| Literature DB >> 20592218 |
Stefan Mitterreiter1, Richard M Page, Frits Kamp, Jessika Hopson, Edith Winkler, Huy-Riem Ha, Runa Hamid, Jochen Herms, Thomas U Mayer, Deborah J Nelson, Harald Steiner, Tobias Stahl, Ulrike Zeitschel, Steffen Rossner, Christian Haass, Stefan F Lichtenthaler.
Abstract
The two proteases beta-secretase and gamma-secretase generate the amyloid beta peptide and are drug targets for Alzheimer's disease. Here we tested the possibility of targeting the cellular environment of beta-secretase cleavage instead of the beta-secretase enzyme itself. beta-Secretase has an acidic pH optimum and cleaves the amyloid precursor protein in the acidic endosomes. We identified two drugs, bepridil and amiodarone, that are weak bases and are in clinical use as calcium antagonists. Independently of their calcium-blocking activity, both compounds mildly raised the membrane-proximal, endosomal pH and inhibited beta-secretase cleavage at therapeutically achievable concentrations in cultured cells, in primary neurons, and in vivo in guinea pigs. This shows that an alkalinization of the cellular environment could be a novel therapeutic strategy to inhibit beta-secretase. Surprisingly, bepridil and amiodarone also modulated gamma-secretase cleavage independently of endosomal alkalinization. Thus, both compounds act as dual modulators that simultaneously target beta- and gamma-secretase through distinct molecular mechanisms. In addition to Alzheimer's disease, compounds with dual properties may also be useful for drug development targeting other membrane proteins.Entities:
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Year: 2010 PMID: 20592218 PMCID: PMC6632893 DOI: 10.1523/JNEUROSCI.1199-10.2010
Source DB: PubMed Journal: J Neurosci ISSN: 0270-6474 Impact factor: 6.167