Research Paper Volume 10, Issue 11 pp 3117—3135

Transferrin is responsible for mediating the effects of iron ions on the regulation of anterior pharynx-defective-1α/β and Presenilin 1 expression via PGE2 and PGD2 at the early stage of Alzheimer’s Disease

Figure 8. Fe accelerated cognitive decline in APP/PS1 Tg mice by enhancing the aggregation and deposition of Aβ. 3-month-old APP/PS1 Tg mice were treated with Fe (25 mg/ml in water) for 3 months in the absence or presence of M-30 (intranasal administration, 0.5 mg/kg/d) or NS398 (intranasal administration, 1 mg/kg/d) before their learning abilities were evaluated (n=6). (A) The immunoreactivity of Aβ was determined by immunohistochemistry with an anti-Aβ antibody. These images are representative of 6 independent mouse experiments, all of which produced similar results. (B-D) In the hidden-platform tests, Fe-treated APP/PS1 Tg mice showed the longest latency and escape path lengths, whereas those in the M-30 and NS398 treatment groups showed clear decreases in escape latency and path length. (E) In the probe trial, the mice in the Fe-treated APP/PS1 group had the fewest times passing through the platform’s former location, and the M-30- or NS398-treated mice showed partially reversed effects of APP/PS1 damage and improved cognition and memory. *p<0.05 compared with APP/PS1 controls. # p<0.05 with respect to the Fe-treated APP/PS1 mice alone.