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Issue title: Oxidative Stress, Reactive Metabolites, Inflammation, and RAGE – Building a Bridge from Alzheimer's Disease to Diabetes and Vice Versa
Guest editors: Angelika Bierhaus
Article type: Research Article
Authors: Muhammad, Sajjada | Bierhaus, Angelikab | Schwaninger, Markusa; *
Affiliations: [a] Institute of Pharmacology, University of Heidelberg, Heidelberg, Germany | [b] Department of Internal Medicine, University of Heidelberg, Heidelberg, Germany
Correspondence: [*] Corresponding author: Markus Schwaninger, Institute of Pharmacology, University of Heidelberg, Im Neuenheimer Feld 366, 69120 Heidelberg, Germany. Tel: +49 6221 548691; Fax: +49 6221 548549; E-mail: markus.schwaninger@pharma.uni-heidelberg.de.
Abstract: A morphological hallmark of Alzheimer's disease (AD) is the deposition of amyloid-β peptide in plaques and along blood vessels. As several lines of evidence suggest that vascular dysfunction contributes to AD, the pathophysiology of diabetic vasculopathy and stroke may cast light on the vascular component of AD. In this review, we compile some recent findings on the role of reactive oxygen species in diabetes-induced vascular dysfunction and the consequent cerebral ischemia and compare them with key findings in AD. Overall, there is compelling evidence that reactive oxygen species play a key role in the pathophysiology of AD. Unfortunately, this insight has not yet led to a new treatment of AD.
Keywords: Antioxidants, endothelial dysfunction, mitochondrial dysfunction, neurodegeneration, oxidative stress
DOI: 10.3233/JAD-2009-0982
Journal: Journal of Alzheimer's Disease, vol. 16, no. 4, pp. 775-785, 2009
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