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In Alzheimer's disease, 6-month treatment with GLP-1 analog prevents decline of brain glucose metabolism: Randomized, placebo-controlled, double-blind clinical trial

Publikation: Forskning - peer reviewTidsskriftartikel

Standard

In Alzheimer's disease, 6-month treatment with GLP-1 analog prevents decline of brain glucose metabolism : Randomized, placebo-controlled, double-blind clinical trial. / Gejl, Michael; Gjedde, Albert; Egefjord, Lærke; Møller, Arne; Hansen, Søren B.; Vang, Kim; Rodell, Anders; Brændgaard, Hans; Gottrup, Hanne; Schacht, Anna C.; Møller, Niels; Brock, Birgitte; Rungby, Jørgen.

I: Frontiers in Aging Neuroscience, Bind 8, 108, 2016.

Publikation: Forskning - peer reviewTidsskriftartikel

Harvard

Gejl, M, Gjedde, A, Egefjord, L, Møller, A, Hansen, SB, Vang, K, Rodell, A, Brændgaard, H, Gottrup, H, Schacht, AC, Møller, N, Brock, B & Rungby, J 2016, 'In Alzheimer's disease, 6-month treatment with GLP-1 analog prevents decline of brain glucose metabolism: Randomized, placebo-controlled, double-blind clinical trial' Frontiers in Aging Neuroscience, bind 8, 108. DOI: 10.3389/fnagi.2016.00108

APA

Gejl, M., Gjedde, A., Egefjord, L., Møller, A., Hansen, S. B., Vang, K., ... Rungby, J. (2016). In Alzheimer's disease, 6-month treatment with GLP-1 analog prevents decline of brain glucose metabolism: Randomized, placebo-controlled, double-blind clinical trial. Frontiers in Aging Neuroscience, 8, [108]. DOI: 10.3389/fnagi.2016.00108

Vancouver

Gejl M, Gjedde A, Egefjord L, Møller A, Hansen SB, Vang K o.a. In Alzheimer's disease, 6-month treatment with GLP-1 analog prevents decline of brain glucose metabolism: Randomized, placebo-controlled, double-blind clinical trial. Frontiers in Aging Neuroscience. 2016;8. 108. Tilgængelig fra, DOI: 10.3389/fnagi.2016.00108

Author

Gejl, Michael ; Gjedde, Albert ; Egefjord, Lærke ; Møller, Arne ; Hansen, Søren B. ; Vang, Kim ; Rodell, Anders ; Brændgaard, Hans ; Gottrup, Hanne ; Schacht, Anna C. ; Møller, Niels ; Brock, Birgitte ; Rungby, Jørgen. / In Alzheimer's disease, 6-month treatment with GLP-1 analog prevents decline of brain glucose metabolism : Randomized, placebo-controlled, double-blind clinical trial. I: Frontiers in Aging Neuroscience. 2016 ; Bind 8.

Bibtex

@article{3c5d2f40eecd46de8d8284dfa50a7527,
title = "In Alzheimer's disease, 6-month treatment with GLP-1 analog prevents decline of brain glucose metabolism: Randomized, placebo-controlled, double-blind clinical trial",
abstract = "In animal models, the incretin hormone GLP-1 affects Alzheimer's disease (AD). We hypothesized that treatment with GLP-1 or an analog of GLP-1 would prevent accumulation of Aβ and raise, or prevent decline of, glucose metabolism (CMRglc) in AD. In this 26-week trial, we randomized 38 patients with AD to treatment with the GLP-1 analog liraglutide (n = 18), or placebo (n = 20). We measured Aβ load in brain with tracer [11C]PIB (PIB), CMRglc with [18F]FDG (FDG), and cognition with the WMS-IV scale (ClinicalTrials.gov NCT01469351). The PIB binding increased significantly in temporal lobe in placebo and treatment patients (both P = 0.04), and in occipital lobe in treatment patients (P = 0.04). Regional and global increases of PIB retention did not differ between the groups (P ≥ 0.38). In placebo treated patients CMRglc declined in all regions, significantly so by the following means in precuneus (P = 0.009, 3.2 μmol/hg/min, 95% CI: 5.45; 0.92), and in parietal (P = 0.04, 2.1 μmol/hg/min, 95% CI: 4.21; 0.081), temporal (P = 0.046, 1.54 μmol/hg/min, 95% CI: 3.05; 0.030), and occipital (P = 0.009, 2.10 μmol/hg/min, 95% CI: 3.61; 0.59) lobes, and in cerebellum (P = 0.04, 1.54 μmol/hg/min, 95% CI: 3.01; 0.064). In contrast, the GLP-1 analog treatment caused a numerical but insignificant increase of CMRglc after 6 months. Cognitive scores did not change. We conclude that the GLP-1 analog treatment prevented the decline of CMRglc that signifies cognitive impairment, synaptic dysfunction, and disease evolution. We draw no firm conclusions from the Aβ load or cognition measures, for which the study was underpowered.",
keywords = "Alzheimer's disease, Amyloid, Cerebral glucose metabolism, Glucagon-like peptide-1, Liraglutide",
author = "Michael Gejl and Albert Gjedde and Lærke Egefjord and Arne Møller and Hansen, {Søren B.} and Kim Vang and Anders Rodell and Hans Brændgaard and Hanne Gottrup and Schacht, {Anna C.} and Niels Møller and Birgitte Brock and Jørgen Rungby",
year = "2016",
doi = "10.3389/fnagi.2016.00108",
volume = "8",
journal = "Frontiers in Aging Neuroscience",
issn = "1663-4365",
publisher = "Frontiers Research Foundation",

}

RIS

TY - JOUR

T1 - In Alzheimer's disease, 6-month treatment with GLP-1 analog prevents decline of brain glucose metabolism

T2 - Frontiers in Aging Neuroscience

AU - Gejl,Michael

AU - Gjedde,Albert

AU - Egefjord,Lærke

AU - Møller,Arne

AU - Hansen,Søren B.

AU - Vang,Kim

AU - Rodell,Anders

AU - Brændgaard,Hans

AU - Gottrup,Hanne

AU - Schacht,Anna C.

AU - Møller,Niels

AU - Brock,Birgitte

AU - Rungby,Jørgen

PY - 2016

Y1 - 2016

N2 - In animal models, the incretin hormone GLP-1 affects Alzheimer's disease (AD). We hypothesized that treatment with GLP-1 or an analog of GLP-1 would prevent accumulation of Aβ and raise, or prevent decline of, glucose metabolism (CMRglc) in AD. In this 26-week trial, we randomized 38 patients with AD to treatment with the GLP-1 analog liraglutide (n = 18), or placebo (n = 20). We measured Aβ load in brain with tracer [11C]PIB (PIB), CMRglc with [18F]FDG (FDG), and cognition with the WMS-IV scale (ClinicalTrials.gov NCT01469351). The PIB binding increased significantly in temporal lobe in placebo and treatment patients (both P = 0.04), and in occipital lobe in treatment patients (P = 0.04). Regional and global increases of PIB retention did not differ between the groups (P ≥ 0.38). In placebo treated patients CMRglc declined in all regions, significantly so by the following means in precuneus (P = 0.009, 3.2 μmol/hg/min, 95% CI: 5.45; 0.92), and in parietal (P = 0.04, 2.1 μmol/hg/min, 95% CI: 4.21; 0.081), temporal (P = 0.046, 1.54 μmol/hg/min, 95% CI: 3.05; 0.030), and occipital (P = 0.009, 2.10 μmol/hg/min, 95% CI: 3.61; 0.59) lobes, and in cerebellum (P = 0.04, 1.54 μmol/hg/min, 95% CI: 3.01; 0.064). In contrast, the GLP-1 analog treatment caused a numerical but insignificant increase of CMRglc after 6 months. Cognitive scores did not change. We conclude that the GLP-1 analog treatment prevented the decline of CMRglc that signifies cognitive impairment, synaptic dysfunction, and disease evolution. We draw no firm conclusions from the Aβ load or cognition measures, for which the study was underpowered.

AB - In animal models, the incretin hormone GLP-1 affects Alzheimer's disease (AD). We hypothesized that treatment with GLP-1 or an analog of GLP-1 would prevent accumulation of Aβ and raise, or prevent decline of, glucose metabolism (CMRglc) in AD. In this 26-week trial, we randomized 38 patients with AD to treatment with the GLP-1 analog liraglutide (n = 18), or placebo (n = 20). We measured Aβ load in brain with tracer [11C]PIB (PIB), CMRglc with [18F]FDG (FDG), and cognition with the WMS-IV scale (ClinicalTrials.gov NCT01469351). The PIB binding increased significantly in temporal lobe in placebo and treatment patients (both P = 0.04), and in occipital lobe in treatment patients (P = 0.04). Regional and global increases of PIB retention did not differ between the groups (P ≥ 0.38). In placebo treated patients CMRglc declined in all regions, significantly so by the following means in precuneus (P = 0.009, 3.2 μmol/hg/min, 95% CI: 5.45; 0.92), and in parietal (P = 0.04, 2.1 μmol/hg/min, 95% CI: 4.21; 0.081), temporal (P = 0.046, 1.54 μmol/hg/min, 95% CI: 3.05; 0.030), and occipital (P = 0.009, 2.10 μmol/hg/min, 95% CI: 3.61; 0.59) lobes, and in cerebellum (P = 0.04, 1.54 μmol/hg/min, 95% CI: 3.01; 0.064). In contrast, the GLP-1 analog treatment caused a numerical but insignificant increase of CMRglc after 6 months. Cognitive scores did not change. We conclude that the GLP-1 analog treatment prevented the decline of CMRglc that signifies cognitive impairment, synaptic dysfunction, and disease evolution. We draw no firm conclusions from the Aβ load or cognition measures, for which the study was underpowered.

KW - Alzheimer's disease

KW - Amyloid

KW - Cerebral glucose metabolism

KW - Glucagon-like peptide-1

KW - Liraglutide

U2 - 10.3389/fnagi.2016.00108

DO - 10.3389/fnagi.2016.00108

M3 - Journal article

VL - 8

JO - Frontiers in Aging Neuroscience

JF - Frontiers in Aging Neuroscience

SN - 1663-4365

M1 - 108

ER -

ID: 179128277