10 October 2015 4 4K Report

As we know, hippocampus is a widely recognized area Alzheimer's disease affects, and reportedly makes a difference in conventional cognitive assessments, e.g. Morris water maze. And stereotaxic infusion of abeta oligomer can be used to generate acute AD model of rodent.

But to my surprise, most researches with this acute AD model didn't choose hippocampus as their injected site. Instead they injected abeta i.c.v. and reported this can induce neuronal death in hippocampus[1]. Previous study revealed i.h. may have more sereve impairment in memory[2], so why still people prefer so much i.c.v. over i.h.?

Many thanks for your answer. This will help us decide in our own experiment.

[1] Li L, Xu B, Zhu Y, et al. DHEA prevents Aβ 25–35-impaired survival of newborn neurons in the dentate gyrus through a modulation of PI 3 K-Akt-mTOR signaling[J]. Neuropharmacology, 2010, 59(4): 323-333.

[2] Flood J F, Morley J E, Roberts E. Amnestic effects in mice of four synthetic peptides homologous to amyloid beta protein from patients with Alzheimer disease[J]. Proceedings of the National Academy of Sciences, 1991, 88(8): 3363-3366.

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