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    BACE inhibitors as potential therapeutics for Alzheimer's disease.

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    27
    Author
    Evin, G; Kenche, VB
    Date
    2007-11
    Source Title
    Recent Pat CNS Drug Discov
    Publisher
    Bentham Science Publishers Ltd.
    University of Melbourne Author/s
    Evin, Genevieve; Kenche, Vijaya
    Affiliation
    Pathology
    Metadata
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    Document Type
    Journal Article
    Citations
    Evin, G. & Kenche, V. B. (2007). BACE inhibitors as potential therapeutics for Alzheimer's disease.. Recent Pat CNS Drug Discov, 2 (3), pp.188-199. https://doi.org/10.2174/157488907782411783.
    Access Status
    This item is currently not available from this repository
    URI
    http://hdl.handle.net/11343/28831
    DOI
    10.2174/157488907782411783
    Description

    C1 - Journal Articles Refereed

    Abstract
    Accumulation of Abeta peptide in the brain results in the formation of amyloid plaques characteristic of Alzheimer's disease (AD) pathology. Abeta soluble oligomers and protofibrils are neurotoxic and these are believed to be a major cause of neurodegeneration in AD. Abeta is derived from a precursor protein by two sequential cleavage steps involving beta- and gamma-secretases, two proteolytic enzymes that represent rational drug targets. beta-secretase was identified as the membrane-anchored aspartyl protease BACE (or BACE1) and found to be elevated in brain cortex of patients with sporadic Alzheimer's disease. In this review, we summarize current approaches towards the development of BACE inhibitors with focus on bioactive compounds and related patents. Recent reports have described drugs that are effective at inhibiting Abeta production in the brain of transgenic mouse models. The beginning of Phase I clinical trials has been approved for one of them and we can expect that in the near future BACE inhibitors will provide novel effective therapeutics to treat AD.
    Keywords
    Neurology and Neuromuscular Diseases; Neurodegenerative Disorders Related to Ageing

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