医学
利拉鲁肽
内科学
脑血流
阿尔茨海默病
随机对照试验
神经退行性变
认知功能衰退
糖尿病
内分泌学
2型糖尿病
疾病
痴呆
作者
Lærke Egefjord,Michael Gejl,Arne Møller,Hans Brændgaard,Hanne Gottrup,Olga Antropova,Niels Møller,Henrik Enghusen Poulsen,Albert Gjedde,Birgitte Brock,Jørgen Rungby
出处
期刊:PubMed
日期:2012-10-01
卷期号:59 (10): A4519-A4519
被引量:30
摘要
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.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.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.The trial is investigator-initiated and investigator-driven and is supported by Novo Nordisk Scandinavia.ClinicalTrials.gov: NCT01469351.
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