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Mediators of Inflammation
Volume 2015, Article ID 105828, 17 pages
Review Article

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

1School of Biomedical Sciences, Curtin Health Innovation Research Institute, Biosciences, Curtin University, Kent Street, Bentley, Perth, WA 6102, Australia
2Centre of Excellence for Alzheimer’s Disease Research and Care, School of Medical Sciences, Edith Cowan University, 270 Joondalup Drive, Joondalup, Perth, WA 6027, Australia
3Department 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
4University of Toronto, Tanz Centre for Research in Neurodegenerative Diseases, Department of Medical Biophysics, Krembil Discovery Tower, 60 Leonard Avenue, Toronto, ON, Canada M5T 2S8

Received 28 July 2015; Accepted 29 September 2015

Academic Editor: Antonio Macciò

Copyright © 2015 Giuseppe Verdile et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.