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      Effect of Advanced Glycation End Products on the Progression of Alzheimer’s Disease

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          Inflammation, defective insulin signaling, and mitochondrial dysfunction as common molecular denominators connecting type 2 diabetes to Alzheimer disease.

          A growing body of evidence supports an intriguing clinical/epidemiological connection between Alzheimer disease (AD) and type 2 diabetes (T2D). T2D patients have significantly increased risk of developing AD and vice versa. Recent studies have begun to reveal common pathogenic mechanisms shared by AD and metabolic disorders, notably obesity and T2D. In T2D and obesity, low-grade chronic inflammation is a key mechanism leading to peripheral insulin resistance, which progressively causes tissue deterioration and overall health decline. In the brain, proinflammatory signaling was recently found to mediate impaired neuronal insulin signaling, synapse deterioration, and memory loss. Here, we review evidence indicating that inflammation, insulin resistance, and mitochondrial dysfunction are common features in AD and T2D. We further propose the hypothesis that dementia and its underlying neuronal dysfunction are exacerbated or driven by peripheral inflammation. Identification of central and peripheral inflammation as potential mediators of brain dysfunction in AD may lead to the development of effective treatments for this devastating disease. © 2014 by the American Diabetes Association.
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            Diabetes and advanced glycation endproducts.

            Bio-reactive advanced glycation endproducts (AGE) alter the structure and function of molecules in biological systems and increase oxidative stress. These adverse effects of both exogenous and endogenously derived AGE have been implicated in the pathogenesis of diabetic complications and changes associated with ageing including atherosclerosis, renal, eye and neurological disease. Specific AGE receptors and nonreceptor mechanisms contribute to these processes but also assist in the removal and degradation of AGE. The final disposal of AGE depends on renal clearance. Promising pharmacologic strategies to prevent AGE formation, reduce AGE toxicity, and/or inactivate AGE are under investigation.
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              Cerebrovascular disease and threshold for dementia in the early stages of Alzheimer's disease.

              Cerebrovascular disease and Alzheimer's disease commonly occur together in the elderly and each may contribute to dementia. Here we present evidence that cerebrovascular disease significantly worsens cognitive performance in the earliest stages of Alzheimer's disease.
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                Author and article information

                Journal
                Journal of Alzheimer's Disease
                JAD
                IOS Press
                13872877
                18758908
                October 29 2019
                October 29 2019
                : 72
                : 1
                : 191-197
                Affiliations
                [1 ]Department of Neurology, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
                [2 ]Department of and Master’s Program in Neurology, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
                [3 ]Department of Environmental and Occupational Medicine, and Health Management Center, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
                [4 ]Department of Environmental and Occupational Medicine, and Health Management Center, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung, Taiwan
                [5 ]Department of Family Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
                [6 ]Department of Family Medicine, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung, Taiwan
                [7 ]Neuroscience Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan
                [8 ]Department of Neurology, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung, Taiwan
                Article
                10.3233/JAD-190639
                25d88cec-ff97-4db0-bc9c-a2b8dc64cea2
                © 2019

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