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What does complement do in Alzheimer’s disease? Old molecules with new insights

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Material Information

Title:
What does complement do in Alzheimer’s disease? Old molecules with new insights
Physical Description:
Mixed Material
Language:
English
Creator:
Shen, Yong
Yang, Libang
Li, Rena
Publisher:
Bio-Med Central (Translational Neurodegeneration)
Publication Date:

Notes

Abstract:
Increasing evidence suggests that inflammatory and immune components in brain are important in Alzheimer’s disease (AD) and anti-inflammatory and immunotherapeutic approaches may be amenable to AD treatment. It is known that complement activation occurs in the brain of patients with AD, and contributes to a local inflammatory state development which is correlated with cognitive impairment. In addition to the complement’s critical role in the innate immune system recognizing and killing, or targeting for destruction, complement proteins can also interact with cell surface receptors to promote a local inflammatory response and contributes to the protection and healing of the host. On the other hand, complement activation also causes inflammation and cell damage as an essential immune function to eliminate cell debris and potentially toxic protein aggregates. It is the balance of these seemingly competing events that influences the ultimate state of neuronal function. Our mini review will be focusing on the unique molecular interactions happening in the AD development, the functional outcomes of those interactions, as well as the contribution of each element to AD.
General Note:
Shen et al. Translational Neurodegeneration 2013, 2:21 http://www.translationalneurodegeneration.com/content/2/1/21; Pages 1-11
General Note:
doi:10.1186/2047-9158-2-21 Cite this article as: Shen et al.: What does complement do in Alzheimer’s disease? Old molecules with new insights. Translational Neurodegeneration 2013 2:21

Record Information

Source Institution:
University of Florida
Holding Location:
University of Florida
Rights Management:
All rights reserved by the source institution.
Resource Identifier:
oclc -
System ID:
AA00018754:00001

Material Information

Title:
What does complement do in Alzheimer’s disease? Old molecules with new insights
Physical Description:
Mixed Material
Language:
English
Creator:
Shen, Yong
Yang, Libang
Li, Rena
Publisher:
Bio-Med Central (Translational Neurodegeneration)
Publication Date:

Notes

Abstract:
Increasing evidence suggests that inflammatory and immune components in brain are important in Alzheimer’s disease (AD) and anti-inflammatory and immunotherapeutic approaches may be amenable to AD treatment. It is known that complement activation occurs in the brain of patients with AD, and contributes to a local inflammatory state development which is correlated with cognitive impairment. In addition to the complement’s critical role in the innate immune system recognizing and killing, or targeting for destruction, complement proteins can also interact with cell surface receptors to promote a local inflammatory response and contributes to the protection and healing of the host. On the other hand, complement activation also causes inflammation and cell damage as an essential immune function to eliminate cell debris and potentially toxic protein aggregates. It is the balance of these seemingly competing events that influences the ultimate state of neuronal function. Our mini review will be focusing on the unique molecular interactions happening in the AD development, the functional outcomes of those interactions, as well as the contribution of each element to AD.
General Note:
Shen et al. Translational Neurodegeneration 2013, 2:21 http://www.translationalneurodegeneration.com/content/2/1/21; Pages 1-11
General Note:
doi:10.1186/2047-9158-2-21 Cite this article as: Shen et al.: What does complement do in Alzheimer’s disease? Old molecules with new insights. Translational Neurodegeneration 2013 2:21

Record Information

Source Institution:
University of Florida
Holding Location:
University of Florida
Rights Management:
All rights reserved by the source institution.
Resource Identifier:
oclc -
System ID:
AA00018754:00001