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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

In physiological and pathological conditions, microglia transmit signal to astrocytes and astrocytes inhibit inflammation by dopamine receptors. In degenerative brain disease, microglia activation weakened, astrocytes' Drd2 signals descend too, resulting in excessive inflammation expression. DA: Dopamine.
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fig2: In physiological and pathological conditions, microglia transmit signal to astrocytes and astrocytes inhibit inflammation by dopamine receptors. In degenerative brain disease, microglia activation weakened, astrocytes' Drd2 signals descend too, resulting in excessive inflammation expression. DA: Dopamine.

Mentions: Dopamine receptor is a vital member of the dopamine signal system of the neurotransmitter in the brain and plays a key role, including emotion, the neural activity of addiction, voluntary movement, and many other advanced functions. The studies suggest that dopamine D2 receptor (Drd2) is also expressed in microglial cells [25] and can affect the activation of CD4+ T lymphocyte; 18 elderly people's average level of Drd2 declined obviously [26, 27], which indicated that Drd2 may participate in the regulation of innate immunity of the central nervous system. In 2009, in the United States, Dr. Glass said that, in the inflammatory response process induced by bacterial endotoxin LPS, microglial cells were first activated, and then astrocytes accepted the immune signal of microglia and were passively activated; in both, mutual cooperation ultimately promoted the neuronal damage and degradation [28] (Figure 2). There is a kind of Cryab protein expressed in astrocytes; Cryab protein is a kind of small molecular heat shock protein, which plays the role of inhibiting inflammation and neuroprotection [29]. In the condition of outside harmful stimulations, due to the inhibitory effect of proinflammatory factor expression of Cryab, inflammation can be controlled within a certain range when the Drd2 signaling pathways of microglia to astrocytes are weakened; Cryab expression level is reduced when the outside world harmful stimulus arrives, microglia could not effectively cope with and lose effective restriction for the inflammatory response and then involve in the neuronal degeneration and aging process.


Microglia in Alzheimer's disease.

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

In physiological and pathological conditions, microglia transmit signal to astrocytes and astrocytes inhibit inflammation by dopamine receptors. In degenerative brain disease, microglia activation weakened, astrocytes' Drd2 signals descend too, resulting in excessive inflammation expression. DA: Dopamine.
© Copyright Policy
Related In: Results  -  Collection

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

fig2: In physiological and pathological conditions, microglia transmit signal to astrocytes and astrocytes inhibit inflammation by dopamine receptors. In degenerative brain disease, microglia activation weakened, astrocytes' Drd2 signals descend too, resulting in excessive inflammation expression. DA: Dopamine.
Mentions: Dopamine receptor is a vital member of the dopamine signal system of the neurotransmitter in the brain and plays a key role, including emotion, the neural activity of addiction, voluntary movement, and many other advanced functions. The studies suggest that dopamine D2 receptor (Drd2) is also expressed in microglial cells [25] and can affect the activation of CD4+ T lymphocyte; 18 elderly people's average level of Drd2 declined obviously [26, 27], which indicated that Drd2 may participate in the regulation of innate immunity of the central nervous system. In 2009, in the United States, Dr. Glass said that, in the inflammatory response process induced by bacterial endotoxin LPS, microglial cells were first activated, and then astrocytes accepted the immune signal of microglia and were passively activated; in both, mutual cooperation ultimately promoted the neuronal damage and degradation [28] (Figure 2). There is a kind of Cryab protein expressed in astrocytes; Cryab protein is a kind of small molecular heat shock protein, which plays the role of inhibiting inflammation and neuroprotection [29]. In the condition of outside harmful stimulations, due to the inhibitory effect of proinflammatory factor expression of Cryab, inflammation can be controlled within a certain range when the Drd2 signaling pathways of microglia to astrocytes are weakened; Cryab expression level is reduced when the outside world harmful stimulus arrives, microglia could not effectively cope with and lose effective restriction for the inflammatory response and then involve in the neuronal degeneration and aging process.

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