Drug Design and Discovery in Alzheimer’s Disease

by

Atta-ur-Rahman, Mohammad Iqbal Choudhary

DOI: 10.2174/97816080582281150101
eISBN: 978-1-60805-822-8, 2014
ISBN: 978-1-60805-823-5
ISSN: 1574-0889 (Print)
ISSN: 2212-1064 (Online)



Indexed in: Book Citation Index, Science Edition, BIOSIS Previews, Scopus, EMBASE, EBSCO, Ulrich's Periodicals Directory.

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Modulation of BACE1 Activity as a Potential Therapeutic Strategy for Treating Alzheimer’s Disease

- Pp. 478-517 (40)

Abstract

Inhibiting the generation of β-amyloid (Aβ) from the amyloid precursor protein (APP) by targeting the protease BACE1, the Alzheimer’s disease β-secretase, is a key strategy for the development of therapeutic compounds aimed at treating Alzheimer’s disease. However, progress in developing biologically active inhibitors has been slow. This is in part because BACE1 possesses a broad and open active site, which cannot be effectively inhibited by small molecules capable of penetrating the bloodbrain barrier. Therefore, there is a great interest in developing modulators of BACE1 activity that are not associated with active site inhibition, rather disrupting the physiological function of the enzyme. This review will discuss the regulation of BACE1 transcriptional expression and modulation of activity by other cellular components, in particular lipids, proteins that interact directly with BACE1, and ubiquitination, as well as BACE1 immunotherapy. This review will also examine the potential of each of these as therapeutic strategies for the treatment of AD.

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