Cholinergic dysfunction in a mouse model
of Alzheimer disease is reversed
by an anti-Aβ antibody
J. Clin. Invest. Kelly R. Bales, et al. 116:825 doi:10.1172/JCI27120 [
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Figure 2Hippocampal ACh release in PDAPP mice is restored to WT levels after anti-Aβ treatment. (
A) Hippocampal ACh release in WT and PDAPP transgenic mice following exposure to a novel environment (Novelty) and after treatment of PDAPP mice with the anti-Aβ antibody m266 (PDAPP + m266; 500 μg i.p.). The arrows indicate the time at which mice were placed into a novel environment (novelty) and back into their home cage. (
B) Release of ACh from the hippocampus of WT and PDAPP mice following administration of scopolamine (0.3 mg/kg i.p.) and after administration of m266.
n = 7–10 mice per group, 4–6 months of age. (
C) Extracellular levels of choline in brain measured by in vivo microdialysis from WT and PDAPP mice.
n = 5 mice per group, 4–6 months of age. (
D) Basal levels of hippocampal ACh release in WT, PDAPP, and PDAPP mice administered m266.
n = 7–10 mice per group, 4–6 months of age. *
P < 0.05 versus WT;
#P < 0.05, PDAPP versus PDAPP + m266.