This site uses cookies to measure how you use the website so it can be updated and improved based on your needs and also uses cookies to help remember the notifications you’ve seen, like this one, so that we don’t show them to you again. If you could also tell us a little bit about yourself, this information will help us understand how we can support you better and make this site even easier for you to use and navigate.

Effects of liraglutide on neurodegeneration, blood flow and cognition in Alzheimer´s disease – protocol for a controlled, randomized double-blinded trial


Egefjord, Lærke, Gejl, Michael, Møller, Arne, Brændgaard, Hans, Gottrup, Hanne, Antropova, Olga, Møller, Niels, Poulsen, Henrik E., Gjedde, Albert, Brock, Birgitte, Rungby, Jørgen


Danish Medical Journal, Volume: 59, No.: 10, Pages.: A4519-A4519

Year of Publication



Introduction: Type 2 diabetes (DM-2) increases the risk of developing Alzheimer´s disease (AD), and patients with AD are more likely to develop DM-2. DM-2 and AD share some pathophysiological features. In AD, amyloid-β (Aβ) is accumulated as extracellular plaques in the gray matter of the brain, while in DM-2 islet amyloid polypeptide (IAPP) is accumulated in the pancreas. Premature cellular degeneration is seen in both diseases. Glucagon-like peptide-1 (GLP-1) reduces the amount of Aβ and improves cognition in animal studies. The present study tests the hypothesis that treatment with the long-acting GLP-1 receptor agonist liraglutide affects the accumulation of Aβ in patients with AD.; Material and Methods: This is a randomized, controlled, double-blinded intervention study with AD patients treated for six months with liraglutide (n = 20) or placebo (n = 20). The primary outcome is change in deposition of Aβ in the central nervous system (CNS) by Pittsburgh compound B positron emission tomography (PET). The secondary outcome is evaluation of cognition using a neuro-psychological test battery, and examination of changes in glucose uptake in the CNS by 18F-fluoro-deoxy-glucose PET. Finally, a perfusion-weighted magnetic resonance imaging with contrast will be performed to evaluate blood flow.; Conclusion: No registered drug affects the deposition of Aβ in the brain of AD patients. Our goal is to find a new therapeutic agent that alters the pathophysiology in AD patients by decreasing the formation of Aβ plaques and thereby presumably improves the cognitive function.; Funding: The trial is investigator-initiated and investigator-driven and is supported by Novo Nordisk Scandinavia.; Trial Registration: NCT01469351.;


administration & dosage, alzheimer disease, amyloid, amyloid betapeptides, analogs derivatives, beta, blood flow velocity, brain, cerebrovascular circulation, cognition, diagnosis, doseresponse relationship drug, doubleblind method, drug effects, drug therapy, followup studies, glucagonlike peptide 1, glucose, humans, levels, liraglutide, magnetic resonance imaging, metabolism, methods, physiology, physiopathology, positronemission tomography, treatment outcome

Countries of Study


Types of Dementia

Alzheimer’s Disease

Types of Study

Randomised Controlled Trial

Type of Outcomes

Cognition, Other

Type of Interventions

Pharmaceutical Interventions

Diagnostic Targets

Neuroimaging (e.g. MRI, PET, CAT etc.)

Pharmaceutical Interventions