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https://www.readbyqxmd.com/read/28231054/alzheimer-s-disease-as-an-inflammatory-disease
#1
Marta Bolós, Juan Ramón Perea, Jesús Avila
Alzheimer's disease (AD) is a neurodegenerative condition characterized by the formation of amyloid-β plaques, aggregated and hyperphosphorylated tau protein, activated microglia and neuronal cell death, ultimately leading to progressive dementia. In this short review, we focus on neuroinflammation in AD. Specifically, we describe the participation of microglia, as well as other factors that may contribute to inflammation, in neurodegeneration.
February 23, 2017: Biomolecular Concepts
https://www.readbyqxmd.com/read/28226226/microglia-function-in-the-central-nervous-system-during-health-and-neurodegeneration
#2
Marco Colonna, Oleg Butovsky
Microglia are resident cells of the brain that regulate brain development, maintenance of neuronal networks, and injury repair. Microglia serve as brain macrophages but are distinct from other tissue macrophages owing to their unique homeostatic phenotype and tight regulation by the central nervous system (CNS) microenvironment. They are responsible for the elimination of microbes, dead cells, redundant synapses, protein aggregates, and other particulate and soluble antigens that may endanger the CNS. Furthermore, as the primary source of proinflammatory cytokines, microglia are pivotal mediators of neuroinflammation and can induce or modulate a broad spectrum of cellular responses...
February 9, 2017: Annual Review of Immunology
https://www.readbyqxmd.com/read/28224343/amphotericin-b-increases-transglutaminase-2-expression-associated-with-upregulation-of-endocytotic-activity-in-mouse-microglial-cell-line-bv-2
#3
Kenji Kawabe, Katsura Takano, Mitsuaki Moriyama, Yoichi Nakamura
Amphotericin B (AmB), a polyene antibiotic, is reported to cause the microglial activation to induce nitric oxide (NO) production and proinflammatory cytokines expression, and change neurotrophic factors expression in cultured microglia (Motoyoshi et al. in Neurochem Int 52:1290-1296, 2008). On the other hand, tissue-type transglutaminase (TG2) is involved in connection to phagocytes with apoptotic cells. Engulfment of neurons by activated microglia is thought to cause neurodegenerative diseases but detail is unclear, and involvement of TG2 in phagocytosis has been reported in our previous study using lipopolysaccharide-stimulated BV-2 cells (Kawabe et al...
February 21, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28224333/anti-neuroinflammatory-effects-of-grossamide-from-hemp-seed-via-suppression-of-tlr-4-mediated-nf-%C3%AE%C2%BAb-signaling-pathways-in-lipopolysaccharide-stimulated-bv2-microglia-cells
#4
Qian Luo, Xiaoli Yan, Larisa Bobrovskaya, Mei Ji, Huiqing Yuan, Hongxiang Lou, Peihong Fan
Grossamide, a representative lignanamide in hemp seed, has been reported to possess potential anti-inflammatory effects. However, the potential anti-neuroinflammatory effects and underlying mechanisms of action of grossamide are still unclear. Therefore, the present study investigated the possible effects and underlying mechanisms of grossamide against lipopolysaccharide (LPS)-induced inflammatory response in BV2 microglia cells. BV2 microglia cells were pre-treated with various concentrations of grossamide before being stimulated with LPS to induce inflammation...
February 21, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28214532/smn1-functions-as-a-novel-inhibitor-for-traf6-mediated-nf-%C3%AE%C2%BAb-signaling
#5
Eun Kyung Kim, Eui-Ju Choi
Survival motor neuron (SMN) is a 38-kDa protein, whose deficiency in humans develops spinal muscular atrophy (SMA), an autosomal recessive neurodegenerative disease with muscular atrophy due to motor neuron death in the spinal cord. We now report that SMN prevents the activation of TRAF6 and IκB kinase (IKK) and thereby negatively regulates the NF-κB signaling processes. SMN physically interacted with TRAF6 and with each component of the IKK complex, IKK-α, IKK-β, and IKK-γ in BV2 microglia cells. Moreover, SMN1 inhibited the E3 ubiquitin ligase activity of TRAF6 as well as the kinase activity of IKK...
February 15, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28210209/lactate-shuttles-in-neuroenergetics-homeostasis-allostasis-and-beyond
#6
REVIEW
Shayne Mason
Understanding brain energy metabolism-neuroenergetics-is becoming increasingly important as it can be identified repeatedly as the source of neurological perturbations. Within the scientific community we are seeing a shift in paradigms from the traditional neurocentric view to that of a more dynamic, integrated one where astrocytes are no longer considered as being just supportive, and activated microglia have a profound influence. Lactate is emerging as the "good guy," contrasting its classical "bad guy" position in the now superseded medical literature...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28202680/cross-talk-between-lrrk2-and-pka-implication-for-parkinson-s-disease
#7
REVIEW
Elisa Greggio, Luigi Bubacco, Isabella Russo
Evidence indicates that leucine-rich repeat kinase 2 (LRRK2) controls multiple processes in neurons and glia cells. Deregulated LRRK2 activity due to gene mutation represents the most common cause of autosomal dominant Parkinson's disease (PD). Protein kinase A (PKA)-mediated signaling is a key regulator of brain function. PKA-dependent pathways play an important role in brain homeostasis, neuronal development, synaptic plasticity, control of microglia activation and inflammation. On the other hand, a decline of PKA signaling was shown to contribute to the progression of several neurodegenerative diseases, including PD...
February 8, 2017: Biochemical Society Transactions
https://www.readbyqxmd.com/read/28202666/lrrk2-in-peripheral-and-central-nervous-system-innate-immunity-its-link-to-parkinson-s-disease
#8
REVIEW
Heyne Lee, William S James, Sally A Cowley
Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are found in familial and idiopathic cases of Parkinson's disease (PD), but are also associated with immune-related disorders, notably Crohn's disease and leprosy. Although the physiological function of LRRK2 protein remains largely elusive, increasing evidence suggests that it plays a role in innate immunity, a process that also has been implicated in neurodegenerative diseases, including PD. Innate immunity involves macrophages and microglia, in which endogenous LRRK2 expression is precisely regulated and expression is strongly up-regulated upon cell activation...
February 8, 2017: Biochemical Society Transactions
https://www.readbyqxmd.com/read/28202386/paraquat-and-maneb-co-exposure-induces-noradrenergic-locus-coeruleus-neurodegeneration-through-nadph-oxidase-mediated-microglial-activation
#9
Liyan Hou, Cong Zhang, Ke Wang, Xiaofang Liu, Hongwei Wang, Yuning Che, Fuqiang Sun, Xueying Zhou, Xiulan Zhao, Qingshan Wang
Co-exposure to paraquat (PQ) and maneb (Mb) has been shown to increase the risk of Parkinson's disease (PD) and dopaminergic (DA) neurodegeneration in the substantia nigra pars compacta (SNpc) is observed in PQ and Mb-treated experimental animals. The loss of noradrenergic locus coeruleus (LC/NE) neurons in brainstem is a common feature shared by multiple neurodegenerative diseases, including PD. However, whether PQ and Mb is able to damage LC/NE neurons remains undefined. In this study, mice treated with combined PQ and Mb displayed progressive LC/NE neurodegeneration...
February 13, 2017: Toxicology
https://www.readbyqxmd.com/read/28188715/-multiple-sclerosis-current-immunological-aspects
#10
Carlos Cuevas-García
Multiple sclerosis is the most common inflammatory, chronic and degenerative condition of the central nervous system, and represents the first cause of disability in young adults. In Mexico, 11 to 20 out of every 100 000 people suffer from this disease. The causes of multiple sclerosis remain unknown, but several theories have been proposed: the interaction of environmental factors, viral infectious factors and genetic and immune susceptibility of each individual patient, which induce an autoimmune response and promote neuronal/axonal degeneration...
January 2017: Revista Alergia Mexico: Organo Oficial de la Sociedad Mexicana de Alergia e Inmunología, A.C
https://www.readbyqxmd.com/read/28188247/neurodegeneration-enhances-the-development-of-arthritis
#11
Stefanie C Lang, Ulrike Harre, Pavitra Purohit, Katharina Dietel, Deborah Kienhöfer, Jonas Hahn, Wolfgang Baum, Martin Herrmann, Georg Schett, Dirk Mielenz
The prevalence of neurodegenerative disease and arthritis increases with age. Despite both processes being associated with immune activation and inflammation, little is known about the mechanistic interactions between neurodegenerative disease and arthritis. In this article, we show that tau-transgenic (tau-tg) mice that develop neurodegenerative disease characterized by deposition of tau tangles in the brain are highly susceptible to developing arthritis. Already at steady-state conditions, tau-tg mice exhibit peripheral immune activation that is manifested by higher numbers of granulocytes, plasmablasts, and inflammatory Ly6C(hi) CCR2(+) monocytes, as well as increased levels of proinflammatory cytokines, such as TNF-α and IL-17...
February 10, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28183245/ykl-40-as-a-potential-biomarker-and-a-possible-target-in-therapeutic-strategies-of-alzheimer-s-disease
#12
Paweł Muszyński, Magdalena Groblewska, Agnieszka Kulczyńska-Przybik, Alina Kułakowska, Barbara Mroczko
BACKGROUND: Growing body of evidence suggests that pathogenesis of Alzheimer's disease (AD), a progressing neurodegenerative condition, is not limited to the neuronal compartment, but also involves various immunological mechanisms. Insoluble Aβ aggregates in the brain can induce the activation of microglia, resulting in synthesis of proinflammatory mediators, which further can stimulate astrocytic expression of YKL-40. Therefore, the aim of the current review is to present up-to-date data about the role of YKL-40 as a biomarker of AD as well as the possibility of therapeutic strategies targeting neuroinflammation...
February 8, 2017: Current Neuropharmacology
https://www.readbyqxmd.com/read/28174214/excitotoxicity-induced-immediate-prostaglandin-d2-production-induces-sustained-microglial-activation-and-delayed-neuronal-death-in-the-hippocampus
#13
Kensuke Iwasa, Shinji Yamamoto, Sosuke Yagishita, Kei Maruyama, Keisuke Yoshikawa
Excitotoxicity is the pivotal mechanism of neuronal death. Prostaglandins (PGs) produced during excitotoxicity play important roles in neurodegenerative conditions. Previously, we demonstrated that initial burst productions of PGD2, PGE2 and PGF2alpha are produced by Cyclooxygenase-2 (COX-2) in the hippocampus following a single systemic kainic acid (KA) administration. In addition, we showed that blocking of all PG productions ameliorated hippocampal delayed neuronal death at 30 days after KA administration...
February 7, 2017: Journal of Lipid Research
https://www.readbyqxmd.com/read/28168207/additive-amelioration-of-als-by-co-targeting-independent-pathogenic-mechanisms
#14
Ashley E Frakes, Lyndsey Braun, Laura Ferraiuolo, Denis C Guttridge, Brian K Kaspar
OBJECTIVE: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease in which glia are central mediators of motor neuron (MN) death. Since multiple cell types are involved in disease pathogenesis, the objective of this study was to determine the benefit of co-targeting independent pathogenic mechanisms in a familial ALS mouse model. METHODS: Recently, our laboratory identified that ALS microglia induce MN death in an NF-κB-dependent mechanism. We also demonstrated that a single, post-natal, intravenous injection of adeno-associated viral vector serotype 9 encoding a shRNA against mutant SOD1 is able to traverse the blood-brain barrier of ALS mice and reduce SOD1-expression in astrocytes and MNs...
February 2017: Annals of Clinical and Translational Neurology
https://www.readbyqxmd.com/read/28167258/protective-effect-of-nrf2-are-activator-isolated-from-green-perilla-leaves-on-dopaminergic-neuronal-loss-in-a-parkinson-s-disease-model
#15
Yuta Masaki, Yasuhiko Izumi, Atsuko Matsumura, Akinori Akaike, Toshiaki Kume
Parkinson's disease (PD) is a neurodegenerative disorder characterized by a selective loss of dopaminergic neurons in the substantia nigra (SN), and oxidative stress is thought to contribute to the pathogenesis. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway, which is a cellular defense system against oxidative stress, is a promising target for therapeutics aimed at reducing neuronal death in PD. Previously, we have isolated 2',3'-dihydroxy-4',6'-dimethoxychalcone (DDC) from green perilla leaves as an activator of the Nrf2-ARE pathway...
February 4, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28164283/monocytes-microglia-and-cd200-cd200r1-signaling-are-essential-in-the-transmission-of-inflammation-from-the-periphery-to-the-central-nervous-system
#16
Xin Xie, Xiaoguang Luo, Na Liu, Xiaohong Li, Fan Lou, Yumin Zheng, Yan Ren
Peripheral inflammation is known to trigger neuroinflammation and neurodegenerative disease. However, the key components during the propagation of inflammation from the periphery to the central nervous system (CNS) remain unclear. Lipopolysaccharide (LPS) was administered to Sprague-Dawley rats to induce peripheral inflammation. An intravenous injection and an intranigral injection of clodronate liposomes (CL) were given to deplete monocytes and microglia, respectively. Recombinant CD200 fusion protein (CD200Fc) or an anti-CD200R1 antibody was injected into the substantia nigra (SN) to manipulate the involvement of CD200 and CD200R1...
February 6, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28163132/aging-leads-to-altered-microglial-function-that-reduces-brain-resiliency-increasing-vulnerability-to-neurodegenerative-diseases
#17
Paula C Bickford, Antwoine Flowers, Bethany Grimmig
Aging is the primary risk factor for many neurodegenerative diseases. Thus, understanding the basic biological changes that take place with aging that lead to the brain being less resilient to disease progression of neurodegenerative diseases such as Parkinson's disease or Alzheimer's disease or insults to the brain such as stroke or traumatic brain injuries. Clearly this will not cure the disease per se, yet increasing the ability of the brain to respond to injury could improve long term outcomes. The focus of this review is examining changes in microglia with age and possible therapeutic interventions involving the use of polyphenol rich dietary supplements...
February 2, 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/28154566/histological-architecture-underlying-brain-immune-cell-cell-interactions-and-the-cerebral-response-to-systemic-inflammation
#18
Atsuyoshi Shimada, Sanae Hasegawa-Ishii
Although the brain is now known to actively interact with the immune system under non-inflammatory conditions, the site of cell-cell interactions between brain parenchymal cells and immune cells has been an open question until recently. Studies by our and other groups have indicated that brain structures such as the leptomeninges, choroid plexus stroma and epithelium, attachments of choroid plexus, vascular endothelial cells, cells of the perivascular space, circumventricular organs, and astrocytic endfeet construct the histological architecture that provides a location for intercellular interactions between bone marrow-derived myeloid lineage cells and brain parenchymal cells under non-inflammatory conditions...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28153013/effects-of-dexamethasone-and-meloxicam-on-borrelia-burgdorferi-induced-inflammation-in-glial-and-neuronal-cells-of-the-central-nervous-system
#19
Geeta Ramesh, Alejandra N Martinez, Dale S Martin, Mario T Philipp
BACKGROUND: Lyme neuroborreliosis (LNB), caused by the spirochete Borrelia burgdorferi (Bb), affects both the central and peripheral nervous systems. Previously, we reported that in a model of acute LNB in rhesus monkeys, treatment with the anti-inflammatory drug dexamethasone significantly reduced both pleocytosis and levels of cerebrospinal fluid (CSF) immune mediators that were induced by Bb. Dexamethasone also inhibited the formation of inflammatory, neurodegenerative, and demyelinating lesions in the brain and spinal cord of these animals...
February 2, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/28143498/neuroprotective-effects-of-intrastriatal-injection-of-rapamycin-in-a-mouse-model-of-excitotoxicity-induced-by-quinolinic-acid
#20
Soraya Wilke Saliba, Erica Leandro Marciano Vieira, Rebeca Priscila de Melo Santos, Eduardo Candelario-Jalil, Bernd L Fiebich, Luciene Bruno Vieira, Antonio Lucio Teixeira, Antonio Carlos Pinheiro de Oliveira
BACKGROUND: The mammalian target of rapamycin (mTOR) is a kinase involved in a variety of physiological and pathological functions. However, the exact role of mTOR in excitotoxicity is poorly understood. Here, we investigated the effects of mTOR inhibition with rapamycin against neurodegeneration, and motor impairment, as well as inflammatory profile caused by an excitotoxic stimulus. METHODS: A single and unilateral striatal injection of quinolinic acid (QA) was used to induce excitotoxicity in mice...
January 31, 2017: Journal of Neuroinflammation
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