Neuroinflammation in Alzheimer’s disease
Fengjin Zhang,1,2 Linlan Jiang11Department of Pharmacy, General Hospital of Guangzhou Military Command, Guangzhou City, People’s Republic of China; 2School of Bioscience and Bioengineering, South China University of Technology, Guangzhou City, People’s Republic of ChinaAbstract:...
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Dove Medical Press
2015
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oai:doaj.org-article:5827a1386e0940a8bc068001f0382efc2021-12-02T00:25:49ZNeuroinflammation in Alzheimer’s disease1178-2021https://doaj.org/article/5827a1386e0940a8bc068001f0382efc2015-01-01T00:00:00Zhttp://www.dovepress.com/neuroinflammation-in-alzheimerrsquos-disease-peer-reviewed-article-NDThttps://doaj.org/toc/1178-2021 Fengjin Zhang,1,2 Linlan Jiang11Department of Pharmacy, General Hospital of Guangzhou Military Command, Guangzhou City, People’s Republic of China; 2School of Bioscience and Bioengineering, South China University of Technology, Guangzhou City, People’s Republic of ChinaAbstract: Amyloid-β plaques and neurofibrillary tangles are the main neuropathological hallmarks in Alzheimer’s disease (AD), the most common cause of dementia in the elderly. However, it has become increasingly apparent that neuroinflammation plays a significant role in the pathophysiology of AD. This review summarizes the current status of neuroinflammation research related to AD, focusing on the connections between neuroinflammation and some inflammation factors in AD. Among these connections, we discuss the dysfunctional blood–brain barrier and alterations in the functional responses of microglia and astrocytes in this process. In addition, we summarize and discuss the role of intracellular signaling pathways involved in inflammatory responses in astrocytes and microglia, including the mitogen-activated protein kinase pathways, nuclear factor-kappa B cascade, and peroxisome proliferator–activated receptor-gamma transcription factors. Finally, the dysregulation of the control and release of pro- and anti-inflammatory cytokines and classic AD pathology (amyloid plaques and neurofibrillary tangles) in AD is also reviewed.Keywords: inflammation, blood–brain barrier, glial cells, intracellular signaling pathways, inflammatory factorsZhang FJJiang LLDove Medical PressarticleNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571Neurology. Diseases of the nervous systemRC346-429ENNeuropsychiatric Disease and Treatment, Vol 2015, Iss default, Pp 243-256 (2015) |
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Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429 |
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Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429 Zhang FJ Jiang LL Neuroinflammation in Alzheimer’s disease |
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Fengjin Zhang,1,2 Linlan Jiang11Department of Pharmacy, General Hospital of Guangzhou Military Command, Guangzhou City, People’s Republic of China; 2School of Bioscience and Bioengineering, South China University of Technology, Guangzhou City, People’s Republic of ChinaAbstract: Amyloid-β plaques and neurofibrillary tangles are the main neuropathological hallmarks in Alzheimer’s disease (AD), the most common cause of dementia in the elderly. However, it has become increasingly apparent that neuroinflammation plays a significant role in the pathophysiology of AD. This review summarizes the current status of neuroinflammation research related to AD, focusing on the connections between neuroinflammation and some inflammation factors in AD. Among these connections, we discuss the dysfunctional blood–brain barrier and alterations in the functional responses of microglia and astrocytes in this process. In addition, we summarize and discuss the role of intracellular signaling pathways involved in inflammatory responses in astrocytes and microglia, including the mitogen-activated protein kinase pathways, nuclear factor-kappa B cascade, and peroxisome proliferator–activated receptor-gamma transcription factors. Finally, the dysregulation of the control and release of pro- and anti-inflammatory cytokines and classic AD pathology (amyloid plaques and neurofibrillary tangles) in AD is also reviewed.Keywords: inflammation, blood–brain barrier, glial cells, intracellular signaling pathways, inflammatory factors |
format |
article |
author |
Zhang FJ Jiang LL |
author_facet |
Zhang FJ Jiang LL |
author_sort |
Zhang FJ |
title |
Neuroinflammation in Alzheimer’s disease |
title_short |
Neuroinflammation in Alzheimer’s disease |
title_full |
Neuroinflammation in Alzheimer’s disease |
title_fullStr |
Neuroinflammation in Alzheimer’s disease |
title_full_unstemmed |
Neuroinflammation in Alzheimer’s disease |
title_sort |
neuroinflammation in alzheimer’s disease |
publisher |
Dove Medical Press |
publishDate |
2015 |
url |
https://doaj.org/article/5827a1386e0940a8bc068001f0382efc |
work_keys_str_mv |
AT zhangfj neuroinflammationinalzheimerrsquosdisease AT jiangll neuroinflammationinalzheimerrsquosdisease |
_version_ |
1718403739050573824 |