Emerging and potential therapies for Alzheimer's disease.
BACKGROUND
The amyloid beta (Abeta) peptide is critical to the development of Alzheimer's disease (AD), the major neurodegenerative disease of the elderly for which there is currently no cure.


OBJECTIVE
To review the literature on emerging treatments and potential therapeutic strategies for AD.


METHODS
Available published literature and information from pharmaceutical companies was utilised.


CONCLUSIONS
Several of the current treatments to combat AD are aimed at inhibiting the production, blocking the oligomerisation/aggregation or enhancing the degradation of Abeta. In our opinion, albeit based on limited available data, a future potential therapeutic strategy is to mimic the mechanism by which the normal cellular form of the prion protein inhibits the beta-secretase beta-site amyloid precursor protein cleaving enzyme-1 (BACE1), and hence the production of Abeta.
Griffiths
Heledd H
HH
University of Leeds, Proteolysis Research Group, Institute of Molecular and Cellular Biology, Faculty of Biological Sciences and Leeds Institute of Genetics, Health and Therapeutics, Leeds LS2 9JT, UK.
Morten
Isobel J
IJ
Hooper
Nigel M
NM
D000544:Alzheimer Disease / Q000188:drug therapy* / Q000378:metabolism; D053829:Amyloid Precursor Protein Secretases / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D000818:Animals; D016282:Aspartic Acid Endopeptidases / Q000378:metabolism; D006801:Humans; D011328:Prions / Q000378:metabolism
D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D011328:Prions; D053829:Amyloid Precursor Protein Secretases; D016282:Aspartic Acid Endopeptidases