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Microglia in Alzheimer's disease.

Li Y, Tan MS, Jiang T, Tan L - Biomed Res Int (2014)

Bottom Line: In this paper, we will review current viewpoints of microglial activation, inflammatory regulatory systems, and their relationship with AD pathology and etiology.Microglia cells have dual roles: they provoke the release of inflammatory factors and cytotoxins leading to neuronal injuries and death; on the other hand, they have the neuroprotective effects.Through this, we hope to illustrate that the anti-inflammatory defenses of neurons can be practiced in the future strategy for recuperating the balance between the levels of inflammatory mediators and immune regulators in AD.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, No. 5 Donghai Middle Road, Qingdao 266071, China ; Department of Pathology, Qingdao Municipal Hospital, Qingdao 266071, China.

ABSTRACT
Alzheimer's disease (AD) is a familiar neurodegenerative disease in the elderly. In this paper, we will review current viewpoints of microglial activation, inflammatory regulatory systems, and their relationship with AD pathology and etiology. Microglia cells are macrophage and representative of the innate immune system in brain. AD brain is marked by obvious inflammatory features, in which microglial activation is the driving force. β-amyloid protein sedimentation activates microglia cells, which causes the inflammation in AD. Microglia cells have dual roles: they provoke the release of inflammatory factors and cytotoxins leading to neuronal injuries and death; on the other hand, they have the neuroprotective effects. Through this, we hope to illustrate that the anti-inflammatory defenses of neurons can be practiced in the future strategy for recuperating the balance between the levels of inflammatory mediators and immune regulators in AD.

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Related in: MedlinePlus

A beta activates inflammatory mediators and the complement system on microglia and then generates free radicals and makes toxic effects on neurons; on the other hand glial cells phagocytize A beta chips.
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fig1: A beta activates inflammatory mediators and the complement system on microglia and then generates free radicals and makes toxic effects on neurons; on the other hand glial cells phagocytize A beta chips.

Mentions: Looking from the ultrastructure, microglia into phagocytes can remove necrotic neurons and then protect the integrity of the necrotic neurons surviving around them. From the point of views of function, microglia can be activated by releasing oxygen free radical, nitric oxide, protease, and inflammatory cytokines and take the cytotoxic effect. At the same time it also can secrete nerve growth factor for supporting tissue repair [4]. Many signal molecules including many cytokines in the central nervous system of normal brain development process play an important role in neural immune regulation, which also participate in the neural pathological immune reaction in neurodegenerative diseases. These related molecules in cell surface or internal can be used as a marker of microglia and differ from the other cells in the central nervous system, such as ILB4, CD11b, and so forth. Aging and the brain A beta deposition are considered to be the major risk factors for the nerve degeneration of AD and associated with the activation of microglia (Figure 1). A beta activate microglial cells to produce a variety of inflammatory factors and make neurotoxic effect, cell inflammatory molecules which include tumor necrosis factor (TNF alpha), interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6), chemokine macrophage inflammatory protein-1 (MIP-1), monocyte chemotactic protein 1 (MCP-1), complement and reactive oxygen species (ROS), and so forth [5]. These injured neurons and nerve toxic substances can cause microglia activation, which trigger a long-standing neurotoxicity cycle referred as a reactive cycle to microglial cells. Microglia activation prompts nerve injury to sustain the development for a long time, leading to reactive microglia cycle, which will exist permanently. As a result, the damage in neurons is a long-term chronic process, and it eventually leads to the development of AD. Microglia neurotransmitter receptors also express receptors, such as glutamate receptor, GABA receptors, dopamine receptor; neural hormone receptor, neuromodulation receptor, histamine receptor, cannabinoid receptor, opioid peptide receptor, chemokine receptors, TNF alpha receptors, interleukin receptors, and so forth; some recognition receptors: toll-like receptor; other receptors: formyl peptide receptor (FPR), calcium receptor, leukotriene receptor, notch receptors, and so forth. A lot of slow release of these factors may be involved in the substantia nigra striatum dopaminergic neuron degeneration necrosis of the system. A lot of studies of this view confirm that their application of dexamethasone, indomethacin, and minocycline against inflammation can protect in the model of AD dopaminergic neurons necrosis [6].


Microglia in Alzheimer's disease.

Li Y, Tan MS, Jiang T, Tan L - Biomed Res Int (2014)

A beta activates inflammatory mediators and the complement system on microglia and then generates free radicals and makes toxic effects on neurons; on the other hand glial cells phagocytize A beta chips.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4150406&req=5

fig1: A beta activates inflammatory mediators and the complement system on microglia and then generates free radicals and makes toxic effects on neurons; on the other hand glial cells phagocytize A beta chips.
Mentions: Looking from the ultrastructure, microglia into phagocytes can remove necrotic neurons and then protect the integrity of the necrotic neurons surviving around them. From the point of views of function, microglia can be activated by releasing oxygen free radical, nitric oxide, protease, and inflammatory cytokines and take the cytotoxic effect. At the same time it also can secrete nerve growth factor for supporting tissue repair [4]. Many signal molecules including many cytokines in the central nervous system of normal brain development process play an important role in neural immune regulation, which also participate in the neural pathological immune reaction in neurodegenerative diseases. These related molecules in cell surface or internal can be used as a marker of microglia and differ from the other cells in the central nervous system, such as ILB4, CD11b, and so forth. Aging and the brain A beta deposition are considered to be the major risk factors for the nerve degeneration of AD and associated with the activation of microglia (Figure 1). A beta activate microglial cells to produce a variety of inflammatory factors and make neurotoxic effect, cell inflammatory molecules which include tumor necrosis factor (TNF alpha), interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6), chemokine macrophage inflammatory protein-1 (MIP-1), monocyte chemotactic protein 1 (MCP-1), complement and reactive oxygen species (ROS), and so forth [5]. These injured neurons and nerve toxic substances can cause microglia activation, which trigger a long-standing neurotoxicity cycle referred as a reactive cycle to microglial cells. Microglia activation prompts nerve injury to sustain the development for a long time, leading to reactive microglia cycle, which will exist permanently. As a result, the damage in neurons is a long-term chronic process, and it eventually leads to the development of AD. Microglia neurotransmitter receptors also express receptors, such as glutamate receptor, GABA receptors, dopamine receptor; neural hormone receptor, neuromodulation receptor, histamine receptor, cannabinoid receptor, opioid peptide receptor, chemokine receptors, TNF alpha receptors, interleukin receptors, and so forth; some recognition receptors: toll-like receptor; other receptors: formyl peptide receptor (FPR), calcium receptor, leukotriene receptor, notch receptors, and so forth. A lot of slow release of these factors may be involved in the substantia nigra striatum dopaminergic neuron degeneration necrosis of the system. A lot of studies of this view confirm that their application of dexamethasone, indomethacin, and minocycline against inflammation can protect in the model of AD dopaminergic neurons necrosis [6].

Bottom Line: In this paper, we will review current viewpoints of microglial activation, inflammatory regulatory systems, and their relationship with AD pathology and etiology.Microglia cells have dual roles: they provoke the release of inflammatory factors and cytotoxins leading to neuronal injuries and death; on the other hand, they have the neuroprotective effects.Through this, we hope to illustrate that the anti-inflammatory defenses of neurons can be practiced in the future strategy for recuperating the balance between the levels of inflammatory mediators and immune regulators in AD.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, No. 5 Donghai Middle Road, Qingdao 266071, China ; Department of Pathology, Qingdao Municipal Hospital, Qingdao 266071, China.

ABSTRACT
Alzheimer's disease (AD) is a familiar neurodegenerative disease in the elderly. In this paper, we will review current viewpoints of microglial activation, inflammatory regulatory systems, and their relationship with AD pathology and etiology. Microglia cells are macrophage and representative of the innate immune system in brain. AD brain is marked by obvious inflammatory features, in which microglial activation is the driving force. β-amyloid protein sedimentation activates microglia cells, which causes the inflammation in AD. Microglia cells have dual roles: they provoke the release of inflammatory factors and cytotoxins leading to neuronal injuries and death; on the other hand, they have the neuroprotective effects. Through this, we hope to illustrate that the anti-inflammatory defenses of neurons can be practiced in the future strategy for recuperating the balance between the levels of inflammatory mediators and immune regulators in AD.

Show MeSH
Related in: MedlinePlus