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    Diet, nutrients and metabolism: Cogs in the wheel driving Alzheimer's disease pathology?

    259257.pdf (365.2Kb)
    Access Status
    Open access
    Authors
    Creegan, Rhona
    Hunt, Wendy
    McManus, Alexandra
    Rainey-Smith, S.
    Date
    2015
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Creegan, R. and Hunt, W. and McManus, A. and Rainey-Smith, S. 2015. Diet, nutrients and metabolism: Cogs in the wheel driving Alzheimer's disease pathology? British Journal of Nutrition. 113 (10): pp. 1499-1517.
    Source Title
    British Journal of Nutrition
    DOI
    10.1017/S0007114515000926
    ISSN
    0007-1145
    School
    Centre of Excellence for Science Seafood & Health
    Remarks

    This article has been published in a revised form in British Journal of Nutrition http://doi.org/10.1017/S0007114515000926. This version is free to view and download for private research and study only. Not for re-distribution, re-sale or use in derivative works.

    URI
    http://hdl.handle.net/20.500.11937/61638
    Collection
    • Curtin Research Publications
    Abstract

    Alzheimer's disease (AD), the most common form of dementia, is a chronic, progressive neurodegenerative disease that manifests clinically as a slow global decline in cognitive function, including deterioration of memory, reasoning, abstraction, language and emotional stability, culminating in a patient with end-stage disease, totally dependent on custodial care. With a global ageing population, it is predicted that there will be a marked increase in the number of people diagnosed with AD in the coming decades, making this a significant challenge to socio-economic policy and aged care. Global estimates put a direct cost for treating and caring for people with dementia at $US604 billion, an estimate that is expected to increase markedly. According to recent global statistics, there are 35.6 million dementia sufferers, the number of which is predicted to double every 20 years, unless strategies are implemented to reduce this burden. Currently, there is no cure for AD; while current therapies may temporarily ameliorate symptoms, death usually occurs approximately 8 years after diagnosis. A greater understanding of AD pathophysiology is paramount, and attention is now being directed to the discovery of biomarkers that may not only facilitate pre-symptomatic diagnosis, but also provide an insight into aberrant biochemical pathways that may reveal potential therapeutic targets, including nutritional ones. AD pathogenesis develops over many years before clinical symptoms appear, providing the opportunity to develop therapy that could slow or stop disease progression well before any clinical manifestation develops.

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