Results: 3

1.
Figure 2

Figure 2. From: The Effects of NOS2 Gene Deletion on Mice Expressing Mutated Human A?PP.

Neuronal loss in APPSw/NOS2−/− compared to APPSw mice at 52–54 weeks of age. A,C,E = tyical views of hippocampus in APPSw mice. B,D,F = same areas in APPSw/NOS2−/− mice. Neurons were identified using NeuN immunochemistry. G: Unbaised stereology was used to count neurons in specific brain regions. A significant decrease (*** = p < 0.001) was observed in all regions in the APPSw/NOS2−/− (abbreviated AN2) mice compared to APPSw (abbreviated A), WT, NOS2−/− (abbreviated N2) mice. H: Summary of the percent changes in neuronal number.

Carol A. Colton, et al. J Alzheimers Dis. ;15(4):571-587.
2.
Figure 3

Figure 3. From: The Effects of NOS2 Gene Deletion on Mice Expressing Mutated Human A?PP.

Behavioral deficits in the APPsw/NOS2−/− compared to APPSw mice at 52–54 weeks age. The 2-day radial arm water maze was used to test learning and memory as described [136]. Data points represent the average (± SEM) number of errors in each of the 5 blocks of trials on day 2 of the testing paradym. *** p < 0.001 compared to either NOS2−/− or to APPSw, n = 7–14 mice/group.

Carol A. Colton, et al. J Alzheimers Dis. ;15(4):571-587.
3.
Figure 1

Figure 1. From: The Effects of NOS2 Gene Deletion on Mice Expressing Mutated Human A?PP.

Panel A: Average fold change (± SEM) in mRNA levels of pro-inflammatory (TNFα; NOS2) and repair [arginase 1 (AG1) and chitinase 3-like-1 (CH3L1)] cytokines from mixed cortical lysates from humans with AD (average age approximately 78 yrs; Stage 4–5 Braak scale). Quantitative RT-PCR data from AD samples were compared to brain samples from aged matched normal individuals. De-identified autopsied brain samples were provided by the Kathleen Bryan Brain Bank at Duke University Medical Center, Durham, NC as described [30].
Panel B: Average fold change (± SEM) in mRNA from aged (52–54 week old) APPSwDI/NOS2−/− mice compared to aged matched wild type (WT) mice. Pro-inflammatory genes were TNFα and IL-6 and repair genes were AG1 and YM1 (mouse homolog for CH3L1). All values are significantly greater than control with p ≤ 0.05 (Student’s t test) (for humans, n = 29 control; AD; mixed gender; for mice n = 5–6 mice, mixed gender).

Carol A. Colton, et al. J Alzheimers Dis. ;15(4):571-587.

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