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microglia neuroinflammation parkinson' disease

Francis Herman, Susan Westfall, Justin Brathwaite, Giulio M Pasinetti
Neurodegenerative disorders constitute a group of multifaceted conditions characterized by the progressive loss of neurons and synaptic connections consequent to a combination of specific genetic predispositions and stochastic stressors. The neuropathologies observed in both Alzheimer's and Parkinson's disease are in part attributed to compounding intrinsic and extrinsic environmental stressors, which we propose may be limited by the administration of specific grape derived phytochemicals and their metabolized derivatives, specifically polyphenols isolated from grape botanicals...
2018: Frontiers in Pharmacology
Gregory P Williams, Aubrey M Schonhoff, Asta Jurkuvenaite, Aaron D Thome, David G Standaert, Ashley S Harms
BACKGROUND: Parkinson's disease (PD) is characterized by intracellular alpha-synuclein (α-syn) inclusions, progressive death of dopaminergic neurons in the substantia nigra pars compacta (SNpc), and activation of the innate and adaptive immune systems. Disruption of immune signaling between the central nervous system (CNS) and periphery, such as through targeting the chemokine receptor type 2 (CCR2) or the major histocompatibility complex II (MHCII), is neuroprotective in rodent models of PD, suggesting a key role for innate and adaptive immunity in disease progression...
August 30, 2018: Journal of Neuroinflammation
Neelima Gupta, Sukanya Shyamasundar, Radhika Patnala, Aparna Karthikeyan, Thiruma V Arumugam, Eng-Ang Ling, S Thameem Dheen
Chronic activation of microglia is the hallmark of numerous neuropathologies such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis. The activated microglia perpetuate inflammation by releasing an array of pro-inflammatory and neurotoxic factors, which eventually exacerbate neurotoxicity and neurodegeneration upon chronic activation of these cells. However, under acute conditions, activated microglia elicit pro-inflammatory as well as anti-inflammatory responses that are associated with neuroprotection...
September 10, 2018: Expert Opinion on Therapeutic Targets
Katharine M von Herrmann, Lucas A Salas, Eileen M Martinez, Alison L Young, Joseph M Howard, Mary S Feldman, Brock C Christensen, Owen M Wilkins, Stephen L Lee, William F Hickey, Matthew C Havrda
Neuroinflammation is a well-characterized pathophysiology occurring in association with the progression of Parkinson's disease. Characterizing the cellular and molecular basis of neuroinflammation is critical to understanding its impact on the incidence and progression of PD and other neurologic disorders. Inflammasomes are intracellular pro-inflammatory pattern-recognition receptors capable of initiating and propagating inflammation. These cellular complexes are well characterized in the innate immune system and activity of the NLRP3 inflammasome has been reported in microglia...
2018: NPJ Parkinson's Disease
Hiroyuki Konishi, Hiroshi Kiyama
Microglia are activated after neuronal injury and in neurodegenerative diseases, and trigger neuroinflammation in the central nervous system (CNS). Microglia-derived neuroinflammation has both beneficial and detrimental effects on neurons. Because the timing and magnitude of microglial activation is thought to be a critical determinant of neuronal fate, understanding the molecular mechanisms underlying microglial activation is required to enable establishment of microglia-targeted therapies for neural diseases...
2018: Frontiers in Cellular Neuroscience
Bridget Martinez, Philip V Peplow
Parkinson's disease (PD) is an age-related neurodegenerative disease for which the characteristic motor symptoms emerge after an extensive loss of dopamine containing neurons. The cell bodies of these neurons are present in the substantia nigra, with the nerve terminals being in the striatum. Both innate and adaptive immune responses may contribute to dopaminergic neurodegeneration and disease progression is potentially linked to these. Studies in the last twenty years have indicated an important role for neuroinflammation in PD through degeneration of the nigrostriatal dopaminergic pathway...
September 2018: Neural Regeneration Research
Xu Jiang, Palanivel Ganesan, Thamaraiselvan Rengarajan, Dong-Kug Choi, Palanisamy Arulselvan
Pathogenesis of Parkinson's disease (PD) is undoubtedly a multifactorial phenomenon, with diverse etiological agents. Pro-inflammatory mediators act as a skew that directs disease progression during neurodegenerative diseases. Understanding the dynamics of inflammation and inflammatory mediators in preventing or reducing disease progression has recently gained much attention. Inflammatory neuro-degeneration is regulated via cytokines, chemokines, lipid mediators and immune cell subsets; however, individual cellular phenotypes in the Central Nervous System (CNS) acts in diverse ways whose persistent activation leads to unresolving inflammation often causing unfavorable outcomes in neurodegenerative disease like PD...
October 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
Mi Eun Kim, Ju Yong Na, Yong-Duk Park, Jun Sik Lee
Microglia, resident macrophages of the central nervous system (CNS), is responsible for immune responses and homeostasis of the CNS. Microglia plays a complex role in neuroinflammation, which has been implicated in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Therefore, therapeutic agents that suppress the microglia-mediated inflammatory response could potentially be used in the prevention or treatment of neurodegenerative diseases. Vanillin, a primary component of vanilla bean extract, has anti-inflammatory, anticancer, and antitumor properties...
August 10, 2018: Applied Biochemistry and Biotechnology
Shahnawaz Ali Bhat, Anika Sood, Rakesh Shukla, Kashif Hanif
Microglia-induced reactive oxygen species (ROS) production and inflammation play an imperative role in neurodegenerative diseases like Alzheimer's disease (AD) and Parkinson's disease (PD). It has been established that angiotensin II type-2 receptor (AT2R) activation is neuroprotective in central nervous system diseases like stroke and AD. However, the involvement of AT2R in NADPH oxidase (NOX)-mediated microglia activation is still elusive. Therefore, the present study investigated the role of AT2R in angiotensin II (Ang II) or Phorbol 12-myristate 13-acetate (PMA)-induced microglia activation in BV2 cells, primary microglia, p47phox knockout (p47KO) microglia, and in vivo...
August 3, 2018: Molecular Neurobiology
Pedro Elói Antunes Dionísio, Sara Rodrigues Oliveira, Joana São José Dias Amaral, Cecília Maria Pereira Rodrigues
Parkin is an E3 ubiquitin ligase involved in Parkinson's disease (PD). Necroptosis is a regulated form of cell death that depends on receptor interacting protein 1 (RIP1) and 3 (RIP3). Importantly, parkin has been implicated in ubiquitination events that can alter inflammation and necroptosis. Here, we investigated how parkin influences microglial function. Incubation of BV-2 microglial cells with zVAD.fmk (zVAD) induced high levels of cell death and viability loss, while N9 microglial cells and primary microglia required further stimuli...
August 3, 2018: Molecular Neurobiology
Dewei He, Bingxu Huang, Shoupeng Fu, Yuhang Li, Xin Ran, Yandan Liu, Guangxin Chen, Juxiong Liu, Dianfeng Liu
Parkinson's disease (PD), a frequent degenerative disease in the elderly, is characterized by dopaminergic neurodegeneration in the substantia nigra pars compacta (SNpc). Neuroinflammation caused by over-activated microglia plays a crucial role in the pathogenesis of PD. Tubeimoside I (TBMS1) has a broad anti-inflammatory effect in peripheral tissues, but the effect on neuroinflammation has not been reported. Therefore, we explored whether TBMS1 could protect dopaminergic neurons by inhibiting the activation of microglia in lipopolysaccharide (LPS)-induced PD rat model...
July 31, 2018: International Journal of Molecular Sciences
Saurabh Srivastava, Elizaveta Katorcha, Natallia Makarava, James P Barrett, David J Loane, Ilia V Baskakov
Neuroinflammation is recognized as one of the obligatory pathogenic features of neurodegenerative diseases including Alzheimer's, Parkinson's or prion diseases. In prion diseases, space and time correlations between deposition of disease-associated, pathogenic form of the prion protein or PrPSc and microglial-mediated neuroinflammation has been established. Yet, it remains unclear whether activation of microglia is triggered directly by a contact with PrPSc , and what molecular features of PrPSc microglia sense and respond to that drive microglia to inflammatory states...
July 27, 2018: Scientific Reports
Bingqing Cao, Tao Wang, Qiumin Qu, Tao Kang, Qian Yang
Parkinson's disease (PD) is the second most common neurodegenerative disorders. Neuroinflammation plays an important role in the pathogenesis of PD. Long noncoding RNA small nucleolar RNA host gene 1 (SNHG1) was elevated in the brain specimens of PD patients and MPP+-treated SH-SY5Y cells. The expression of mouse Snhg1 and miR-7 was firstly determined in lipopolysaccharide (LPS)-induced BV2 cells. The role and mechanism of SNHG1 in the neuroinflammation of PD were investigated using gain- and loss-of function approaches both in vitro and in vivo...
September 15, 2018: Neuroscience
Dong Hwan Ho, A Reum Je, Haejin Lee, Ilhong Son, Hee-Seok Kweon, Hyung-Gun Kim, Wongi Seol
Leucine-rich repeat kinase 2 (LRRK2) mutations are the most common genetic cause of Parkinson's disease (PD). LRRK2 contains a functional kinase domain and G2019S, the most prevalent LRRK2 pathogenic mutation, increases its kinase activity. LRRK2 regulates mitochondria morphology and autophagy in neurons. LPS treatment increases LRRK2 protein level and mitochondrial fission in microglia, and down-regulation of LRRK2 expression or inhibition of its kinase activity attenuates microglia activation. Here, we evaluated the direct role of LRRK2 G2019S in mitochondrial dynamics in microglia...
June 2018: Experimental Neurobiology
Muhammad M Hossain, Blair Weig, Kenneth Reuhl, Marla Gearing, Long-Jun Wu, Jason R Richardson
Parkinson's disease (PD), the second most common age-related progressive neurodegenerative disorder, is characterized by dopamine depletion and the loss of dopaminergic (DA) neurons with accompanying neuroinflammation. Zonisamide is an-anti-convulsant drug that has recently been shown to improve clinical symptoms of PD through its inhibition of monoamine oxidase B (MAO-B). However, zonisamide has additional targets, including voltage-gated sodium channels (Nav ), which may contribute to its reported neuroprotective role in preclinical models of PD...
October 2018: Experimental Neurology
Rituraj Niranjan
Neuroinflammation is associated with the pathogenesis of many neurological disorders including Parkinson's disease, Alzheimer's disease, Amyotrophic lateral sclerosis and Huntington disease. Current studies in this area have advanced the mechanism of neuroinflammation and its role in neurodegeneration. Studies from epidemiologic, clinical and animal models also contributed in the various new mechanisms of neuroinflammation. In this line, activation of monocytes is an important emerging mechanism that has a, profound role in neuroinflammation and neurodegeneration...
July 19, 2018: Neurochemistry International
Kai Yao, Yong-Fei Zhao
As the crucial etiological factor, aging-related microglia activation promotes the development of Parkinson's disease (PD). However, the molecular and functional changes of aged-microglia and their contribution to neurodegeneration in PD are only partially understood, which was investigated in our study. Female C57BL/6 mice were randomly divided into four groups, included young-control group, young-MPTP group, aged-control group and aged-MPTP group. Pole test and adhesive removal test were firstly performed...
October 1, 2018: Experimental Gerontology
Teemu A Natunen, Mikko Gynther, Hannah Rostalski, Külli Jaako, Aaro J Jalkanen
Prolyl oligopeptidase (PREP) is an abundant peptidase in the brain and periphery, but its physiological functions are still largely unknown. Recent findings point to a role for PREP in inflammatory processes. This study assessed the cellular and extracellular PREP activities in cultures of mouse primary cortical neurons, microglial cells and astrocytes, and immortalized microglial BV-2 cells under neuroinflammatory conditions induced by lipopolysaccharide (LPS) and interferon gamma (IFNγ). Furthermore, we evaluated the neuroprotective effect of a specific PREP inhibitor, KYP-2047, in a neuroinflammation model based on a coculture of primary cortical neurons and activated BV-2 cells...
July 11, 2018: Basic & Clinical Pharmacology & Toxicology
Mi Eun Kim, Pu Reum Park, Ju Yong Na, Inae Jung, Jun Hwi Cho, Jun Sik Lee
Neuroinflammation resulting from microglial activation is involved in the pathogenesis of neurodegenerative diseases, including Parkinson's diseases. Microglial activation plays an important role in neuroinflammation and contributes to several neurological disorders. Hence, inhibition of both microglial activation and the generation of pro-inflammatory cytokines may lead to an effective treatment for neurodegenerative diseases. In the present study, the anti-neuroinflammatory effects of galangin were investigated in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells...
July 11, 2018: Molecular and Cellular Biochemistry
Namkwon Kim, Jimin Do, Jae-Sung Bae, Hee Kyung Jin, Jong-Ho Kim, Kyung-Soo Inn, Myung Sook Oh, Jong Kil Lee
Inflammatory processes in the central nervous system are feature among biological reactions to harmful stimuli such as pathogens and damaged cells. In resting conditions, microglia are involved in immune surveillance and brain homeostasis. However, the activation of abnormal microglia can be detrimental to neurons, even resulting in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease and Huntington's disease. Therefore, normalization of microglial activation is considered a promising strategy for developing drugs that can treat or prevent inflammation-related brain diseases...
June 2018: Journal of Pharmacological Sciences
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