The Journal of Neuroscience, January 24, 2007, ():
Disturbed Cross Talk between Insulin-Like Growth Factor I and AMP-Activated Protein Kinase as a Possible Cause of Vascular Dysfunction in the Amyloid Precursor Protein/Presenilin 2 Mouse Model of Alzheimer's Disease
J. Neurosci. Lopez-Lopez et al.
27: 824
Supplemental Data
Files in this Data Supplement:
- supplemental material
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Supplementary Figure 1. Brain cortex sections of APP/PS2 mice were stained with anti-Aβ and anti-MHCII (a marker of activated microglia) antibodies. While a positive control section from a representative older APPPS2 mice (14 months old) shows Aβ+ plaques and MHCII+ profiles, similar brain cortex sections from two representative young mice (6 months) show no staining. Weak intra-neuronal Aβ+ staining is found in the younger mice (arrows). No microglia reactivity associated to Aβ+ profiles was detected in any of the young APP/PS2 mice used in this experiment (n=7).
- supplemental material
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Supplementary Figure 2. Metabolic activity of brain endothelial cells after IGF-I and AICAR administration. Metabolic activity of the cells, as measured by peroxide production (A), mitochondrial activity (MTT levels, B) or mitochondrial biogenesis (C, PGC-1 levels) were not further modified by conjoint addition of AICAR and IGF-I. Similar increases were found after AICAR, IGF-I, or when both were given together. Endothelial cultures were stimulated and 24 h later peroxide levels were monitored by assessing production of fluorescent dichofluorescein by the cells (n= 8). Levels of MTT in treated cultures were quantified with a commercial system (n= 4) 24 h after the different treatments, while PGC-1 levels were assessed in cell extracts by immunoblot 24h after treatments (n=4). *p<0.001 vs control. A representative blot is shown.
