1. These are main factors in the etiology of monocyte activation-induced inflammatory and neurodegenerative diseases. Importantly, the protective action of hydroxychloroquine (HCQ) treatment via the inhibition of TRPV1 on the levels of inflammatory factors, cROS, and apoptosis in acute INF (lipopolysaccharide, LPS)-exposed neuronal cells was recently reported. However, the relationships between acute INF via TRPV1 activation and HCQ in monocytes have not been fully clarified yet. The cell membrane of U937 human monocytes contains natural TRPV1. In the study plan, we used U937 cells in four main groups, namely control, HCQ (60 μM for 48 h), INF (1 μg/mL LPS for 16 h), and HCQ + INF. The current data indicate that LPS-induced acute INF caused the upregulation of excessive cytosolic Ca²⁺ accumulation via the stimulation of TRPV1 in the cells. The treatment of INF additionally upregulated the levels of apoptosis and cytokines (IL6, IL1β, and TNFα), due to upregulated cROS and lipid peroxidation levels as well as upregulated generation of caspase -3 (CAS3) and -9 (CAS9) but a decrease in glutathione and glutathione peroxidase. The expression levels of TRPV1, Bax, CAS3, and CAS9 were also upregulated by the treatment of LPS. However, treatment with HCQ and TRPV1 blocker (capsazepine) modulated the levels of cytokines, caspases, cROS, Ca²⁺ influx, and apoptosis through the modulation of TRPV1 in the U937 that were stimulated with LPS. In summary, the present data suggest TRPV1 activation through the acute INF (LPS)-induced inflammatory, oxidant, and apoptotic adverse actions in monocyte cells, whereas HCQ prevented adverse actions via the modulation of TRPV1. The results may be significant in the modulation of monocyte activation-caused inflammatory and neurodegenerative diseases. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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17 pages, 2798 KiB

Open AccessArticle

Neuroprotective Effects of Glochidion zeylanicum Leaf Extract against H₂O₂/Glutamate-Induced Toxicity in Cultured Neuronal Cells and Aβ-Induced Toxicity in Caenorhabditis elegans

by Chatrawee Duangjan, Panthakarn Rangsinth, Shaoxiong Zhang, Xiaojie Gu, Michael Wink and Tewin Tencomnao

Biology 2021, 10(8), 800; https://doi.org/10.3390/biology10080800 - 19 Aug 2021

Cited by 11 | Viewed by 4174

Abstract

Oxidative stress plays a crucial role in the development of age-related neurodegenerative diseases. Previously, Glochidion zeylanicum methanol (GZM) extract has been reported to have antioxidant and anti-aging properties. However, the effect of GZM on neuroprotection has not been reported yet; furthermore, the mechanism [...] Read more.

Oxidative stress plays a crucial role in the development of age-related neurodegenerative diseases. Previously, Glochidion zeylanicum methanol (GZM) extract has been reported to have antioxidant and anti-aging properties. However, the effect of GZM on neuroprotection has not been reported yet; furthermore, the mechanism involved in its antioxidant properties remains unresolved. The study is aimed to demonstrate the neuroprotective properties of GZM extract and their underlying mechanisms in cultured neuronal (HT-22 and Neuro-2a) cells and Caenorhabditis elegans models. GZM extract exhibited protective effects against glutamate/H₂O₂-induced toxicity in cultured neuronal cells by suppressing the intracellular reactive oxygen species (ROS) generation and enhancing the expression of endogenous antioxidant enzymes (SODs, GPx, and GSTs). GZM extract also triggered the expression of SIRT1/Nrf2 proteins and mRNA transcription of antioxidant genes (NQO1, GCLM, and EAAT3) which are the master regulators of cellular defense against oxidative stress. Additionally, GZM extract exhibited protective effects to counteract β-amyloid (Aβ)-induced toxicity in C. elegans and promoted neuritogenesis properties in Neuro-2a cells. Our observations suggest that GZM leaf extract has interesting neuritogenesis and neuroprotective potential and can possibly act as potential contender for the treatment of oxidative stress-induced Alzheimer’s disease (AD) and related neurodegenerative conditions; however, this needs to be studied further in other in vivo systems. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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15 pages, 2104 KiB

Open AccessArticle

Increased Levels of IL-16 in the Central Nervous System during Neuroinflammation Are Associated with Infiltrating Immune Cells and Resident Glial Cells

by Shehla U Hridi, Mark Barbour, Chelsey Wilson, Aimee JPM Franssen, Tanith Harte, Trevor J Bushell and Hui-Rong Jiang

Biology 2021, 10(6), 472; https://doi.org/10.3390/biology10060472 - 27 May 2021

Cited by 22 | Viewed by 4736

Abstract

Interleukin (IL)-16, a CD4⁺ immune cell specific chemoattractant cytokine, has been shown to be involved in the development of multiple sclerosis, an inflammatory demyelinating disease of the central nervous system (CNS). While immune cells such as T cells and macrophages are reported [...] Read more.

Interleukin (IL)-16, a CD4⁺ immune cell specific chemoattractant cytokine, has been shown to be involved in the development of multiple sclerosis, an inflammatory demyelinating disease of the central nervous system (CNS). While immune cells such as T cells and macrophages are reported to be the producers of IL-16, the cellular source of IL-16 in the CNS is less clear. This study investigates the correlation of IL-16 expression levels in the CNS with the severity of neuroinflammation and determines the phenotype of cells which produce IL-16 in the CNS of experimental autoimmune encephalomyelitis (EAE) mice. Our data show that IL-16 expression is significantly increased in the brain and spinal cord tissues of EAE mice compared to phosphate buffered saline (PBS) immunised controls. Dual immunofluorescence staining reveals that the significantly increased IL-16⁺ cells in the CNS lesions of EAE mice are likely to be the CD45⁺ infiltrating immune cells such as CD4⁺ or F4/80⁺ cells and the CNS resident CD11b⁺ microglia and GFAP⁺ astrocytes, but not NeuN+ neurons. Our data suggest cytokine IL-16 is closely involved in EAE pathology as evidenced by its increased expression in the glial and infiltrating immune cells, which impacts the recruitment and activation of CD4⁺ immune cells in the neuroinflammation. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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18 pages, 3380 KiB

Open AccessArticle

Deletion of Mitochondrial Translocator Protein (TSPO) Gene Decreases Oxidative Retinal Pigment Epithelial Cell Death via Modulation of TRPM2 Channel

by Dilek Özkaya, Xinhua Shu and Mustafa Nazıroğlu

Biology 2021, 10(5), 382; https://doi.org/10.3390/biology10050382 - 28 Apr 2021

Cited by 7 | Viewed by 2908

Abstract

The current results indicated the possible protective actions of 18 kDa mitochondrial translocator protein (TSPO) deletion on TRPM2 stimulation, mitochondrial free ROS (Mito-fROS) and apoptotic harmful actions in the cells of adult retinal pigment epithelial19 (ARPE19). There was a direct relationship between TSPO [...] Read more.

The current results indicated the possible protective actions of 18 kDa mitochondrial translocator protein (TSPO) deletion on TRPM2 stimulation, mitochondrial free ROS (Mito-fROS) and apoptotic harmful actions in the cells of adult retinal pigment epithelial19 (ARPE19). There was a direct relationship between TSPO and the disease of age-related macular degeneration. The nature of TSPO implicates upregulation of Mito-fROS and apoptosis via the activation of Ca²⁺ channels in ARPE19, although deletion of TSPO gene downregulates the activation. The decrease of oxidative cytotoxicity and apoptosis might induce in TSPO gene deleted cells by the inhibition of Mito-fROS and PARP-1 activation-induced TRPM2 cation channel activation. The ARPE19 cells were divided into two main groups as TSPO expressing (ARPE19) and non-expressing cells (ARPE19-KO). The levels of caspase -3 (Casp -3), caspase -9 (Casp -9), apoptosis, Mito-fROS, TRPM2 current and intracellular free Ca²⁺ were upregulated in the ARPE19 by the stimulations of H₂O₂ and ADP-ribose, although their levels were downregulated in the cells by the modulators of PARP-1 (DPQ and PJ34), TRPM2 (ACA and 2APB) and glutathione. However, the H₂O₂ and ADP-ribose-mediated increases were not observed in the ARPE19-KO. The expression levels of Bax, Casp -3, Casp -9 and PARP-1 were higher in the ARPE19 group as compared to the ARPE19-KO group. In summary, current results confirmed that TRPM2-mediated cell death and oxidative cytotoxicity in the ARPE19 cells were occurred by the presence of TSPO. The deletion of TSPO may be considered as a therapeutic way to TRPM2 activation-mediated retinal oxidative injury. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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19 pages, 4700 KiB

Open AccessArticle

Kaempferia parviflora Rhizome Extract Inhibits Glutamate-Induced Toxicity in HT-22 Mouse Hippocampal Neuronal Cells and Extends Longevity in Caenorhabditis elegans

by Aunchalee Tonsomboon, Mani Iyer Prasanth, Waluga Plaingam and Tewin Tencomnao

Biology 2021, 10(4), 264; https://doi.org/10.3390/biology10040264 - 26 Mar 2021

Cited by 13 | Viewed by 5334

Abstract

Kaempferia parviflora Wall. ex Baker (KP) or “Kra-chai-dam” has been shown to exhibit several pharmacological effects including anti-inflammation, antimicrobial, and sexual-enhancing activity. The objectives of this study included an investigation of the effect of KP rhizome extract against glutamate-induced toxicity in mouse hippocampal [...] Read more.

Kaempferia parviflora Wall. ex Baker (KP) or “Kra-chai-dam” has been shown to exhibit several pharmacological effects including anti-inflammation, antimicrobial, and sexual-enhancing activity. The objectives of this study included an investigation of the effect of KP rhizome extract against glutamate-induced toxicity in mouse hippocampal HT-22 neuronal cells, determination of the underlying mechanism of neuroprotection, and an evaluation of the effect of KP extract on the longevity of Caenorhabditis elegans. HT-22 cells were co-treated with glutamate (5 mM) and KP extract (25, 50, and 75 μg/mL) for 14 h. Cell viability, intracellular reactive oxygen species (ROS) assay, fluorescence-activated cell sorting (FACS) analysis, and Western blotting were performed. The longevity effect of KP extract on C. elegans was studied by lifespan measurement. In HT-22 cells, co-treatment of glutamate with KP extract significantly inhibited glutamate-mediated cytotoxicity and decreased intracellular ROS production. Additionally, the glutamate-induced apoptosis and apoptotic-inducing factor (AIF) translocation were blocked by KP extract co-treatment. Western blot analysis also demonstrated that KP extract significantly diminished extracellular signal-regulated kinase (ERK) phosphorylation induced by glutamate, and brain-derived neurotrophic factor (BDNF) was recovered to the control. Moreover, this KP extract treatment prolonged the lifespan of C. elegans. Altogether, this study suggested that KP extract possesses both neuroprotective and longevity-inducing properties, thus serving as a promising candidate for development of innovative health products. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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16 pages, 3719 KiB

Open AccessArticle

Neuroprotective Effects of Extracts from Tiger Milk Mushroom Lignosus rhinocerus Against Glutamate-Induced Toxicity in HT22 Hippocampal Neuronal Cells and Neurodegenerative Diseases in Caenorhabditis elegans

by Parinee Kittimongkolsuk, Nattaporn Pattarachotanant, Siriporn Chuchawankul, Michael Wink and Tewin Tencomnao

Biology 2021, 10(1), 30; https://doi.org/10.3390/biology10010030 - 5 Jan 2021

Cited by 18 | Viewed by 7798

Abstract

Despite the Tiger Milk Mushroom Lignosus rhinocerus (LR) having been used as a traditional medicine, little is known about the neuroprotective effects of LR extracts. This study aims to investigate the neuroprotective effect of three extracts of LR against glutamate-induced oxidative stress in [...] Read more.

Despite the Tiger Milk Mushroom Lignosus rhinocerus (LR) having been used as a traditional medicine, little is known about the neuroprotective effects of LR extracts. This study aims to investigate the neuroprotective effect of three extracts of LR against glutamate-induced oxidative stress in mouse hippocampal (HT22) cells as well as to determine their effect in Caenorhabditis elegans. In vitro, we assessed the toxicity of three LR extracts (ethanol extract (LRE), cold-water extract (LRC) and hot-water extract (LRH)) and their protective activity by MTT assay, Annexin V-FITC/propidium iodide staining, Mitochondrial Membrane Potential (MMP) and intracellular ROS accumulation. Furthermore, we determined the expression of antioxidant genes (catalase (CAT), superoxide dismutase (SOD1 and SOD2) and glutathione peroxidase (GPx)) by qRT-PCR. In vivo, we investigated the neuroprotective effect of LRE, not only against an Aβ-induced deficit in chemotaxis behavior (Alzheimer model) but also against PolyQ40 formation (model for Morbus Huntington) in transgenic C. elegans. Only LRE significantly reduced both apoptosis and intracellular ROS levels and significantly increased the expression of antioxidant genes after glutamate-induced oxidative stress in HT22 cells. In addition, LRE significantly improved the Chemotaxis Index (CI) in C. elegans and significantly decreased PolyQ40 aggregation. Altogether, the LRE exhibited neuroprotective properties both in vitro and in vivo. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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Review

Jump to: Research

42 pages, 17546 KiB

Open AccessReview

Stem Cell Transplantation Therapy and Neurological Disorders: Current Status and Future Perspectives

by Md. Mominur Rahman, Md. Rezaul Islam, Mohammad Touhidul Islam, Md. Harun-Or-Rashid, Mahfuzul Islam, Sabirin Abdullah, Mohammad Borhan Uddin, Sumit Das, Md. Saidur Rahaman, Muniruddin Ahmed, Fahad A. Alhumaydhi, Talha Bin Emran, Amany Abdel-Rahman Mohamed, Mohammad Rashed Iqbal Faruque, Mayeen Uddin Khandaker and Gomaa Mostafa-Hedeab

Biology 2022, 11(1), 147; https://doi.org/10.3390/biology11010147 - 17 Jan 2022

Cited by 46 | Viewed by 16383

Abstract

Neurodegenerative diseases are a global health issue with inadequate therapeutic options and an inability to restore the damaged nervous system. With advances in technology, health scientists continue to identify new approaches to the treatment of neurodegenerative diseases. Lost or injured neurons and glial [...] Read more.

Neurodegenerative diseases are a global health issue with inadequate therapeutic options and an inability to restore the damaged nervous system. With advances in technology, health scientists continue to identify new approaches to the treatment of neurodegenerative diseases. Lost or injured neurons and glial cells can lead to the development of several neurological diseases, including Parkinson’s disease, stroke, and multiple sclerosis. In recent years, neurons and glial cells have successfully been generated from stem cells in the laboratory utilizing cell culture technologies, fueling efforts to develop stem cell-based transplantation therapies for human patients. When a stem cell divides, each new cell has the potential to either remain a stem cell or differentiate into a germ cell with specialized characteristics, such as muscle cells, red blood cells, or brain cells. Although several obstacles remain before stem cells can be used for clinical applications, including some potential disadvantages that must be overcome, this cellular development represents a potential pathway through which patients may eventually achieve the ability to live more normal lives. In this review, we summarize the stem cell-based therapies that have been explored for various neurological disorders, discuss the potential advantages and drawbacks of these therapies, and examine future directions for this field. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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16 pages, 1066 KiB

Open AccessReview

ALS2-Related Motor Neuron Diseases: From Symptoms to Molecules

by Marcello Miceli, Cécile Exertier, Marco Cavaglià, Elena Gugole, Marta Boccardo, Rossana Rita Casaluci, Noemi Ceccarelli, Alessandra De Maio, Beatrice Vallone and Marco A. Deriu

Biology 2022, 11(1), 77; https://doi.org/10.3390/biology11010077 - 5 Jan 2022

Cited by 10 | Viewed by 3403

Abstract

Infantile-onset Ascending Hereditary Spastic Paralysis, Juvenile Primary Lateral Sclerosis and Juvenile Amyotrophic Lateral Sclerosis are all motor neuron diseases related to mutations on the ALS2 gene, encoding for a 1657 amino acids protein named Alsin. This ~185 kDa multi-domain protein is ubiquitously expressed [...] Read more.

Infantile-onset Ascending Hereditary Spastic Paralysis, Juvenile Primary Lateral Sclerosis and Juvenile Amyotrophic Lateral Sclerosis are all motor neuron diseases related to mutations on the ALS2 gene, encoding for a 1657 amino acids protein named Alsin. This ~185 kDa multi-domain protein is ubiquitously expressed in various human tissues, mostly in the brain and the spinal cord. Several investigations have indicated how mutations within Alsin’s structured domains may be responsible for the alteration of Alsin’s native oligomerization state or Alsin’s propensity to interact with protein partners. In this review paper, we propose a description of differences and similarities characterizing the above-mentioned ALS2-related rare neurodegenerative disorders, pointing attention to the effects of ALS2 mutation from molecule to organ and at the system level. Known cases were collected through a literature review and rationalized to deeply elucidate the neurodegenerative clinical outcomes as consequences of ALS2 mutations. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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25 pages, 2209 KiB

Open AccessReview

Metabolomics in Retinal Diseases: An Update

by Xing Li, Shichang Cai, Zhiming He, James Reilly, Zhihong Zeng, Niall Strang and Xinhua Shu

Biology 2021, 10(10), 944; https://doi.org/10.3390/biology10100944 - 22 Sep 2021

Cited by 15 | Viewed by 4610

Abstract

Retinal diseases are a leading cause of visual loss and blindness, affecting a significant proportion of the population worldwide and having a detrimental impact on quality of life, with consequent economic burden. The retina is highly metabolically active, and a number of retinal [...] Read more.

Retinal diseases are a leading cause of visual loss and blindness, affecting a significant proportion of the population worldwide and having a detrimental impact on quality of life, with consequent economic burden. The retina is highly metabolically active, and a number of retinal diseases are associated with metabolic dysfunction. To better understand the pathogenesis underlying such retinopathies, new technology has been developed to elucidate the mechanism behind retinal diseases. Metabolomics is a relatively new “omics” technology, which has developed subsequent to genomics, transcriptomics, and proteomics. This new technology can provide qualitative and quantitative information about low-molecular-weight metabolites (M.W. < 1500 Da) in a given biological system, which shed light on the physiological or pathological state of a cell or tissue sample at a particular time point. In this article we provide an extensive review of the application of metabolomics to retinal diseases, with focus on age-related macular degeneration (AMD), diabetic retinopathy (DR), retinopathy of prematurity (ROP), glaucoma, and retinitis pigmentosa (RP). Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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23 pages, 1178 KiB

Open AccessReview

Mutual Interactions between Brain States and Alzheimer’s Disease Pathology: A Focus on Gamma and Slow Oscillations

by Nicole Byron, Anna Semenova and Shuzo Sakata

Biology 2021, 10(8), 707; https://doi.org/10.3390/biology10080707 - 23 Jul 2021

Cited by 18 | Viewed by 9628

Abstract

Brain state varies from moment to moment. While brain state can be defined by ongoing neuronal population activity, such as neuronal oscillations, this is tightly coupled with certain behavioural or vigilant states. In recent decades, abnormalities in brain state have been recognised as [...] Read more.

Brain state varies from moment to moment. While brain state can be defined by ongoing neuronal population activity, such as neuronal oscillations, this is tightly coupled with certain behavioural or vigilant states. In recent decades, abnormalities in brain state have been recognised as biomarkers of various brain diseases and disorders. Intriguingly, accumulating evidence also demonstrates mutual interactions between brain states and disease pathologies: while abnormalities in brain state arise during disease progression, manipulations of brain state can modify disease pathology, suggesting a therapeutic potential. In this review, by focusing on Alzheimer’s disease (AD), the most common form of dementia, we provide an overview of how brain states change in AD patients and mouse models, and how controlling brain states can modify AD pathology. Specifically, we summarise the relationship between AD and changes in gamma and slow oscillations. As pathological changes in these oscillations correlate with AD pathology, manipulations of either gamma or slow oscillations can modify AD pathology in mouse models. We argue that neuromodulation approaches to target brain states are a promising non-pharmacological intervention for neurodegenerative diseases. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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16 pages, 2337 KiB

Open AccessReview

The Relationship of the Mechanisms of the Pathogenesis of Multiple Sclerosis and the Expression of Endogenous Retroviruses

by Vera R. Lezhnyova, Ekaterina V. Martynova, Timur I. Khaiboullin, Richard A. Urbanowicz, Svetlana F. Khaiboullina and Albert A. Rizvanov

Biology 2020, 9(12), 464; https://doi.org/10.3390/biology9120464 - 11 Dec 2020

Cited by 7 | Viewed by 3879

Abstract

Two human endogenous retroviruses of the HERV-W family can act as cofactors triggering multiple sclerosis (MS): MS-associated retrovirus (MSRV) and ERVWE1. Endogenous retroviral elements are believed to have integrated in our ancestors’ DNA millions of years ago. Their involvement in the pathogenesis of [...] Read more.

Two human endogenous retroviruses of the HERV-W family can act as cofactors triggering multiple sclerosis (MS): MS-associated retrovirus (MSRV) and ERVWE1. Endogenous retroviral elements are believed to have integrated in our ancestors’ DNA millions of years ago. Their involvement in the pathogenesis of various diseases, including neurodegenerative pathologies, has been demonstrated. Numerous studies have shown a correlation between the deterioration of patients’ health and increased expression of endogenous retroviruses. The exact causes and mechanisms of endogenous retroviruses activation remains unknown, which hampers development of therapeutics. In this review, we will summarize the main characteristics of human endogenous W retroviruses and describe the putative mechanisms of activation, including epigenetic mechanisms, humoral factors as well as the role of the exogenous viral infections. Full article

(This article belongs to the Special Issue Neurodegenerative Diseases: Molecular Mechanisms and Therapeutic Applications)

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