Open Access

Erratum to: A multifunctional therapeutic approach to disease modification in multiple familial mouse models and a novel sporadic model of Alzheimer’s disease

  • Jia Luo1,
  • Sue H. Lee1,
  • Lawren VandeVrede1,
  • Zhihui Qin1,
  • Manel Ben Aissa1, 5,
  • John Larson2,
  • Andrew F. Teich3,
  • Ottavio Arancio3,
  • Yohan D’Souza4,
  • Ahmed Elharram4,
  • Kevin Koster5,
  • Leon M. Tai5,
  • Mary Jo LaDu5,
  • Brian M. Bennett4 and
  • Gregory R. J. Thatcher1Email author
Molecular Neurodegeneration201611:40

https://doi.org/10.1186/s13024-016-0104-5

Received: 9 May 2016

Accepted: 11 May 2016

Published: 18 May 2016

The original article was published in Molecular Neurodegeneration 2016 11:35

Unfortunately, after publication of this article, it was noticed that Fig. 6 (Fig. 1 here) was incorrect. The corrected figure can be seen below.
Fig. 1

NMZ-treated Aldh2−/− mice show rescued learning, memory and CREB responsiveness in carbachol treated hippocampal slices. Reversal of the age-dependent decline in the spontaneous alternation rate and discrimination index in the Y-maze task (a) and NOR task (b), respectively, was observed in male and female Aldh2 −/− mice: after obtaining baseline measurements at 2.5–3 months, mice were randomized to drug or vehicle control groups (n = 8–11) and treated with NMZ (20/mg/kg/day p.o.) or vehicle at 3 months of age for a period of 12 weeks. Pre-randomization data were compared by an unpaired t-test and post-randomization groups by a one-way ANOVA with a Bonferroni post-hoc test. Hippocampal slices from 6 month old wild type and Aldh2 −/− mice that had been treated with NMZ or vehicle control for 12 weeks, were incubated with 50 μM carbachol or vehicle (Basal) for 30 mins and snap frozen. Immunoblot analysis for pCREB was performed using 30 μg protein of hippocampal homogenate, and immunoreactive bands were quantitated by densitometry (c). Data are presented as the mean ± S.D. (n = 3) and were analyzed by a one-way ANOVA with a Bonferroni post-hoc test: * significant differences from basal (** p < 0.01, ***p < 0.001); ψ significant difference compared to basal in all other groups (p < 0.05)

Notes

Declarations

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors’ Affiliations

(1)
Department of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, University of Illinois at Chicago
(2)
Department of Psychiatry, Neuropsychiatric Institute, University of Illinois at Chicago
(3)
Department of Pathology, The Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, Columbia University
(4)
Department of Biomedical & Molecular Sciences, Faculty of Health Sciences, Queen’s University
(5)
Department of Anatomy and Cell Biology, College of Medicine, University of Illinois at Chicago

Reference

  1. Luo J, Lee SH, VandeVrede L, Qin Z, Aissa MB, Larson J, Teich AF, Arancio O, D’Souza Y, Elharram A, Koster K, Tai LM, LaDu MJ, Bennett BM, Thatcher GRJ. A multifunctional therapeutic approach to disease modification in multiple familial mouse models and a novel sporadic model of Alzheimer’s disease. Mol Neurodegeneration. 2016;11:35. doi:https://doi.org/10.1186/s13024-016-0103-6.

Copyright

© Luo et al. 2016

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