Acta Anatomica Sinica ›› 2018, Vol. 49 ›› Issue (2): 158-165.doi: 10.16098/j.issn.0529-1356.2018.02.004

• Neurobiology • Previous Articles     Next Articles

Kinesin1-mediated neuronal axoplasmic transport disorder in cerebral cortex of amyloid precursor protein/presenilin-1 transgenic mice

WANG Qian1 FAN Wen-juan 1,2 SUN Yi-zheng1 WANG Lai1 DENG Jin-bo 1*   

  1. 1.Institute of Neurobiology, College of Life Science, He’nan University, He’nan Kaifeng 475004, China; 2.Molecular Medical Laboratory, Luohe Medical College, He’nan Luohe 462002, China
  • Received:2017-02-21 Revised:2017-05-22 Online:2017-04-06 Published:2018-04-06
  • Contact: DENG Jin-bo E-mail:jinbo_deng@henu.edu.cn

Abstract:

Objective To understand the roles of axonal transport proteins, kinesin1 and SIM-312, in the pathogenesis and development of Alzheimer’s disease. Methods Amyloid precursor protein(APP)/ presenilin-1(PS1)transgenic mice (n=40) and wild type mice (n=40) from postnatal day 30 to postnatal day 360 were used in the study. Amyloid beta-peptides(Aβ)plaques and astrocytes in cerebral cortex were visualized with immunofluorescent labeling and Western blotting. Results Compared with wild type mice, Aβ plaques and astrocytes increased in cerebral cortex of APP/PS1 mutant mice, especially after 9 months, with statistical significance. However, after 9 months, the number of kinesin1-positive cells decreased in APP/PS1 transgenic mice, and SIM-312 positive neurofilaments appeared tangled in the cerebral cortex of AD mice as well. Conclusion Abnormal kinesin1 and SIM-312 are involved in axonal transportation disorder in AD mice, suggesting they are the important pathogenic factors of AD.

Key words: Alzheimer's disease, Axial transport barrier, Neurofilament, Kinesin1, Western blotting, Mouse