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. 2017 Dec 13;7:17490. doi: 10.1038/s41598-017-17718-y

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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The GLP-1 analog treatment appeared to reduce the effects of disease duration. The results are consistent with the claims (1) that the maximum blood-brain transfer capacity declines with duration of Alzheimer’s disease, and (2) that GLP-1 analog treatment raises the GLUT1 activity in the barrier as a potential future target for treatment of the neurovascular dysfunction in Alzheimer’s disease. Estimates of K _t averaged 9.3 mM (± 0.28 RSDR, robust standard deviation of residuals) in the placebo treated group at baseline, 10.1 mM (± 0.19 RSDR) at six months, and 5.9 mM (± 0.18 RSDR) in the liraglutide group at baseline, and 11.1 mM (± 0.25 RSDR) at six months of treatment. The points representing the averages of the healthy control group were not included in the analysis.