Journal
PROGRESS IN NEUROBIOLOGY
Volume 162, Issue -, Pages 17-36Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pneurobio.2017.12.002
Keywords
Amyloid aggregation; Antibiotic; Drug repurposing; Neuroprotection
Categories
Funding
- FAPESP/CONICET [PIP-CONICET0183, PICT-MINCyT2012-2882, PIUNT-UNTD542/1]
- BecAr Program from Jefatura de Gabinete de Ministros de Argentina
- CAMPUS FRANCE
- Bernardo Houssay Program, MINCyT-CONICET-CAMPUS FRANCE
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Neurodegenerative diseases are chronic and progressive disorders that affect specific regions of the brain, causing gradual disability and suffering that results in a complete inability of patients to perform daily functions. Amyloid aggregation of specific proteins is the most common biological event that is responsible for neuronal death and neurodegeneration in various neurodegenerative diseases. Therapeutic agents capable of interfering with the abnormal aggregation are required, but traditional drug discovery has fallen short. The exploration of new uses for approved drugs provides a useful alternative to fill the gap between the increasing incidence of neurodegenerative diseases and the long-term assessment of classical drug discovery technologies. Drug re-profiling is currently the quickest possible transition from bench to bedside. In this way, experimental evidence shows that some antibiotic compounds exert neuroprotective action through anti-aggregating activity on disease-associated proteins. The finding that many antibiotics can cross the blood-brain barrier and have been used for several decades without serious toxic effects makes them excellent candidates for therapeutic switching towards neurological disorders. The present review is, to our knowledge, the first extensive evaluation and analysis of the anti-amyloidogenic effect of different antibiotics on well-known disease-associated proteins. In addition, we propose a common structural signature derived from the antiaggregant antibiotic molecules that could be relevant to rational drug discovery. (c) 2017 Elsevier Ltd. All rights reserved.
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