Journal
EXPERT OPINION ON EMERGING DRUGS
Volume 13, Issue 2, Pages 255-271Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1517/14728214.13.2.255
Keywords
Alzheimer's disease; amyloid beta (A beta) peptides; beta-amyloid cleavage enzyme 1 (BACE-1, beta-secretase); beta-amyloid precursor protein (beta APP); gamma secretase (gamma-secretase); neurodegenerative disease; presenilin-1 (PS1); secretase; selective A beta 42-lowering agents (SALA); statins
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Funding
- NIA NIH HHS [AG18031] Funding Source: Medline
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Background: According to the amyloid cascade hypothesis' of Alzheimer's disease (AD), abnormal processing of beta-amyloid precursor protein (PAPP) into toxic amyloid beta (A beta)-peptides is central to the etiopathology of this uniquely human brain disorder. Objective: To review current AD drugs, pharmacological approaches and strategies aimed at modulating A beta-pepticle generation and/or aggregation in the treatment of AD. Methods: Data searches at various websites: Alzheimer Research Forum; individual drug company databases; Medline; Pharmaprojects database; unpublished research; inter-University research communications. Results/conclusion: Considerable research effort has focused on secretase-mediated mechanisms of PAPP processing, and the latest pharmacological strategies have used selective A beta-peptide-lowering agents (SALA) to provide therapeutic benefit against A beta-initiated neurodegenerative pathology. Currently, dedicated anticholinesterase, glutamatergic agonist and A beta-peptide immunization have had little impact in the clinical treatment of AD. One unexpected benefit of statins (HMG-CoA inhibitors), besides their cholesterol lowering abilities, has been their ancillary effects in potentiating the enzymatic mechanisms that generate A beta-peptides. The long-term benefits or complications of statin-based therapies for use in the clinical management of AD are not known.
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