Type your tag names separated by a space and hit enter

Inflammation and Oxidative Stress: The Molecular Connectivity between Insulin Resistance, Obesity, and Alzheimer's Disease.

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.

Links

  • PMC Free PDF
  • PMC Free Full Text
  • FREE Publisher Full Text
  • Authors+Show Affiliations

    ,

    School of Biomedical Sciences, Curtin Health Innovation Research Institute, Biosciences, Curtin University, Kent Street, Bentley, Perth, WA 6102, Australia ; Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical Sciences, Edith Cowan University, 270 Joondalup Drive, Joondalup, Perth, WA 6027, Australia.

    ,

    School of Biomedical Sciences, Curtin Health Innovation Research Institute, Biosciences, Curtin University, Kent Street, Bentley, Perth, WA 6102, Australia.

    ,

    School of Biomedical Sciences, Curtin Health Innovation Research Institute, Biosciences, Curtin University, Kent Street, Bentley, Perth, WA 6102, Australia ; Department of Physiology and Biophysics, Institute of Biomedical Sciences (ICB-I), University of São Paulo (USP), Avenida Prof. Lineu Prestes 1524, Butantã, 05508-000 São Paulo, SP, Brazil.

    ,

    School of Biomedical Sciences, Curtin Health Innovation Research Institute, Biosciences, Curtin University, Kent Street, Bentley, Perth, WA 6102, Australia.

    ,

    School of Biomedical Sciences, Curtin Health Innovation Research Institute, Biosciences, Curtin University, Kent Street, Bentley, Perth, WA 6102, Australia.

    ,

    School of Biomedical Sciences, Curtin Health Innovation Research Institute, Biosciences, Curtin University, Kent Street, Bentley, Perth, WA 6102, Australia.

    ,

    University of Toronto, Tanz Centre for Research in Neurodegenerative Diseases, Department of Medical Biophysics, Krembil Discovery Tower, 60 Leonard Avenue, Toronto, ON, Canada M5T 2S8.

    ,

    Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical Sciences, Edith Cowan University, 270 Joondalup Drive, Joondalup, Perth, WA 6027, Australia.

    ,

    University of Toronto, Tanz Centre for Research in Neurodegenerative Diseases, Department of Medical Biophysics, Krembil Discovery Tower, 60 Leonard Avenue, Toronto, ON, Canada M5T 2S8.

    School of Biomedical Sciences, Curtin Health Innovation Research Institute, Biosciences, Curtin University, Kent Street, Bentley, Perth, WA 6102, Australia.

    Source

    Mediators of inflammation 2015: 2015 pg 105828

    MeSH

    Alzheimer Disease
    Amyloid beta-Peptides
    Animals
    Diabetes Mellitus, Type 2
    Glycogen Synthase Kinase 3
    Glycogen Synthase Kinase 3 beta
    Heme Oxygenase-1
    Humans
    Inflammation
    Insulin Resistance
    NADP
    Obesity
    Oxidative Stress
    eIF-2 Kinase

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Review

    Language

    eng

    PubMed ID

    26693205

    Citation

    Verdile, Giuseppe, et al. "Inflammation and Oxidative Stress: the Molecular Connectivity Between Insulin Resistance, Obesity, and Alzheimer's Disease." Mediators of Inflammation, vol. 2015, 2015, p. 105828.
    Verdile G, Keane KN, Cruzat VF, et al. Inflammation and Oxidative Stress: The Molecular Connectivity between Insulin Resistance, Obesity, and Alzheimer's Disease. Mediators Inflamm. 2015;2015:105828.
    Verdile, G., Keane, K. N., Cruzat, V. F., Medic, S., Sabale, M., Rowles, J., ... Newsholme, P. (2015). Inflammation and Oxidative Stress: The Molecular Connectivity between Insulin Resistance, Obesity, and Alzheimer's Disease. Mediators of Inflammation, 2015, p. 105828. doi:10.1155/2015/105828.
    Verdile G, et al. Inflammation and Oxidative Stress: the Molecular Connectivity Between Insulin Resistance, Obesity, and Alzheimer's Disease. Mediators Inflamm. 2015;2015:105828. PubMed PMID: 26693205.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Inflammation and Oxidative Stress: The Molecular Connectivity between Insulin Resistance, Obesity, and Alzheimer's Disease. AU - Verdile,Giuseppe, AU - Keane,Kevin N, AU - Cruzat,Vinicius F, AU - Medic,Sandra, AU - Sabale,Miheer, AU - Rowles,Joanne, AU - Wijesekara,Nadeeja, AU - Martins,Ralph N, AU - Fraser,Paul E, AU - Newsholme,Philip, Y1 - 2015/11/26/ PY - 2015/07/28/received PY - 2015/09/29/accepted PY - 2015/12/23/entrez PY - 2015/12/23/pubmed PY - 2016/9/27/medline SP - 105828 EP - 105828 JF - Mediators of inflammation JO - Mediators Inflamm. VL - 2015 N2 - 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. SN - 1466-1861 UR - https://www.unboundmedicine.com/medline/citation/26693205/full_citation L2 - https://dx.doi.org/10.1155/2015/105828 DB - PRIME DP - Unbound Medicine ER -