Effect Analysis of Different Interventions to Improve Neuroinflammation in The Treatment of Alzheimer’s Disease
10.16476/j.pibb.2024.0354
- VernacularTitle:不同干预手段改善神经炎症在治疗阿尔茨海默病中的效果分析
- Author:
Jiang-Hui SHAN
1
;
Chao-Yang CHU
1
;
Shi-Yu CHEN
1
;
Zhi-Cheng LIN
1
;
Yu-Yu ZHOU
1
;
Tian-Yuan FANG
1
;
Chu-Xia ZHANG
1
;
Biao XIAO
1
;
Kai XIE
2
;
Qing-Juan WANG
2
;
Zhi-Tao LIU
3
;
Li-Ping LI
1
Author Information
1. Department of Physiology and Pharmacology, Health Science Centre, Ningbo University, Ningbo 315211, China
2. Rehabilitative Department, the First Affiliated Hospital of Ningbo University, Ningbo 315211, China
3. Department of Science and Education, Ningbo Rehabilitation Hospital, Ningbo 315040, China
- Publication Type:Journal Article
- Keywords:
Alzheimer’s disease;
drug therapy;
gene therapy;
gut microbiome therapy;
neuroinflammation;
physical intervention;
stem cell therapy
- From:
Progress in Biochemistry and Biophysics
2025;52(2):310-333
- CountryChina
- Language:Chinese
-
Abstract:
Alzheimer’s disease (AD) is a central neurodegenerative disease characterized by progressive cognitive decline and memory impairment in clinical. Currently, there are no effective treatments for AD. In recent years, a variety of therapeutic approaches from different perspectives have been explored to treat AD. Although the drug therapies targeted at the clearance of amyloid β-protein (Aβ) had made a breakthrough in clinical trials, there were associated with adverse events. Neuroinflammation plays a crucial role in the onset and progression of AD. Continuous neuroinflammatory was considered to be the third major pathological feature of AD, which could promote the formation of extracellular amyloid plaques and intracellular neurofibrillary tangles. At the same time, these toxic substances could accelerate the development of neuroinflammation, form a vicious cycle, and exacerbate disease progression. Reducing neuroinflammation could break the feedback loop pattern between neuroinflammation, Aβ plaque deposition and Tau tangles, which might be an effective therapeutic strategy for treating AD. Traditional Chinese herbs such as Polygonum multiflorum and Curcuma were utilized in the treatment of AD due to their ability to mitigate neuroinflammation. Non-steroidal anti-inflammatory drugs such as ibuprofen and indomethacin had been shown to reduce the level of inflammasomes in the body, and taking these drugs was associated with a low incidence of AD. Biosynthetic nanomaterials loaded with oxytocin were demonstrated to have the capability to anti-inflammatory and penetrate the blood-brain barrier effectively, and they played an anti-inflammatory role via sustained-releasing oxytocin in the brain. Transplantation of mesenchymal stem cells could reduce neuroinflammation and inhibit the activation of microglia. The secretion of mesenchymal stem cells could not only improve neuroinflammation, but also exert a multi-target comprehensive therapeutic effect, making it potentially more suitable for the treatment of AD. Enhancing the level of TREM2 in microglial cells using gene editing technologies, or application of TREM2 antibodies such as Ab-T1, hT2AB could improve microglial cell function and reduce the level of neuroinflammation, which might be a potential treatment for AD. Probiotic therapy, fecal flora transplantation, antibiotic therapy, and dietary intervention could reshape the composition of the gut microbiota and alleviate neuroinflammation through the gut-brain axis. However, the drugs of sodium oligomannose remain controversial. Both exercise intervention and electromagnetic intervention had the potential to attenuate neuroinflammation, thereby delaying AD process. This article focuses on the role of drug therapy, gene therapy, stem cell therapy, gut microbiota therapy, exercise intervention, and brain stimulation in improving neuroinflammation in recent years, aiming to provide a novel insight for the treatment of AD by intervening neuroinflammation in the future.
