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胶质细胞介导的阿尔茨海默病神经炎症。

Glial Cell-Mediated Neuroinflammation in Alzheimer's Disease.

机构信息

Department of Drug Discovery and Development, Harrison College of Pharmacy, Auburn University, 720 S Donahue Dr., Auburn, AL 36849, USA.

Division of Pharmaceutics & Pharmacology, College of Pharmacy, The Ohio State University, Columbus, OH 43210, USA.

出版信息

Int J Mol Sci. 2022 Sep 12;23(18):10572. doi: 10.3390/ijms231810572.


DOI:10.3390/ijms231810572
PMID:36142483
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9502483/
Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder; it is the most common cause of dementia and has no treatment. It is characterized by two pathological hallmarks, the extracellular deposits of amyloid beta (Aβ) and the intraneuronal deposits of Neurofibrillary tangles (NFTs). Yet, those two hallmarks do not explain the full pathology seen with AD, suggesting the involvement of other mechanisms. Neuroinflammation could offer another explanation for the progression of the disease. This review provides an overview of recent advances on the role of the immune cells' microglia and astrocytes in neuroinflammation. In AD, microglia and astrocytes become reactive by several mechanisms leading to the release of proinflammatory cytokines that cause further neuronal damage. We then provide updates on neuroinflammation diagnostic markers and investigational therapeutics currently in clinical trials to target neuroinflammation.

摘要

阿尔茨海默病(AD)是一种进行性神经退行性疾病;它是痴呆症的最常见原因,目前尚无治疗方法。它的特征是两种病理特征,细胞外淀粉样蛋白β(Aβ)沉积和神经元内神经原纤维缠结(NFTs)沉积。然而,这两个特征并不能解释 AD 患者的全部病理,这表明可能存在其他机制。神经炎症可能为疾病的进展提供另一种解释。这篇综述概述了免疫细胞小胶质细胞和星形胶质细胞在神经炎症中的作用的最新进展。在 AD 中,小胶质细胞和星形胶质细胞通过几种机制变得活跃,导致释放促炎细胞因子,从而导致进一步的神经元损伤。然后,我们将介绍目前正在临床试验中针对神经炎症的神经炎症诊断标志物和研究性治疗方法的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98e7/9502483/ea1146d12981/ijms-23-10572-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98e7/9502483/f692728c59b1/ijms-23-10572-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98e7/9502483/ea1146d12981/ijms-23-10572-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98e7/9502483/f692728c59b1/ijms-23-10572-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98e7/9502483/ea1146d12981/ijms-23-10572-g001.jpg

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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
CRISPRi screens in human iPSC-derived astrocytes elucidate regulators of distinct inflammatory reactive states.

Nat Neurosci. 2022-11

[2]
Targeting NLRP3-Mediated Neuroinflammation in Alzheimer's Disease Treatment.

Int J Mol Sci. 2022-8-11

[3]
Role of NLRP3 Inflammasome and Its Inhibitors as Emerging Therapeutic Drug Candidate for Alzheimer's Disease: a Review of Mechanism of Activation, Regulation, and Inhibition.

Inflammation. 2023-2

[4]
Microglial TYROBP/DAP12 in Alzheimer's disease: Transduction of physiological and pathological signals across TREM2.

Mol Neurodegener. 2022-8-24

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YKL-40 changes are not detected in post-mortem brain of patients with Alzheimer's disease and frontotemporal lobar degeneration.

Alzheimers Res Ther. 2022-7-25

[6]
Physical Exercise-Induced Astrocytic Neuroprotection and Cognitive Improvement Through Primary Cilia and Mitogen-Activated Protein Kinases Pathway in Rats With Chronic Cerebral Hypoperfusion.

Front Aging Neurosci. 2022-6-1

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An Overview of Oxidative Stress, Neuroinflammation, and Neurodegenerative Diseases.

Int J Mol Sci. 2022-5-25

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Addressing Blood-Brain Barrier Impairment in Alzheimer's Disease.

Biomedicines. 2022-3-22

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Treadmill exercise improve recognition memory by TREM2 pathway to inhibit hippocampal microglial activation and neuroinflammation in Alzheimer's disease model.

Physiol Behav. 2022-7-1

[10]
Advances in the development of new biomarkers for Alzheimer's disease.

Transl Neurodegener. 2022-4-21

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