Allan Jones, Philipp Kulozik, Anke Ostertag, and Stephan Herzig review common metabolic and inflammatory processes implicated in the pathogenesis of both T2D and AD. In particular, they emphasize the role of critical transcriptional checkpoints in the control of cellular metabolism, insulin sensitivity, and inflammation. These transcriptional regulators might hold great promise as new therapeutic targets in the potentially combined treatment of type 2 diabetes and Alzheimer's disease. Other inflammatory processes might be involved in both AD and T2D. Ivica Granic, Amalia M. Dolga, Ingrid M. Nijholt, Gertjan van Dijk, and Ulrich L. M. Eisel investigate how both inflammation and the inducible nuclear factor NF- B might be involved in both diabetes mellitus and Alzheimer's disease. Clement T. Loy and Stephen M. Twigg discuss how advanced glycation end products (AGEs) and growth factor dysregulation may link diabetes and AD.

Receptor for Advanced Glycation Endproducts (RAGE) is a superfamily of cell molecules which serves as a receptor for amyloid- peptide (A ). Increased expression of RAGE is observed in regions of the brain affected by Alzheimer's disease (AD), and A -RAGE interaction in vitro leads to cell stress with the generation of reactive oxygen species and activation of downstream signaling. Shi Du Yan, Angelika Bierhaus, Peter P. Nawroth, and David M. Stern suggest that RAGE may be a therapeutic target for AD.

Masayoshi Takeuchi and Sho-ichi Yamagishi contribute a study of Toxic Advanced Glycation End-products (TAGE). These AGEs can cause oxidative stress in numerous types of cells, which could contribute to the pathological changes of diabetic vascular complications and AD. Akihiko Taguchi discusses how RAGE-mediated chronic inflammation can initiate a degenerative positive feedback loop between endothelium and neuronal cells. Elzbieta Kojro and Rolf Postina explore how RAGE and Amyloid-beta protein precursor (A PP) proteolysis can be affected by insulin and how proteolysis of RAGE may prevent transport of A across the blood-brain barrier.

A contributing factor to oxidative stress can be excess free iron. Sandro Altamura and Martina U. Muckenthaler review experimental evidences for an involvement of iron in Alzheimer's disease and Parkinson's disease. They also propose a role for iron in atherosclerosis, another frequent disorder of aging.

Michael Morcos and Harald Hutter report that the classical model organism in aging research, the nematode Caenorhabditis elegans (C. elegans), shares many similarities at the molecular level to pathological processes found in humans. C. elegans has an accessible and well characterized nervous system and features several genes homologous to human genes implicated in AD like amyloid- protein precursor, presenilins and tau.

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