Journal
EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
Volume 150, Issue -, Pages 140-155Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.ejmech.2018.02.084
Keywords
Alzheimer's disease; Amyloid beta; Chelator; Hydrazones; Mechanism of action
Categories
Funding
- Ministry of Education, Youth and Sports of the Czech Republic within the National Sustainability Program II [LQ1604]
- Ministry of Education, Youth and Sports of the Czech Republic within National Programme of Sustainability I - NPU I [LO1304, LO1601]
- Ministry of Education, Youth and Sports of the Czech Republic within EATRIS-CZ [LM2015064]
- project BIOCEV [CZ.1.05/1.1.00/02.0109]
- Grant Agency of the Czech Republic [17-07822S]
- Technology Agency of the Czech Republic [TE01020028]
- [OPPC CZ.2.16/3.1.00/24503]
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder affecting tens of million people. Currently marketed drugs have limited therapeutic efficacy and only slowing down the neurodegenerative process. Interestingly, it has been suggested that biometal cations in the amyloid beta (A beta) aggregate deposits contribute to neurotoxicity and degenerative changes in AD. Thus, chelation therapy could represent novel mode of therapeutic intervention. Here we describe the features of chelators with therapeutically relevant mechanism of action. We have found that the tested compounds effectively reduce the toxicity of exogenous A beta and suppress its endogenous production as well as decrease oxidative stress. Cholyl hydrazones were found to be the most active compounds. In summary, our data show that cation complexation, together with improving transport efficacy may represent basis for eventual treatment strategy in AD. (C) 2018 Published by Elsevier Masson SAS.
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