These authors contributed equally to this work.
β-Secretase-1 elevation in transgenic mouse models of Alzheimer’s disease is associated with synaptic/axonal pathology and amyloidogenesis: implications for neuritic plaque development
Version of Record online: 10 DEC 2009
© The Authors (2009). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd
European Journal of Neuroscience
Volume 30, Issue 12, pages 2271–2283, December 2009
How to Cite
Zhang, X.-M., Cai, Y., Xiong, K., Cai, H., Luo, X.-G., Feng, J.-C., Clough, R. W., Struble, R. G., Patrylo, P. R. and Yan, X.-X. (2009), β-Secretase-1 elevation in transgenic mouse models of Alzheimer’s disease is associated with synaptic/axonal pathology and amyloidogenesis: implications for neuritic plaque development. European Journal of Neuroscience, 30: 2271–2283. doi: 10.1111/j.1460-9568.2009.07017.x
- Issue online: 15 DEC 2009
- Version of Record online: 10 DEC 2009
- Received 16 August 2009, accepted 6 October 2009
Fig. S1. Co-occurrence of BACE1 or Aβ with TH and NADPH-d around swollen/dystrophic axon terminals in the striatum and cortex.
Fig. S2. Initial occurrence of 3D6, 6E10 and BACE1 labeling in 5XFAD mouse brain before plaque onset.
Fig. S3. Age-related pattern of changes in 3D6 and β-secretase-1 labeling around cortical pyramidal neurons and compact plaques in 5XFAD mice.
Fig. S4. Additional trials of correlated measurements of BACE1/3D6 immunoreactivity relative to plaque size.
As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer-reviewed and may be re-organized for online delivery, but are not copy-edited or typeset by Wiley-Blackwell. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors.
|EJN_7017_sm_Fig.S1.doc||3182K||Supporting info item|
|EJN_7017_sm_Fig.S2.doc||2935K||Supporting info item|
|EJN_7017_sm_Fig.S3.doc||1400K||Supporting info item|
|EJN_7017_sm_Fig.S4.doc||186K||Supporting info item|
Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.