Alzheimer's disease (AD) was first described over a century ago; however, at the present its precise etiology remains unknown. Several hypotheses have been postulated to explain the pathogenesis of sporadic AD. Among these, the “amyloid cascade hypothesis” (ACH) has gained enormous relevance based on genetic and biochemical evidence. One of its major predictions is that the interference with Aß aggregation may be therapeutically useful. Interestingly, the outcome of recent clinical trials including vaccination and targeted therapy aimed at reducing extracellular Aß levels suggests that such strategy may not have the expected impact on AD progression and, in some cases, it may even cause life-threatening side effects. Thus, we think it is timely and highly relevant to the AD research community to revisit this subject in a thorough, objective, and open-minded way.

In addition to papers tackling the ACH, we are interested in articles that explore advances in molecular genetics and molecular diagnostics, new insights into neuropathology using animal models, and current concepts in the treatment of AD. Potential topics include, but are not limited to:

• Biomarkers to diagnose AD
• Genetic polymorphisms as risk factors for AD
• New cellular and animal models to understand AD pathogenesis
• Alterations in the metabolism of APP, Aß, and tau protein and their impact on cell membrane, ion-exchange, and key metabolic functions of the cell
• Compensatory processes of the brain to overcome changing conditions in normal and pathologic aging
• Mitochondrial function and biochemical pathways in normal aging and AD brains

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