Experimental Studies on Kinetics and Functions of Monuclear Phagozytes of the Central Nervous System

Oehmichen, M; Grüninger, H; Genčić, M.

doi:10.1007/978-3-662-08456-4_50

Cited by 18 publications

(10 citation statements)

References 7 publications

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“…TNFα, NO, & ROS) aimed at destroying the invading pathogens. Surface molecules associated with the innate immune response, such as complement receptors and MHC molecules, are also upregulated upon microglial activation 47, 48. For example, upregulation of MHC proteins enable microglia to act as antigen-presenting cells to T-cells that will enter the brain during active infections 18…”

Section: Microglial Activation and Functionmentioning

confidence: 99%

Microglial Activation and Chronic Neurodegeneration

2010

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Summary: Microglia, the resident innate immune cells in the brain, have long been implicated in the pathology of neurodegenerative diseases. Accumulating evidence points to activated microglia as a chronic source of multiple neurotoxic factors, including tumor necrosis factor-␣, nitric oxide, interleukin-1␤, and reactive oxygen species (ROS), driving progressive neuron damage. Microglia can become chronically activated by either a single stimulus (e.g., lipopolysaccharide or neuron damage) or multiple stimuli exposures to result in cumulative neuronal loss with time. Although the mechanisms driving these phenomena are just beginning to be understood, reactive microgliosis (the microglial response to neuron damage) and ROS have been implicated as key mechanisms of chronic and neurotoxic microglial activation, particularly in the case of Parkinson's disease. We review the mechanisms of neurotoxicity associated with chronic microglial activation and discuss the role of neuronal death and microglial ROS driving the chronic and toxic microglial phenotype.

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Section: Microglial Activation and Functionmentioning

confidence: 99%

Microglial Activation and Chronic Neurodegeneration

2010

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“…Although 'resting', microglia constantly monitor for changes in the surrounding environment and are ready to get activated to fight off any threats to tissue integrity. When stimulated, microglia acquire an ameboid morphology and present an upregulated catalog of surface molecules (Oehmichen & Gencic 1975, Cho et al 2006, such as MHC, chemokine receptors, and CD14 (Rock et al 2004). This activated state also coincides with the production of soluble mediators both detrimental, such as pro-inflammatory cytokines, reactive oxygen species, and reactive nitrogen species (Sawada et al 1989, Moss & Bates 2001, Viviani et al 2001, Liu et al 2002, Tansey et al 2007, and beneficial (i.e.…”

Section: Neuroinflammation: the Main Featuresmentioning

confidence: 99%

Neuroactive steroids, their metabolites, and neuroinflammation

Giatti¹,

Boraso²,

Melcangi³

et al. 2012

Journal of Molecular Endocrinology

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Neuroinflammation represents a common feature of many neurodegenerative diseases implicated both in their onset and progression. Neuroactive steroids act as physiological regulators and protective agents in the nervous system. Therefore, the attention of biomedical research has been recently addressed in evaluating whether neuroactive steroids, such as progestagens, androgens, and estrogens may also affect neuroinflammatory pathways. Observations so far obtained suggest a general anti-inflammatory effect with a beneficial relapse on several neurodegenerative experimental models, thus confirming the potentiality of a neuroprotective strategy based on neuroactive steroids. In this scenario, neuroactive steroid metabolism and the sophisticated machinery involved in their signaling are becoming especially attractive. In particular, because metabolism of neuroactive steroids as well as expression of their receptors is affected during the course of neurodegenerative events, a crucial role of progesterone and testosterone metabolites in modulating neuroinflammation and neurodegeneration may be proposed. In the present review, we will address this issue, providing evidence supporting the hypothesis that the efficacy of neuroactive steroids could be improved through the use of their metabolites.

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“…Activated microglia undergo dramatic morphologic changes, metamorphosing from resting ramified microglia into activated amoeboid microglia (Kreutzberg 1996). They also exhibit increased expression of surface molecules such as complement receptors and major histocompatibility complex (MHC) molecules Oehmichen and Gencic 1975). At the same time, activated microglia release a variety of soluble factors.…”

Section: Immune Cells In the Brainmentioning

confidence: 99%

Parkinson's disease and exposure to infectious agents and pesticides and the occurrence of brain injuries: role of neuroinflammation.

Liu

Gao

Hong

2003

Environ Health Perspect

256

191

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Idiopathic Parkinson's disease (PD) is a devastating movement disorder characterized by selective degeneration of the nigrostriatal dopaminergic pathway. Neurodegeneration usually starts in the fifth decade of life and progresses over 5-10 years before reaching the fully symptomatic disease state. Despite decades of intense research, the etiology of sporadic PD and the mechanism underlying the selective neuronal loss remain unknown. However, the late onset and slow-progressing nature of the disease has prompted the consideration of environmental exposure to agrochemicals, including pesticides, as a risk factor. Moreover, increasing evidence suggests that early-life occurrence of inflammation in the brain, as a consequence of either brain injury or exposure to infectious agents, may play a role in the pathogenesis of PD. Most important, there may be a self-propelling cycle of inflammatory process involving brain immune cells (microglia and astrocytes) that drives the slow yet progressive neurodegenerative process. Deciphering the molecular and cellular mechanisms governing those intricate interactions would significantly advance our understanding of the etiology and pathogenesis of PD and aid the development of therapeutic strategies for the treatment of the disease.

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Experimental Studies on Kinetics and Functions of Monuclear Phagozytes of the Central Nervous System

Cited by 18 publications

References 7 publications

Microglial Activation and Chronic Neurodegeneration

Microglial Activation and Chronic Neurodegeneration

Neuroactive steroids, their metabolites, and neuroinflammation

Parkinson's disease and exposure to infectious agents and pesticides and the occurrence of brain injuries: role of neuroinflammation.

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