Research Progress of Microglia in the Intervention Effect of Alzheimer's Disease

Tianying Fang; Caiping Han; Qingli Song; Yaning Hao; Wei Yuan; Meng Yu; Lin Zhang

doi:doi:10.11648/j.cmr.20231204.15

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Research Progress of Microglia in the Intervention Effect of Alzheimer's Disease

Tianying Fang, Caiping Han, Qingli Song, Yaning Hao, Wei Yuan, Meng Yu, Lin Zhang

Published in Clinical Medicine Research (Volume 12, Issue 4)

Received: 28 June 2023 Accepted: 24 July 2023 Published: 22 August 2023

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Abstract

Alzheimer's disease (AD) is a degenerative disease of the central nervous system characterized by an insidious onset and progressive worsening of cognitive function. The main pathological features of AD are β-amyloid (Aβ) plaques, neuroprogenitor fibril tangles (NFT) formed by hyperphosphorylated Tau proteins, and other pathological features. In addition, there is growing evidence that AD is strongly associated with microglia activation, due to the fact that most of the risk genes for AD are highly expressed by microglia in the brain. The category of microglia is mainly depending on the milieu in which they become activated and the factors they are stimulated. In the development of AD, microglia can be activated to the M1 type to exert neuroinflammatory effects by producing various pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 to induce neurotoxicity, and to the M2 type to exert anti-inflammation effects through enhancing the expression of neurotrophin, IL-4, and IL-6, and accelerate the clearance of Aβ plaques, which is believed to be promising molecules in AD therapy. This paper summarizes the mechanisms of microglia in AD and reviews the activation of microglia, the triggering receptor expressed on myeloid cells 2 (TREM2), disease-associated microglia (DAM), and gut microbiota to identify new therapeutic targets for AD, which currently lacks effective interventions.

Published in	Clinical Medicine Research (Volume 12, Issue 4)
DOI	10.11648/j.cmr.20231204.15
Page(s)	82-87
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Alzheimer's Disease, Microglia, Neuroinflammation, TREM2, DAM, Gut Microbiota

References

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APA Style

Tianying Fang, Caiping Han, Qingli Song, Yaning Hao, Wei Yuan, et al. (2023). Research Progress of Microglia in the Intervention Effect of Alzheimer's Disease. Clinical Medicine Research, 12(4), 82-87. https://doi.org/10.11648/j.cmr.20231204.15

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ACS Style

Tianying Fang; Caiping Han; Qingli Song; Yaning Hao; Wei Yuan, et al. Research Progress of Microglia in the Intervention Effect of Alzheimer's Disease. Clin. Med. Res. 2023, 12(4), 82-87. doi: 10.11648/j.cmr.20231204.15

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AMA Style

Tianying Fang, Caiping Han, Qingli Song, Yaning Hao, Wei Yuan, et al. Research Progress of Microglia in the Intervention Effect of Alzheimer's Disease. Clin Med Res. 2023;12(4):82-87. doi: 10.11648/j.cmr.20231204.15

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@article{10.11648/j.cmr.20231204.15,
  author = {Tianying Fang and Caiping Han and Qingli Song and Yaning Hao and Wei Yuan and Meng Yu and Lin Zhang},
  title = {Research Progress of Microglia in the Intervention Effect of Alzheimer's Disease},
  journal = {Clinical Medicine Research},
  volume = {12},
  number = {4},
  pages = {82-87},
  doi = {10.11648/j.cmr.20231204.15},
  url = {https://doi.org/10.11648/j.cmr.20231204.15},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cmr.20231204.15},
  abstract = {Alzheimer's disease (AD) is a degenerative disease of the central nervous system characterized by an insidious onset and progressive worsening of cognitive function. The main pathological features of AD are β-amyloid (Aβ) plaques, neuroprogenitor fibril tangles (NFT) formed by hyperphosphorylated Tau proteins, and other pathological features. In addition, there is growing evidence that AD is strongly associated with microglia activation, due to the fact that most of the risk genes for AD are highly expressed by microglia in the brain. The category of microglia is mainly depending on the milieu in which they become activated and the factors they are stimulated. In the development of AD, microglia can be activated to the M1 type to exert neuroinflammatory effects by producing various pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 to induce neurotoxicity, and to the M2 type to exert anti-inflammation effects through enhancing the expression of neurotrophin, IL-4, and IL-6, and accelerate the clearance of Aβ plaques, which is believed to be promising molecules in AD therapy. This paper summarizes the mechanisms of microglia in AD and reviews the activation of microglia, the triggering receptor expressed on myeloid cells 2 (TREM2), disease-associated microglia (DAM), and gut microbiota to identify new therapeutic targets for AD, which currently lacks effective interventions.},
 year = {2023}
}

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TY  - JOUR
T1  - Research Progress of Microglia in the Intervention Effect of Alzheimer's Disease
AU  - Tianying Fang
AU  - Caiping Han
AU  - Qingli Song
AU  - Yaning Hao
AU  - Wei Yuan
AU  - Meng Yu
AU  - Lin Zhang
Y1  - 2023/08/22
PY  - 2023
N1  - https://doi.org/10.11648/j.cmr.20231204.15
DO  - 10.11648/j.cmr.20231204.15
T2  - Clinical Medicine Research
JF  - Clinical Medicine Research
JO  - Clinical Medicine Research
SP  - 82
EP  - 87
PB  - Science Publishing Group
SN  - 2326-9057
UR  - https://doi.org/10.11648/j.cmr.20231204.15
AB  - Alzheimer's disease (AD) is a degenerative disease of the central nervous system characterized by an insidious onset and progressive worsening of cognitive function. The main pathological features of AD are β-amyloid (Aβ) plaques, neuroprogenitor fibril tangles (NFT) formed by hyperphosphorylated Tau proteins, and other pathological features. In addition, there is growing evidence that AD is strongly associated with microglia activation, due to the fact that most of the risk genes for AD are highly expressed by microglia in the brain. The category of microglia is mainly depending on the milieu in which they become activated and the factors they are stimulated. In the development of AD, microglia can be activated to the M1 type to exert neuroinflammatory effects by producing various pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 to induce neurotoxicity, and to the M2 type to exert anti-inflammation effects through enhancing the expression of neurotrophin, IL-4, and IL-6, and accelerate the clearance of Aβ plaques, which is believed to be promising molecules in AD therapy. This paper summarizes the mechanisms of microglia in AD and reviews the activation of microglia, the triggering receptor expressed on myeloid cells 2 (TREM2), disease-associated microglia (DAM), and gut microbiota to identify new therapeutic targets for AD, which currently lacks effective interventions.
VL  - 12
IS  - 4
ER  -

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Author Information

Tianying Fang

Department of Clinical Medicine of 2nd Clinical Medical School, Shaanxi University of Chinese Medicine, Xianyang, China
Caiping Han

Neurology, Xi'an Central Hospital, Xi'an, China
Qingli Song

Department of Clinical Medicine of 2nd Clinical Medical School, Shaanxi University of Chinese Medicine, Xianyang, China
Yaning Hao

Department of Clinical Medicine of 2nd Clinical Medical School, Shaanxi University of Chinese Medicine, Xianyang, China
Wei Yuan

Neurology, Xi'an North Hospital, Xi'an, China
Meng Yu

Neurology, Shaanxi Yejin Hospital, Xi'an, China
Lin Zhang

Neurology, Xi'an People's Hospital (Xi'an Fourth Hospital), Xi'an, China

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APA Style

Tianying Fang, Caiping Han, Qingli Song, Yaning Hao, Wei Yuan, et al. (2023). Research Progress of Microglia in the Intervention Effect of Alzheimer's Disease. Clinical Medicine Research, 12(4), 82-87. https://doi.org/10.11648/j.cmr.20231204.15

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ACS Style

Tianying Fang; Caiping Han; Qingli Song; Yaning Hao; Wei Yuan, et al. Research Progress of Microglia in the Intervention Effect of Alzheimer's Disease. Clin. Med. Res. 2023, 12(4), 82-87. doi: 10.11648/j.cmr.20231204.15

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AMA Style

Tianying Fang, Caiping Han, Qingli Song, Yaning Hao, Wei Yuan, et al. Research Progress of Microglia in the Intervention Effect of Alzheimer's Disease. Clin Med Res. 2023;12(4):82-87. doi: 10.11648/j.cmr.20231204.15

Copy | Download

@article{10.11648/j.cmr.20231204.15,
  author = {Tianying Fang and Caiping Han and Qingli Song and Yaning Hao and Wei Yuan and Meng Yu and Lin Zhang},
  title = {Research Progress of Microglia in the Intervention Effect of Alzheimer's Disease},
  journal = {Clinical Medicine Research},
  volume = {12},
  number = {4},
  pages = {82-87},
  doi = {10.11648/j.cmr.20231204.15},
  url = {https://doi.org/10.11648/j.cmr.20231204.15},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cmr.20231204.15},
  abstract = {Alzheimer's disease (AD) is a degenerative disease of the central nervous system characterized by an insidious onset and progressive worsening of cognitive function. The main pathological features of AD are β-amyloid (Aβ) plaques, neuroprogenitor fibril tangles (NFT) formed by hyperphosphorylated Tau proteins, and other pathological features. In addition, there is growing evidence that AD is strongly associated with microglia activation, due to the fact that most of the risk genes for AD are highly expressed by microglia in the brain. The category of microglia is mainly depending on the milieu in which they become activated and the factors they are stimulated. In the development of AD, microglia can be activated to the M1 type to exert neuroinflammatory effects by producing various pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 to induce neurotoxicity, and to the M2 type to exert anti-inflammation effects through enhancing the expression of neurotrophin, IL-4, and IL-6, and accelerate the clearance of Aβ plaques, which is believed to be promising molecules in AD therapy. This paper summarizes the mechanisms of microglia in AD and reviews the activation of microglia, the triggering receptor expressed on myeloid cells 2 (TREM2), disease-associated microglia (DAM), and gut microbiota to identify new therapeutic targets for AD, which currently lacks effective interventions.},
 year = {2023}
}

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TY  - JOUR
T1  - Research Progress of Microglia in the Intervention Effect of Alzheimer's Disease
AU  - Tianying Fang
AU  - Caiping Han
AU  - Qingli Song
AU  - Yaning Hao
AU  - Wei Yuan
AU  - Meng Yu
AU  - Lin Zhang
Y1  - 2023/08/22
PY  - 2023
N1  - https://doi.org/10.11648/j.cmr.20231204.15
DO  - 10.11648/j.cmr.20231204.15
T2  - Clinical Medicine Research
JF  - Clinical Medicine Research
JO  - Clinical Medicine Research
SP  - 82
EP  - 87
PB  - Science Publishing Group
SN  - 2326-9057
UR  - https://doi.org/10.11648/j.cmr.20231204.15
AB  - Alzheimer's disease (AD) is a degenerative disease of the central nervous system characterized by an insidious onset and progressive worsening of cognitive function. The main pathological features of AD are β-amyloid (Aβ) plaques, neuroprogenitor fibril tangles (NFT) formed by hyperphosphorylated Tau proteins, and other pathological features. In addition, there is growing evidence that AD is strongly associated with microglia activation, due to the fact that most of the risk genes for AD are highly expressed by microglia in the brain. The category of microglia is mainly depending on the milieu in which they become activated and the factors they are stimulated. In the development of AD, microglia can be activated to the M1 type to exert neuroinflammatory effects by producing various pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 to induce neurotoxicity, and to the M2 type to exert anti-inflammation effects through enhancing the expression of neurotrophin, IL-4, and IL-6, and accelerate the clearance of Aβ plaques, which is believed to be promising molecules in AD therapy. This paper summarizes the mechanisms of microglia in AD and reviews the activation of microglia, the triggering receptor expressed on myeloid cells 2 (TREM2), disease-associated microglia (DAM), and gut microbiota to identify new therapeutic targets for AD, which currently lacks effective interventions.
VL  - 12
IS  - 4
ER  -

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