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    Inflammation and oxidative stress: the molecular connectivity between insulin resistance, obesity, and Alzheimer’s disease

    Access Status
    Open access
    Authors
    Verdile, Giuseppe
    Keane, Kevin
    Cruzat, Vinicius
    Medic, S.
    Sabale, M.
    Rowles, J.
    Wijesekara, N.
    Martins, R.
    Fraser, P.
    Newsholme, Philip
    Date
    2015
    Type
    Journal Article
    
    Metadata
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    Citation
    Verdile, G. and Keane, K and Cruzat, V. and Medic, S. and Sabale, M. and Rowles, J. and Wijesekara, N. et al. 2015. Inflammation and oxidative stress: the molecular connectivity between insulin resistance, obesity, and Alzheimer’s disease. Mediators of Inflammation. 2015: 105828.
    Source Title
    Mediators of Inflammation
    DOI
    10.1155/2015/105828
    ISSN
    1466-1861
    School
    School of Biomedical Sciences
    Remarks

    This open access article is distributed under the Creative Commons license http://creativecommons.org/licenses/by/3.0/

    URI
    http://hdl.handle.net/20.500.11937/25620
    Collection
    • Curtin Research Publications
    Abstract

    Type 2 diabetes (T2DM), Alzheimer’s disease (AD), and insulin resistance are age-related conditions and increased prevalence is of public concern. Recent research has provided evidence that insulin resistance and impaired insulin signalling may be a contributory factor to the progression of diabetes, dementia, and other neurological disorders. Alzheimer’s disease (AD) is the most common subtype of dementia. Reduced release (for T2DM) and decreased action of insulin are central to the development and progression of both T2DM and AD. A literature search was conducted to identify molecular commonalities between obesity, diabetes, and AD. Insulin resistance affects many tissues and organs, either through impaired insulin signalling or through aberrant changes in both glucose and lipid (cholesterol and triacylglycerol) metabolism and concentrations in the blood. Although epidemiological and biological evidence has highlighted an increased incidence of cognitive decline and AD in patients with T2DM, the common molecular basis of cell and tissue dysfunction is rapidly gaining recognition. As a cause or consequence, the chronic inflammatory response and oxidative stress associated with T2DM, amyloid-β (Aβ) protein accumulation, and mitochondrial dysfunction link T2DM and AD.

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