Emerging and potential therapies for Alzheimer's disease

H H Griffiths; I J Morten; N M Hooper

doi:10.1517/14728222.12.6.693 10.1517/14728222.12.6.693 [pii]

Emerging and potential therapies for Alzheimer's disease

H H Griffiths, I J Morten, N M Hooper

Research output: Contribution to journal › Article › peer-review

Abstract

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. RESULTS/CONCLUSION: 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.

Original language	English
Pages (from-to)	693-704
Number of pages	12
Journal	Expert Opin Ther Targets
Volume	12
Issue number	6
DOIs	https://doi.org/10.1517/14728222.12.6.693 10.1517/14728222.12.6.693 [pii]
Publication status	Published - 2008

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title = "Emerging and potential therapies for Alzheimer's disease",

abstract = "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. RESULTS/CONCLUSION: 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.",

author = "Griffiths, {H H} and Morten, {I J} and Hooper, {N M}",

note = "Griffiths, Heledd H Morten, Isobel J Hooper, Nigel M United Kingdom Biotechnology and Biological Sciences Research Council United Kingdom Medical Research Council Research Support, Non-U.S. Gov't England Expert opinion on therapeutic targets Expert Opin Ther Targets. 2008 Jun;12(6):693-704.",

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doi = "10.1517/14728222.12.6.693 10.1517/14728222.12.6.693 [pii]",

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TY - JOUR

T1 - Emerging and potential therapies for Alzheimer's disease

AU - Griffiths, H H

AU - Morten, I J

AU - Hooper, N M

N1 - Griffiths, Heledd H Morten, Isobel J Hooper, Nigel M United Kingdom Biotechnology and Biological Sciences Research Council United Kingdom Medical Research Council Research Support, Non-U.S. Gov't England Expert opinion on therapeutic targets Expert Opin Ther Targets. 2008 Jun;12(6):693-704.

PY - 2008

Y1 - 2008

N2 - 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. RESULTS/CONCLUSION: 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.

AB - 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. RESULTS/CONCLUSION: 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.

U2 - 10.1517/14728222.12.6.693 10.1517/14728222.12.6.693 [pii]

DO - 10.1517/14728222.12.6.693 10.1517/14728222.12.6.693 [pii]

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SN - 1744-7631

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Emerging and potential therapies for Alzheimer's disease

Abstract

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