Authors
Guiseppe Verdile, Edith Cowan UniversityFollow
Kevin N. Keane
Vinicius F. Cruzat
Sandra Medic
Miheer Sabale
Joanne Rowles
Nadeeja Wijesekara
Ralph Martins, Edith Cowan UniversityFollow
Paul E. Fraser
Philip Newsholme
Document Type
Journal Article
Publisher
Hindawi Publishing Corporation
Place of Publication
New York, USA
School
School of Medical and Health Sciences
RAS ID
20355
Abstract
Type 2 diabetes (T 2 DM), 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 T 2 DM) and decreased action of insulin are central to the development and progression of both T 2 DM 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 T 2 DM, the common molecular basis of cell and tissue dysfunction is rapidly gaining recognition. As a cause or consequence, the chronic in flammatory response and oxidative stress associated with T 2 DM, amyloid- ! (A ! ) protein accumulation, and mitochondrial dysfunction link T 2 DM and AD.
DOI
10.1155/2015/105828
Creative Commons License
This work is licensed under a Creative Commons Attribution 3.0 License.
Comments
Verdile, G., Keane, K. N., Cruzat, V. F., Medic, S., Sabale, M., Rowles, J., ... Newsholme, P. (2015). Inflamation and oxidative stress : The molecular connectivity between insulin resistance, obesity and Alzheimer's disease. Mediators of Inflammation, 6. doi: 10.1155/2015/105828. Available here