These authors contributed equally.
Reduction and the intracellular translocation of EphB2 in Tg2576 mice and the effects of β-amyloid
Article first published online: 9 SEP 2013
© 2013 British Neuropathological Society
Neuropathology and Applied Neurobiology
Volume 39, Issue 6, pages 612–622, October 2013
How to Cite
Qu, M., Jiang, J., Liu, X.-P., Tian, Q., Chen, L.-M., Yin, G., Liu, D., Wang, J.-Z. and Zhu, L.-Q. (2013), Reduction and the intracellular translocation of EphB2 in Tg2576 mice and the effects of β-amyloid. Neuropathology and Applied Neurobiology, 39: 612–622. doi: 10.1111/nan.12019
- Issue published online: 9 SEP 2013
- Article first published online: 9 SEP 2013
- Accepted manuscript online: 21 JAN 2013 09:34AM EST
- Manuscript Accepted: 19 DEC 2012
- Manuscript Received: 31 JUL 2012
- National Natural Science Foundation of China. Grant Number: 91132725
- Ministry of Science and Technology of China. Grant Number: 2011DFG33250
- New Century Excellent Talent of Education Ministry. Grant Number: NCET-10-0421
- New Investigator Research Grant of Alzheimer's Association. Grant Number: NIRG-11-205737
- Alzheimer's disease;
- olfactory bulb
EphB2 is a member of receptor tyrosine kinases (RTKs) family that is essential for the cell adhesion, neural crest migration, axon guidance and synaptogenesis in the nervous system. Recent studies show that preservation of EphB2 in a transgenic mouse model of Alzheimer's disease (AD) rescues the cognitive deficit, suggesting a crucial role of EphB2 in AD. However, the expression and distribution profiles of EphB2 in the early stage of AD have not been reported.
Immunohistochemistry, immunoblot and immunofluorescence were used to analyse the level of EphB2 in Tg2576 mice at different ages and in cultured neurones with Aβ treatment at different times.
EphB2 was reduced in an age-dependent manner in the olfactory bulb and the hippocampus of Tg2576 mice. The decrease of EphB2 appeared earlier in the olfactory bulb than the hippocampus, and reduction of EphB2 appeared earlier than that of MAP2, a dendritic cytoskeleton marker. In the cortex, EphB2 displayed a significant translocation from the neuronal processes to the cell bodies with ageing. In primary hippocampal neuronal cultures, Aβ42 treatment also induced the decrement of EphB2 that was prior to the decline of MAP2.
Our findings provide the first evidence for an age- and region-dependent reduction and intracellular translocation of EphB2 in Tg2576 mice, and the foremost decrement of EphB2 in the olfactory bulb may represent an early sign of AD.