Endothelial nitric oxide deficiency promotes Alzheimer's disease pathology
Version of Record online: 27 JUN 2013
© 2013 International Society for Neurochemistry
Journal of Neurochemistry
Volume 127, Issue 5, pages 691–700, December 2013
How to Cite
J. Neurochem.(2013) 127, 691–700
- Issue online: 13 NOV 2013
- Version of Record online: 27 JUN 2013
- Accepted manuscript online: 8 JUN 2013 06:42AM EST
- Manuscript Accepted: 5 JUN 2013
- Manuscript Revised: 10 MAY 2013
- Manuscript Received: 25 MAR 2013
- National Institutes of Health. Grant Numbers: HL-111062, HL-91867
- Mayo Alzheimer's Disease Research Center
- AHA. Grant Numbers: 0835436N, 12POST8550003
- Clinical Pharmacology Training Grant. Grant Number: T32 GM08685
- Samuel Johnson Foundation for Genomics of Addiction Program at Mayo Clinic
- Mayo Foundation
Figure S1. Levels of iNOS, nNOS, Tau and pTau are unaltered in the brains of late middle aged eNOS-/- mice as compared with age-matched wild-type control animals.
Figure S2. Hippocampal levels of iNOS, nNOS, Tau, and pTau were not different between late middle aged eNOS-/- and late middle aged wild-type mice.
Figure S3. Levels of CD68, GFAP, and NeuN are unaltered in the hippocampus of late middle aged eNOS-/- mice.
Figure S4. APP and BACE1 protein levels were unaltered in brain microvessels of late middle aged eNOS-/- mice as compared with late middle aged wild-type control animals.
Figure S5. APP and BACE1 protein levels were unaltered in microvessels isolated from the hippocampus of late middle aged eNOS-/- mice as compared with late middle aged wild-type control animals.
Figure S6. No differences in locomotor activity was observed between late middle aged eNOS-/- and late middle aged wild-type mice.
Table S1. Peripheral parameters of 15-month-old wild type and eNOS-/- mice.
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