Acta Anatomica Sinica ›› 2018, Vol. 49 ›› Issue (5): 571-578.doi: 10.16098/j.issn.0529-1356.2018.05.002

• Neurobiology • Previous Articles     Next Articles

Brain barrier structure of APPSWE Tg2576 mice

CUI Zhan-jun1 LIU Fang2 ZHAO Kai-bing3 LI Bing-mei4 LIU Zhong-hua 1*   

  1. 1.Institute of Nano Medicine; 2.Department of Pathology, the First Affiliated Hospital of He’nan University; 3.Department of Anatomy, Medical College of Kaifeng University; 4.Teaching Office,He’nan University Huaihe Hospital, He’nan Kaifeng 475001,China
  • Received:2017-09-26 Revised:2018-05-31 Online:2018-10-06 Published:2018-10-06
  • Contact: LIU Zhong-hua E-mail:cjz1968@126.com

Abstract:

Objective To investigate the basic structure of the blood brain barrier (BBB) and blood cerebrospinal fluid barrier (BCSFB) in mice and their changes in structure, function, and ultrastructure during the development and progression of AD. Methods The APPSWE Tg2576 mice were used and divided into APPSWE transgenic positive mice (model group) and littermates wild type mice (control group), twety mice in each group. After 16 months of feeding, whole body perfusion was performed and the craniotomy was performed to obtain the lateral ventricle wall and its choroid plexus. Immunofluorescence and transmission electron microscopy were used to observe the ultrastructure of BBB and BCSFB, so as to observe the changes of brain barrier of AD model. Results The vascular density was significantly lower in the AD model group than in the control group; the normal structure of the brain barrier in AD mice was impaired, mainly due to the connection between the brain vascular endothelial cells (or choroid plexus endothelial cells) and their organelles being damaged. The ultrastructure of the choroid plexus also showed significant changes. The main manifestations were the widening of the intercellular space, and some of the connecting structures between the cells, such as adhesion and connection, and some vesicle-like structures in the cytoplasm. Conclusion Compared with normal mice, the brain barrier of AD rats is damaged, which may lead to corresponding changes in the brain barrier transport mechanism and affect the clearance of Aβ in the brain, and the steady-state mechanisms existing in the brain barrier, such as secretions and receptors thereof. Mediated signaling may also change, and these factors may be involved in the formation and progression of AD.

Key words: Alzheimer’s disease, Blood brain barrier, Blood cerebrospinal fluid barrier, Choroid plexus, Proliferation, Vascular nerve unit, Immunofluorescence, Mouse