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astrocytes and neurodegenerative disease

Ana Clara Liberman, Emiliano Trias, Luana da Silva Chagas, Pablo Trindade, Marissol Dos Santos Pereira, Damian Refojo, Cecilia Hedin-Pereira, Claudio A Serfaty
An extensive microglial-astrocyte-monocyte-neuronal cross talk seems to be crucial for normal brain function, development, and recovery. However, under certain conditions neuroinflammatory interactions between brain cells and neuroimmune cells influence disease outcome and brain pathology. Microglial cells express a range of functional states with dynamically pleomorphic profiles from a surveilling status of synaptic transmission to an active player in major events of development such as synaptic elimination, regeneration, and repair...
December 5, 2018: Neuroimmunomodulation
Corona Solana, Raquel Tarazona, Rafael Solana
Alzheimer's disease (AD) represents the most common cause of dementia in the elderly. AD is a neurodegenerative disorder characterized by progressive memory loss and cognitive decline. Although the aetiology of AD is not clear, both environmental factors and heritable predisposition may contribute to disease occurrence. In addition, inflammation and immune system alterations have been linked to AD. The prevailing hypothesis as cause of AD is the deposition in the brain of amyloid beta peptides (A β ). Although A β have a role in defending the brain against infections, their accumulation promotes an inflammatory response mediated by microglia and astrocytes...
2018: International Journal of Alzheimer's Disease
Diego S Ojeda, Daniel Grasso, Javier Urquiza, Andreas Till, María Inés Vaccaro, Jorge Quarleri
Despite more than 30 years of extensive research efforts, a complete understanding of the neurological consequences of HIV central nervous system (CNS) infection remains elusive. HIV is not only able to establish a viral reservoir in the CNS but also to initiate manifestation of neurodegenerative diseases. These neurological disorders may arise because of virus-induced activation of the inflammasome in CNS cells, including astrocytes. Nevertheless, in some productive viral infection scenarios, selective autophagy may reduce inflammation through mitochondrial degradation ("mitophagy") to counteract inflammasome activation...
2018: Frontiers in Immunology
Yasuharu Takamori, Yukie Hirahara, Taketoshi Wakabayashi, Tetsuji Mori, Taro Koike, Yosky Kataoka, Yasuhisa Tamura, Shuji Kurebayashi, Kiyoshi Kurokawa, Hisao Yamada
Lamins are type V intermediate filament proteins that are located beneath the inner nuclear membrane. In mammalian somatic cells, LMNB1 and LMNB2 encode somatic lamins B1 and B2, respectively, and the LMNA gene is alternatively spliced to generate somatic lamins A and C. Mutations in lamin genes have been linked to many human hereditary diseases, including neurodegenerative disorders. Knowledge about lamins in the nervous system has been accumulated recently, but a precise analysis of lamin subtypes in glial cells has not yet been reported...
December 2018: IBRO Reports
Yong-Shun Guo, Pei-Zhou Liang, Shen-Zhao Lu, Rong Chen, Yan-Qing Yin, Jia-Wei Zhou
Neuroinflammation is considered a challenging clinical problem. Chronic inflammatory responses play important roles in the onset and progression of various neurodegenerative diseases, including multiple sclerosis (MS). Previous studies have shown that astrocytes express small heat shock protein αB-crystallin (CRYAB) which is capable of inhibiting inflammatory responses in astrocytes per se. However, the underlying mechanisms of CRYAB-induced modulation of neuroinflammation are still not fully understood. In the present study, we investigated the role of extracellular CRYAB in the interaction between microglia and astrocytes in the context of MS-associated neuroinflammation...
November 26, 2018: Biochemical and Biophysical Research Communications
Mona Dehhaghi, Vanessa Tan, Benjamin Heng, Fatemeh Mohammadipanah, Gilles J Guillemin
Astrocytes, the main non-neuronal cells in the brain, have significant roles in the maintenance and survival of neurons. Oxidative stress has been implicated in various neurodegenerative disorders such as Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), and Parkinson's disease (PD). Myxobacteria produce a wide range of bioactive metabolites with notable structures and modes of action, which introduce them as potent natural product producers. In the present study, we evaluated the effects of myxobacterial extracts on hydrogen peroxide (H2 O2 ) mediated toxicity on primary human astrocytes...
November 26, 2018: Neuroscience
Daniele Lana, Filippo Ugolini, Gary L Wenk, Maria Grazia Giovannini, Sandra Zecchi-Orlandini, Daniele Nosi
Aging and neurodegenerative diseases share a condition of neuroinflammation entailing the production of endogenous cell debris in the CNS that must be removed by microglia ( i.e., resident macrophages), to restore tissue homeostasis. In this context, extension of microglial cell branches toward cell debris underlies the mechanisms of microglial migration and phagocytosis. Amoeboid morphology and the consequent loss of microglial branch functionality characterizes dysregulated microglia. Microglial migration is assisted by another glial population, the astroglia, which forms a dense meshwork of cytoplasmic projections...
November 29, 2018: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Andrew R Mendelsohn, James Larrick
Neuroinflammation is thought to play a key role in progression of neurodegenerative disease such as Alzheimer's disease. Given the apparent nexus of inflammatory disease with the secretory associated senescence phenotype (SASP) of cellular senescence, two reports found that tau-mediated neurodegeneration involves induction of senescence in astrocytes, microglia and possibly even neurons. Elimination of senescent cells by pharmacological induced genetic ablation or by senolytic drugs blocks progression of mutant human tau-mediated neurodegeneration in mice...
November 29, 2018: Rejuvenation Research
Simona Federica Spampinato, Agata Copani, Ferdinando Nicoletti, Maria Angela Sortino, Filippo Caraci
Neurodegenerative disorders are characterized by excitotoxicity and neuroinflammation that finally lead to slow neuronal degeneration and death. Although neurons are the principal target, glial cells are important players as they contribute by either exacerbating or dampening the events that lead to neuroinflammation and neuronal damage. A dysfunction of the glutamatergic system is a common event in the pathophysiology of these diseases. Metabotropic glutamate (mGlu) receptors belong to a large family of G protein-coupled receptors largely expressed in neurons as well as in glial cells...
2018: Frontiers in Molecular Neuroscience
Ann C Mckee, Bobak Abdolmohammadi, Thor D Stein
Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy associated with repetitive head trauma, including concussion and subconcussion. CTE was first recognized in boxers nearly a century ago as "dementia pugilistica" or "punch drunk," but has been recently identified in contact sports athletes (including American football, ice hockey, soccer, baseball, rugby, boxing, and wrestling) and military veterans exposed to blast. Similar to many other neurodegenerative diseases, CTE is diagnosed conclusively only by neuropathologic examination of brain tissue...
2018: Handbook of Clinical Neurology
Huanhuan Wang, Wenhai Huang, Meihao Liang, Yingying Shi, Chixiao Zhang, Qin Li, Meng Liu, Yikai Shou, Hongping Yin, Xiaozheng Zhu, Xiaoyan Sun, Yu Hu, Zhengrong Shen
Background: Microglia activation is a crucial event in neurodegenerative disease. The depression of microglial inflammatory response is considered a promising therapeutic strategy. NFκB signaling, including IKK/IκB phosphotylation, p65 nucelus relocalization and NFκB-related genes transcription are prevalent accepted to play important role in microglial activation. (+)-JQ1, a BRD4 inhibitor firstly discovered as an anti-tumor agent, was later confirmed to be an anti-inflammatory compound...
2018: Cell & Bioscience
Sabrina Strobel, Edna Grünblatt, Helmut Heinsen, Peter Riederer, Thomas Espach, Michael Meder, Camelia-Maria Monoranu
Oxidative stress is implicated in the pathogenesis of neurodegenerative diseases, including sporadic Alzheimer's disease (AD). Mitochondrial DNA (mtDNA) deletions are markers of oxidative damage with an age-dependent accumulation. In a previous study, we analyzed mtDNA levels in diverse neuronal cell types in order to unravel the impact of oxidative stress in brains of AD patients. The aim of this study was to identify possible correlations between mtDNA deletion levels of selected astrocytes and microglia from three brain regions with different vulnerability to AD pathology and different stages of disease compared to controls...
November 22, 2018: Journal of Alzheimer's Disease: JAD
D V Telegina, O S Kozhevnikova, N G Kolosova
Age is the major risk factor in the age-related macular degeneration (AMD) which is a complex multifactor neurodegenerative disease of the retina and the main cause of irreversible vision loss in people over 60 years old. The major role in AMD pathogenesis belongs to structure-functional changes in the retinal pigment epithelium cells, while the onset and progression of AMD are commonly believed to be caused by the immune system dysfunctions. The role of retinal glial cells (Muller cells, astrocytes, and microglia) in AMD pathogenesis is studied much less...
September 2018: Biochemistry. Biokhimii︠a︡
Eun-Jung Lee, Jin-Sun Park, Yu-Young Lee, Do-Yeon Kim, Jihee Lee Kang, Hee-Sun Kim
BACKGROUND: Recent evidence suggests that reactive astrocytes play an important role in neuroinflammation and neurodegenerative diseases. Thus, controlling astrocyte reactivity has been suggested as a promising strategy for treating neurodegenerative diseases. In the present study, we investigated whether a matrix metalloproteinase (MMP)-8 inhibitor, M8I, could control neuroinflammation in lipoteichoic acid (LTA)-stimulated rat primary astrocytes. METHODS: The effects of M8I on the expression of inducible nitric oxide synthase, cytokines, and MMPs were examined in LTA-stimulated rat primary astrocytes by ELISA, RT-PCR, and Western blot analysis...
November 23, 2018: Journal of Neuroinflammation
Wen-Ying Chen, Cheng-Yi Chang, Jian-Ri Li, Jiaan-Der Wang, Chih-Cheng Wu, Yu-Hsiang Kuan, Su-Lan Liao, Wen-Yi Wang, Chun-Jung Chen
Microglia polarization of classical activation state is crucial to the induction of neuroinflammation, and has been implicated in the pathogenesis of numerous neurodegenerative diseases. Fungal immunomodulatory proteins are emerging health-promoting natural substances with multiple pharmacological activities, including immunomodulation. Herein, we investigated the anti-inflammatory and neuroprotective potential of fungal immunomodulatory protein extracted from Ganoderma microsporum (GMI) in an in vitro rodent model of primary cultures...
November 21, 2018: International Journal of Molecular Sciences
Irene García-Domínguez, Karolina Veselá, Juan García-Revilla, Alejandro Carrillo-Jiménez, María Angustias Roca-Ceballos, Marti Santiago, Rocío M de Pablos, José L Venero
The impact of systemic inflammation in nigral dopaminergic cell loss remains unclear. Here, we have investigated the role of peripheral inflammation induced by systemic lipopolysaccharide (LPS) administration in the MPTP-based model of Parkinson's disease. Brain inflammation, microglia and astroglia activation, disruption of the blood-brain barrier (BBB) and integrity of the nigrostriatal dopaminergic system were evaluated in response to i.p. injection of LPS, MPTP or the combination of both. Our results showed that combinative treatment exacerbates microglia activation and enhances (i) the appearance of galectin-3-positive microglia, recently identified as microglial disease-associated phenotypic marker, (ii) the up-regulation of pro-inflammatory cytokines, (iii) the occurrence of A1 neurotoxic astrocytes, (iv) the breakdown of the BBB, and (v) the loss of dopaminergic neurons in the substantia nigra...
2018: Frontiers in Cellular Neuroscience
Ana-Maria Zagrean, Dirk M Hermann, Ioan Opris, Leon Zagrean, Aurel Popa-Wagner
Restorative strategies after stroke are focused on the remodeling of cerebral endothelial cells and brain parenchymal cells. The latter, i.e., neurons, neural precursor cells and glial cells, synergistically interact with endothelial cells in the ischemic brain, providing a neurovascular unit (NVU) remodeling that can be used as target for stroke therapies. Intercellular communication and signaling within the NVU, the multicellular brain-vessel-blood interface, including its highly selective blood-brain barrier, are fundamental to the central nervous system homeostasis and function...
2018: Frontiers in Neuroscience
Henna Konttinen, Irina Gureviciene, Minna Oksanen, Alexandra Grubman, Sanna Loppi, Mikko T Huuskonen, Paula Korhonen, Riikka Lampinen, Meike Keuters, Irina Belaya, Heikki Tanila, Katja M Kanninen, Gundars Goldsteins, Gary Landreth, Jari Koistinaho, Tarja Malm
Astrocytes are the gatekeepers of neuronal energy supply. In neurodegenerative diseases, bioenergetics demand increases and becomes reliant upon fatty acid oxidation as a source of energy. Defective fatty acid oxidation and mitochondrial dysfunctions correlate with hippocampal neurodegeneration and memory deficits in Alzheimer's disease (AD), but it is unclear whether energy metabolism can be targeted to prevent or treat the disease. Here we show for the first time an impairment in fatty acid oxidation in human astrocytes derived from induced pluripotent stem cells of AD patients...
November 19, 2018: Glia
Jenny Sassone, Elsa Papadimitriou, Dimitra Thomaidou
Huntington's Disease (HD) is a neurodegenerative disorder caused by a CAG expansion in the exon-1 of the IT15 gene encoding the protein Huntingtin. Expression of mutated Huntingtin in humans leads to dysfunction and ultimately degeneration of selected neuronal populations of the striatum and cerebral cortex. Current available HD therapy relies on drugs to treat chorea and control psychiatric symptoms, however, no therapy has been proven to slow down disease progression or prevent disease onset. Thus, although 24 years have passed since HD gene identification, HD remains a relentless progressive disease characterized by cognitive dysfunction and motor disability that leads to death of the majority of patients, on average 10-20 years after its onset...
2018: Frontiers in Neuroscience
Zahra Jahangiri, Zahra Gholamnezhad, Mahmoud Hosseini
Alzheimer's disease (AD) is a fastest growing neurodegenerative condition with no standard treatment. There are growing evidence about the beneficial effects of exercise in brain health promotion and slowing the cognitive decline. The aim of this study was to review the protective mechanisms of treadmill exercise in different models of rodent memory deficits. Online literature database, including PubMed-Medline, Scopus, Google scholar were searched from 2003 till 2017. Original article with English language were chosen according to following key words in the title: (exercise OR physical activity) AND (memory OR learning)...
November 15, 2018: Metabolic Brain Disease
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