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Biomedicines
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The Contribution of Astrocytes to Human Neurodegenerative Diseases
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The Contribution of Astrocytes to Human Neurodegenerative Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (15 May 2022) | Viewed by 11345

Special Issue Editors

Prof. Dr. Rickie Patani

E-Mail Website
Guest Editor
Department of Neuromuscular Diseases, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK
Interests: neurology; neuroscience; induced pluripotent stem cell models of diseases; RNA metabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Ben Clarke

E-Mail Website
Co-Guest Editor
Department of Neuromuscular Diseases, Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK
Interests: neuroscience; induced pluripotent stem cell models of diseases; astrocyte reactivity

Special Issue Information

Dear Colleagues,

Neurodegeneration occurs in several devastating and incurable diseases, including Alzheimer's disease, Parkinson’s disease, amyotrophic lateral sclerosis (ALS) and multiple sclerosis. The precise mechanisms by which neurons become dysfunctional and ultimately degenerate remain largely unresolved, but there is an increasing recognition for the role of astrocytes in disease pathomechanisms. Astrocytes fulfil multiple supportive roles in aiding neuronal function in the central nervous system (CNS) but have been found to become dysfunctional in several neurodegenerative diseases, sometimes coinciding with the acquisition of neurotoxic immune phenotypes. This Special Issue focuses specifically on novel insights concerning how astrocytes contribute to the molecular and cellular phases of human neurological diseases. Original manuscripts and/or reviews dealing with these issues are most welcome from outstanding experts on the topic.

Prof. Dr. Rickie Patani
Guest Editors
Dr. Ben Clarke
Co-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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • neurodegeneration
  • astrocytes
  • induced pluripotent stem cell (iPSC) models of diseases
  • human postmortem tissue
  • RNA metabolism
  • astrocyte reactivity

Published Papers (4 papers)

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Research

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30 pages, 9018 KiB  
Article
Retinal Changes in Astrocytes and Müller Glia in a Mouse Model of Laser-Induced Glaucoma: A Time-Course Study
by Jose A. Fernández-Albarral, Rosa de Hoz, José A. Matamoros, Lejing Chen, Inés López-Cuenca, Elena Salobrar-García, Lidia Sánchez-Puebla, José M. Ramírez, Alberto Triviño, Juan J. Salazar and Ana I. Ramírez
Biomedicines 2022, 10(5), 939; https://doi.org/10.3390/biomedicines10050939 - 19 Apr 2022
Cited by 10 | Viewed by 2468
Abstract
Macroglia (astrocytes and Müller glia) may play an important role in the pathogenesis of glaucoma. In a glaucoma mouse model, we studied the effects of unilateral laser-induced ocular hypertension (OHT) on macroglia in OHT and contralateral eyes at different time points after laser [...] Read more.
Macroglia (astrocytes and Müller glia) may play an important role in the pathogenesis of glaucoma. In a glaucoma mouse model, we studied the effects of unilateral laser-induced ocular hypertension (OHT) on macroglia in OHT and contralateral eyes at different time points after laser treatment (1, 3, 5, 8 and 15 days) using anti-GFAP and anti-MHC-II, analyzing the morphological changes, GFAP-labelled retinal area (GFAP-PA), and GFAP and MHC-II immunoreactivity intensities ((GFAP-IRI and MHC-II-IRI)). In OHT and contralateral eyes, with respect to naïve eyes, at all the time points, we found the following: (i) astrocytes with thicker somas and more secondary processes, mainly in the intermediate (IR) and peripheral retina (PR); (ii) astrocytes with low GFAP-IRI and only primary processes near the optic disc (OD); (iii) an increase in total GFAP-RA, which was higher at 3 and 5 days, except for at 15 days; (iv) an increase in GFAP-IRI in the IR and especially in the PR; (v) a decrease in GFAP-IRI near the OD, especially at 1 and 5 days; (vi) a significant increase in MHC-II-IRI, which was higher in the IR and PR; and (vii) the Müller glia were GFAP+ and MHC-II+. In conclusion, in this model of glaucoma, there is a bilateral macroglial activation maintained over time involved in the inflammatory glaucoma process. Full article
(This article belongs to the Special Issue The Contribution of Astrocytes to Human Neurodegenerative Diseases)
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17 pages, 3927 KiB  
Article
The AST-120 Recovers Uremic Toxin-Induced Cognitive Deficit via NLRP3 Inflammasome Pathway in Astrocytes and Microglia
by Lung-Chih Li, Wei-Yu Chen, Jin-Bor Chen, Wen-Chin Lee, Chiung-Chih Chang, Hong-Tai Tzeng, Chiang-Chi Huang, Ya-Jen Chang and Jenq-Lin Yang
Biomedicines 2021, 9(9), 1252; https://doi.org/10.3390/biomedicines9091252 - 17 Sep 2021
Cited by 11 | Viewed by 3035
Abstract
Chronic kidney disease (CKD) is characterized by the progressive loss of renal function; moreover, CKD progression commonly leads to multiple comorbidities, including neurological dysfunction and immune disorders. CKD-triggered neuroinflammation significantly contributes to cognitive impairment. This study aimed to investigate the contribution of uremic [...] Read more.
Chronic kidney disease (CKD) is characterized by the progressive loss of renal function; moreover, CKD progression commonly leads to multiple comorbidities, including neurological dysfunction and immune disorders. CKD-triggered neuroinflammation significantly contributes to cognitive impairment. This study aimed to investigate the contribution of uremic toxins to cognitive impairment. Serum creatinine, blood urea nitrogen (BUN), indoxyl sulfate (IS), and p-cresol sulfate (PCS) levels were measured using an enzyme-linked immunosorbent assay and high-performance liquid chromatography. The creatinine, BUN, IS, and PCS levels were increased from 4 weeks after 5/6-nephrectomy in mice, which suggested that 5/6-nephrectomy could yield a CKD animal model. Further, CKD mice showed significantly increased brain and serum indoxyl sulfate levels. Immunohistochemistry analysis revealed hippocampal inflammation and NLRP3-inflammasomes in astrocytes. Further, the Y-maze and Morris water maze tests revealed learning and memory defects in CKD mice. AST-120, which is also an IS absorbent, effectively reduced serum and hippocampal IS levels as well as reversed the cognitive impairment in CKD mice. Additionally, NLRP3-knockout mice that underwent 5/6-nephrectomy showed no change in cognitive function. These findings suggested that IS is an important uremic toxin that induces NLRP3 inflammasome-mediated not only in microglia, but it also occurred in astrocytic inflammation, which subsequently causes cognitive impairment. Full article
(This article belongs to the Special Issue The Contribution of Astrocytes to Human Neurodegenerative Diseases)
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15 pages, 2528 KiB  
Article
Bradykinin, as a Reprogramming Factor, Induces Transdifferentiation of Brain Astrocytes into Neuron-like Cells
by Tsong-Hai Lee, Pei-Shan Liu, Su-Jane Wang, Ming-Ming Tsai, Velayuthaprabhu Shanmugam and Hsi-Lung Hsieh
Biomedicines 2021, 9(8), 923; https://doi.org/10.3390/biomedicines9080923 - 30 Jul 2021
Cited by 3 | Viewed by 2146
Abstract
Kinins are endogenous, biologically active peptides released into the plasma and tissues via the kallikrein-kinin system in several pathophysiological events. Among kinins, bradykinin (BK) is widely distributed in the periphery and brain. Several studies on the neuro-modulatory actions of BK by the B [...] Read more.
Kinins are endogenous, biologically active peptides released into the plasma and tissues via the kallikrein-kinin system in several pathophysiological events. Among kinins, bradykinin (BK) is widely distributed in the periphery and brain. Several studies on the neuro-modulatory actions of BK by the B2BK receptor (B2BKR) indicate that this neuropeptide also functions during neural fate determination. Previously, BK has been shown to induce differentiation of nerve-related stem cells into neuron cells, but the response in mature brain astrocytes is unknown. Herein, we used rat brain astrocyte (RBA) to investigate the effect of BK on cell transdifferentiation into a neuron-like cell morphology. Moreover, the signaling mechanisms were explored by zymographic, RT-PCR, Western blot, and immunofluorescence staining analyses. We first observed that BK induced RBA transdifferentiation into neuron-like cells. Subsequently, we demonstrated that BK-induced RBA transdifferentiation is mediated through B2BKR, PKC-δ, ERK1/2, and MMP-9. Finally, we found that BK downregulated the astrocytic marker glial fibrillary acidic protein (GFAP) and upregulated the neuronal marker neuron-specific enolase (NSE) via the B2BKR/PKC-δ/ERK pathway in the event. Therefore, BK may be a reprogramming factor promoting brain astrocytic transdifferentiation into a neuron-like cell, including downregulation of GFAP and upregulation of NSE and MMP-9 via the B2BKR/PKC-δ/ERK cascade. Here, we also confirmed the transdifferentiative event by observing the upregulated neuronal nuclear protein (NeuN). However, the electrophysiological properties of the cells after BK treatment should be investigated in the future to confirm their phenotype. Full article
(This article belongs to the Special Issue The Contribution of Astrocytes to Human Neurodegenerative Diseases)
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Review

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18 pages, 1053 KiB  
Review
Astrocytes, a Promising Opportunity to Control the Progress of Parkinson’s Disease
by Alberto Sanchez, Ingrid Morales, Clara Rodriguez-Sabate, Miguel Sole-Sabater and Manuel Rodriguez
Biomedicines 2021, 9(10), 1341; https://doi.org/10.3390/biomedicines9101341 - 28 Sep 2021
Cited by 4 | Viewed by 2872
Abstract
At present, there is no efficient treatment to prevent the evolution of Parkinson’s disease (PD). PD is generated by the concurrent activity of multiple factors, which is a serious obstacle for the development of etio-pathogenic treatments. Astrocytes may act on most factors involved [...] Read more.
At present, there is no efficient treatment to prevent the evolution of Parkinson’s disease (PD). PD is generated by the concurrent activity of multiple factors, which is a serious obstacle for the development of etio-pathogenic treatments. Astrocytes may act on most factors involved in PD and the promotion of their neuroprotection activity may be particularly suitable to prevent the onset and progression of this basal ganglia (BG) disorder. The main causes proposed for PD, the ability of astrocytes to control these causes, and the procedures that can be used to promote the neuroprotective action of astrocytes will be commented upon, here. Full article
(This article belongs to the Special Issue The Contribution of Astrocytes to Human Neurodegenerative Diseases)
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