Research Paper Volume 13, Issue 10 pp 14001—14014
Adalimumab ameliorates memory impairments and neuroinflammation in chronic cerebral hypoperfusion rats
- 1 Department of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450002, People’s Republic of China
- 2 Henan Key Laboratory of Tumor Pathology, Zhengzhou 450002, People’s Republic of China
- 3 Department of Pathology, School of Basic Medicine, Zhengzhou University, Zhengzhou 450002, People’s Republic of China
- 4 Department of Medical Laboratory, Henan Provincial People’s Hospital, Zhengzhou, Henan 450003, People’s Republic of China
- 5 Department of Medical Laboratory of Central China Fuwai Hospital, Zhengzhou, Henan 450003, People’s Republic of China
- 6 Central China Fuwai Hospital of Zhengzhou University, Zhengzhou, Henan 450003, People’s Republic of China
- 7 Medical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450002, People’s Republic of China
- 8 Department of Pathology, People’s Hospital of Zhengzhou, Zhengzhou 450000, People’s Republic of China
Received: February 23, 2021 Accepted: April 5, 2021 Published: May 24, 2021https://doi.org/10.18632/aging.203009
How to Cite
Copyright: © 2021 Xu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Vascular dementia (VaD) is the second most common type of dementia worldwide. Although there are five FDA-approved drugs for the treatment of Alzheimer’s disease (AD), none of them have been applied to treat VaD. Adalimumab is a TNF-α inhibitor that is used for the treatment of autoimmune diseases such as rheumatoid arthritis. In a recent retrospective case-control study, the application of adalimumab for rheumatoid or psoriasis was shown to decrease the risk of AD. However, whether adalimumab can be used for the treatment of VaD is not clear. In this study, we used 2VO surgery to generate a VaD rat model and treated the rats with adalimumab or vehicle. We demonstrated that VaD rats treated with adalimumab exhibited significant improvements in memory. In addition, adalimumab treatment significantly alleviated neuronal loss in the hippocampi of VaD rats. Moreover, adalimumab significantly reduced microglial activation and reversed M1/M2 polarization in VaD rats. Furthermore, adalimumab treatment suppressed the activity of NF-κB, an important neuroinflammatory transcription factor. Finally, adalimumab displayed a protective role against oxidative stress in VaD rats. Our results indicate that adalimumab may be applied for the treatment of human patients with VaD.