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https://www.readbyqxmd.com/read/29775624/characterization-and-comparative-analysis-of-a-new-mouse-microglial-cell-model-for-studying-neuroinflammatory-mechanisms-during-neurotoxic-insults
#1
Souvarish Sarkar, Emir Malovic, Deeksha Sarda, Vivek Lawana, Dharmin Rokad, Huajun Jin, Vellareddy Anantharam, Arthi Kanthasamy, Anumantha G Kanthasamy
Microglia are the first responders of the central nervous system, acting as the key modulators of neuroinflammation observed during neurotoxic insults as well as in the pathophysiology of several neurodegenerative disorders including Alzheimer's (AD), Parkinson's (PD), and Huntington's diseases (HD). The number of publications on microglia has increased steadily throughout the past decade because of immense interests in the neuroinflammation that precedes the neurodegenerative process. To study microglial biology and its role in modulating neuroinflammation, immortalized microglial cell lines derived from mice, rats, and humans have been developed...
May 15, 2018: Neurotoxicology
https://www.readbyqxmd.com/read/29768974/brain-phospholipid-precursors-administered-post-injury-reduce-tissue-damage-and-improve-neurological-outcome-in-experimental-traumatic-brain-injury
#2
Orli Thau-Zuchman, Rita Noutel Gomes, Simon Christopher Dyall, Meirion Davis, John V Priestley, Martine Groenendijk, Martijn DE Wilde, Jordi Lopez-Tremoleda, Adina T Michael-Titus
Traumatic brain injury (TBI) leads to cellular loss, destabilisation of membranes, disruption of synapses and altered brain connectivity, and increased risk of neurodegenerative disease. A significant and long-lasting decrease in phospholipids (PL), essential membrane constituents, has recently been reported in plasma and brain tissue, in human and experimental TBI. We hypothesised that supporting PL synthesis post-injury could improve outcome after TBI. We tested this hypothesis using a multi-nutrient combination designed to support the biosynthesis of phospholipids and available for clinical use...
May 17, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29765306/microglial-activation-is-modulated-by-captopril-in-vitro-and-in-vivo-studies
#3
Keren Asraf, Nofar Torika, Ron N Apte, Sigal Fleisher-Berkovich
The renin-angiotensin system (RAS) is an important peripheral system involved in homeostasis modulation, with angiotensin II (Ang II) serving as the main effector hormone. The main enzyme involved in Ang II formation is angiotensin-converting enzyme (ACE). ACE inhibitors (ACEIs) such as captopril (Cap) are predominantly used for the management of hypertension. All of the components of the RAS have also been identified in brain. Centrally located hormones such as Ang II can induce glial inflammation. Moreover, in Alzheimer's disease (AD) models, where glial inflammation occurs and is thought to contribute to the propagation of the disease, increased levels of Ang II and ACE have been detected...
2018: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29759145/thymoquinone-increases-the-expression-of-neuroprotective-proteins-while-decreasing-the-expression-of-pro-inflammatory-cytokines-and-the-gene-expression-nf%C3%AE%C2%BAb-pathway-signaling-targets-in-lps-ifn%C3%AE-activated-bv-2-microglia-cells
#4
Makini K Cobourne-Duval, Equar Taka, Patricia Mendonca, Karam F A Soliman
Neuroinflammation and microglial activation are pathological markers of a number of central nervous system (CNS) diseases. Chronic activation of microglia induces the release of excessive amounts of reactive oxygen species (ROS) and pro-inflammatory cytokines. Additionally, chronic microglial activation has been implicated in several neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. Thymoquinone (TQ) has been identified as one of the major active components of the natural product Nigella sativa seed oil...
July 15, 2018: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/29759078/transcriptome-analysis-of-alcohol-treated-microglia-reveals-downregulation-of-beta-amyloid-phagocytosis
#5
Sergey Kalinin, Marta González-Prieto, Hannah Scheiblich, Lucia Lisi, Handojo Kusumo, Michael T Heneka, Jose L M Madrigal, Subhash C Pandey, Douglas L Feinstein
BACKGROUND: Microglial activation contributes to the neuropathology associated with chronic alcohol exposure and withdrawal, including the expression of inflammatory and anti-inflammatory genes. In the current study, we examined the transcriptome of primary rat microglial cells following incubation with alcohol alone, or alcohol together with a robust inflammatory stimulus. METHODS: Primary microglia were prepared from mixed rat glial cultures. Cells were incubated with 75 mM ethanol alone or with proinflammatory cytokines ("TII": IL1β, IFNγ, and TNFα)...
May 14, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29758264/anti-il17-treatment-ameliorates-down-syndrome-phenotypes-in-mice
#6
Noemí Rueda, Verónica Vidal, Susana García-Cerro, Josep Oriol Narcís, María Llorens-Martín, Andrea Corrales, Sara Lantigua, Marcos Iglesias, Jesús Merino, Ramón Merino, Carmen Martínez-Cué
Down syndrome (DS) is characterized by structural and functional anomalies that are present prenatally and that lead to intellectual disabilities. Later in life, the cognitive abilities of DS individuals progressively deteriorate due to the development of Alzheimer's disease (AD)-associated neuropathology (i.e., β-amyloid (Aβ) plaques, neurofibrillary tangles (NFTs), neurodegeneration, synaptic pathology, neuroinflammation and increased oxidative stress). Increasing evidence has shown that among these pathological processes, neuroinflammation plays a predominant role in AD etiopathology...
May 11, 2018: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/29755324/effect-of-chronic-oxidative-stress-on-neuroinflammatory-response-mediated-by-cd4-t-cells-in-neurodegenerative-diseases
#7
REVIEW
Helena Solleiro-Villavicencio, Selva Rivas-Arancibia
In a state of oxidative stress, there is an increase of reactive species, which induce an altered intracellular signaling, leading to dysregulation of the inflammatory response. The inability of the antioxidant defense systems to modulate the proinflammatory response is key to the onset and progression of neurodegenerative diseases. The aim of this work is to review the effect of the state of oxidative stress on the loss of regulation of the inflammatory response on the microglia and astrocytes, the induction of different CD4+ T cell populations in neuroinflammation, as well as its role in some neurodegenerative diseases...
2018: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29754747/sexual-dimorphism-in-predisposition-to-alzheimer-s-disease
#8
REVIEW
Daniel W Fisher, David A Bennett, Hongxin Dong
Clinical studies indicate that Alzheimer's disease (AD) disproportionately affects women in both disease prevalence and rate of symptom progression, but the mechanisms underlying this sexual divergence are unknown. Although some have suggested this difference in risk is a reflection of the known differences in longevity between men and women, mounting clinical and preclinical evidence supports women also having intrinsic susceptibilities toward the disease. Although a number of potential risk factors have been hypothesized to mediate these differences, none have been definitively verified...
April 17, 2018: Neurobiology of Aging
https://www.readbyqxmd.com/read/29754213/pathogenesis-of-alzheimer-s-disease-examined-using-a-modified-puri-li-model-that-incorporates-calcium-ion-homeostasis
#9
R A Thuraisingham
The Puri-Li kinetic model is modified to include neuronal calcium ion homeostasis to study the effect of calcium ions on the production of amyloid-β peptides (Aβ), microglia, and astroglia during the pathogenesis of Alzheimer's disease (AD). This is carried out by solving the modified Puri-Li model under steady-state conditions. The derived expressions show that the inclusion of calcium ions has altered the steady-state populations of Aβ, microglia, and astroglia. The calcium ions activate the synthesis of Aβ which in turn increases the calcium ions entering the cytoplasm of the neuronal cells, thus creating a positive loop...
May 13, 2018: Journal of Molecular Neuroscience: MN
https://www.readbyqxmd.com/read/29752066/the-microglial-innate-immune-receptor-trem2-is-required-for-synapse-elimination-and-normal-brain-connectivity
#10
Fabia Filipello, Raffaella Morini, Irene Corradini, Valerio Zerbi, Alice Canzi, Bernadeta Michalski, Marco Erreni, Marija Markicevic, Chiara Starvaggi-Cucuzza, Karel Otero, Laura Piccio, Francesca Cignarella, Fabio Perrucci, Matteo Tamborini, Marco Genua, Lawrence Rajendran, Elisabetta Menna, Stefania Vetrano, Margaret Fahnestock, Rosa Chiara Paolicelli, Michela Matteoli
The triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial innate immune receptor associated with a lethal form of early, progressive dementia, Nasu-Hakola disease, and with an increased risk of Alzheimer's disease. Microglial defects in phagocytosis of toxic aggregates or apoptotic membranes were proposed to be at the origin of the pathological processes in the presence of Trem2 inactivating mutations. Here, we show that TREM2 is essential for microglia-mediated synaptic refinement during the early stages of brain development...
May 3, 2018: Immunity
https://www.readbyqxmd.com/read/29743866/dexmedetomidine-inhibits-inflammation-in-microglia-cells-under-stimulation-of-lps-and-atp-by-c-fos-nlrp3-caspase-1-cascades
#11
Hu Li, Xueping Zhang, Mingfu Chen, Jianyan Chen, Tao Gao, Shanglong Yao
NOD-like receptor 3 (NLRP3) plays critical roles in the initiation of inflammasome-mediated inflammation in microglia, thus becomes an important therapeutic target of Alzheimer's disease (AD). Dexmedetomidine (Dex), a new type of clinical anesthetic agent, shows anti-inflammatory properties and inhibits postoperative cognitive dysfunction in AD patients. The present study was aimed to investigate effect of Dex on NLRP3 activity in activated microglia and reveal the underlying mechanisms. The human microglia clone 3 (HMC3) cells were exposed to 100 ng/ml LPS and 5 mM ATP, in the presence and absence of doses of Dex...
2018: EXCLI Journal
https://www.readbyqxmd.com/read/29740062/the-contribution-of-microglia-to-early-synaptic-compensatory-responses-that-precede-%C3%AE-amyloid-induced-neuronal-death
#12
Sara Merlo, Simona Federica Spampinato, Martina Beneventano, Maria Angela Sortino
Glial-neuronal cross-talk has a critical role in the development of neurodegenerative conditions, including Alzheimer's Disease, where it affects neuronal responses to β-amyloid peptide (Aβ)-induced toxicity. We set out to identify factors regulating synaptic responses to Aβ, dissecting the specific role of glial signaling. A low concentration of aggregated Aβ42 induced selective up-regulation of mature brain-derived neurotrophic factor (BDNF) expression and release in rat organotypic hippocampal cultures as well as in cortical pure microglia...
May 8, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29737568/pterostilbene-inhibits-amyloid-%C3%AE-induced-neuroinflammation-in-a-microglia-cell-line-by-inactivating-the-nlrp3-caspase-1-inflammasome-pathway
#13
Qiushi Li, Long Chen, Xuewen Liu, Xidong Li, Yue Cao, Yang Bai, Fengjiao Qi
Neuroinflammation has been known as an important pathogenetic contributor of Alzheimer's disease (AD). Pterostilbene is a natural compound which has neuroprotective activity. However, the effect of pterostilbene on amyloid-β (Aβ)-induced neuroinflammation has not been clarified. The aim of the present study was to investigate the effect of pterostilbene on Aβ-induced neuroinflammation in microglia. The results indicated that pterostilbene attenuated Aβ1-42 -induced cytotoxicity of BV-2 cells. Aβ1-42 induced NO production and iNOS mRNA and protein expression, while pterostilbene inhibited the induction...
May 8, 2018: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/29732971/upregulation-of-suppressor-of-cytokine-signaling-3-in-microglia-by-cinnamic-acid
#14
Sudipta Chakrabarti, Malabendu Jana, Avik Roy, Kalipada Pahan
Neuroinflammation plays an important role in the pathogenesis of various neurodegenerative diseases including Alzheimer's disease (AD). Suppressor of cytokine signaling 3 (SOCS3) is an anti-inflammatory molecule that suppresses cytokine signaling and inflammatory gene expression in different cells including microglia. However, pathways through which SOCS3 could be upregulated are poorly described. Cinnamic acid is a metabolite of cinnamon, a natural compound that is being widely used all over the world as a spice or flavoring agent...
May 6, 2018: Current Alzheimer Research
https://www.readbyqxmd.com/read/29729668/urmc-099-facilitates-amyloid-%C3%AE-clearance-in-a-murine-model-of-alzheimer-s-disease
#15
Tomomi Kiyota, Jatin Machhi, Yaman Lu, Bhagyalaxmi Dyavarshetty, Maryam Nemati, Gang Zhang, R Lee Mosley, Harris A Gelbard, Howard E Gendelman
BACKGROUND: The mixed lineage kinase type 3 inhibitor URMC-099 facilitates amyloid-beta (Aβ) clearance and degradation in cultured murine microglia. One putative mechanism is an effect of URMC-099 on Aβ uptake and degradation. As URMC-099 promotes endolysosomal protein trafficking and reduces Aβ microglial pro-inflammatory activities, we assessed whether these responses affect Aβ pathobiogenesis. To this end, URMC-099's therapeutic potential, in Aβ precursor protein/presenilin-1 (APP/PS1) double-transgenic mice, was investigated in this model of Alzheimer's disease (AD)...
May 5, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29729150/cd200-cx3cl1-and-trem2-mediated-neuron-microglia-interactions-and-their-involvements-in-alzheimer-s-disease
#16
Lihang Zhang, Juan Xu, Jinchao Gao, Yuncheng Wu, Ming Yin, Wenjuan Zhao
Neurons and microglia are two major components in the central nervous system (CNS). The interactions between them play important roles in maintaining homeostasis of the brain. In recent years, substantial studies have focused on the interactions between neurons and microglia, revealing that microglia become reactive when the interactions are pathophysiologically interfered, usually accompanying neuronal injury, which is a common feature for Alzheimer's disease (AD). Many molecules and factors participate in these physiological and pathological processes, either in a contact-dependent or a contact-independent manner...
May 5, 2018: Reviews in the Neurosciences
https://www.readbyqxmd.com/read/29720226/increased-a20-e3-ubiquitin-ligase-interactions-in-bid-deficient-glia-attenuate-tlr3-and-tlr4-induced-inflammation
#17
Sinéad Kinsella, Michael Fichtner, Orla Watters, Hans-Georg König, Jochen H M Prehn
BACKGROUND: Chronic pro-inflammatory signaling propagates damage to neural tissue and affects the rate of disease progression. Increased activation of Toll-like receptors (TLRs), master regulators of the innate immune response, is implicated in the etiology of several neuropathologies including amyotrophic lateral sclerosis, Alzheimer's disease, and Parkinson's disease. Previously, we identified that the Bcl-2 family protein BH3-interacting domain death agonist (Bid) potentiates the TLR4-NF-κB pro-inflammatory response in glia, and specifically characterized an interaction between Bid and TNF receptor associated factor 6 (TRAF6) in microglia in response to TLR4 activation...
May 2, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29720213/pm2-5-exposure-aggravates-oligomeric-amyloid-beta-induced-neuronal-injury-and-promotes-nlrp3-inflammasome-activation-in-an-in-vitro-model-of-alzheimer-s-disease
#18
Bian-Rong Wang, Jian-Quan Shi, Nian-Nian Ge, Zhou Ou, You-Yong Tian, Teng Jiang, Jun-Shan Zhou, Jun Xu, Ying-Dong Zhang
BACKGROUND: Numerous studies suggested that PM2.5 exposure was associated with increased risk of Alzheimer's disease (AD). But the precise mechanisms by which PM2.5 contributed to AD pathogenesis have not been clarified. METHODS: In the presence or absence of neurons, oligomeric amyloid beta (oAβ)-primed microglia were stimulated with PM2.5. Firstly, we determined the effects of PM2.5 exposure on neuronal injury and inflammation in neurons-microglia co-cultures...
May 2, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29710716/brain-inflammation-connects-cognitive-and-non-cognitive-symptoms-in-alzheimer-s-disease
#19
M Clara Selles, Mauricio M Oliveira, Sergio T Ferreira
Alzheimer's disease (AD) is the main form of dementia in the elderly and affects greater than 47 million people worldwide. Care for AD patients poses very significant personal and economic demands on individuals and society, and the situation is expected to get even more dramatic in the coming decades unless effective treatments are found to halt the progression of the disease. Although AD is most commonly regarded as a disease of the memory, the entire brain is eventually affected by neuronal dysfunction or neurodegeneration, which brings about a host of other behavioral disturbances...
April 25, 2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29706957/microglia-and-beyond-innate-immune-cells-as-regulators-of-brain-development-and-behavioral-function
#20
REVIEW
Kathryn M Lenz, Lars H Nelson
Innate immune cells play a well-documented role in the etiology and disease course of many brain-based conditions, including multiple sclerosis, Alzheimer's disease, traumatic brain and spinal cord injury, and brain cancers. In contrast, it is only recently becoming clear that innate immune cells, primarily brain resident macrophages called microglia, are also key regulators of brain development. This review summarizes the current state of knowledge regarding microglia in brain development, with particular emphasis on how microglia during development are distinct from microglia later in life...
2018: Frontiers in Immunology
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