With increasing life expectancy in developed countries, diseases typically associated with old age are becoming more frequent and, thus, increasingly gain in socioeconomic importance. Age is a major risk factor for almost all neurodegenerative diseases, in particular dementia. Currently, more than 4 million people in the United States suffer from dementia, the majority of them from Alzheimer’s disease (AD). The cost of dementia to the United States economy is now well over $100 billion per year. It is expected, however, that the incidence of dementia will double during the next 20 years  and that its cost will exceed $380 billion per year. Therefore, there is considerable effort to unravel the pathophysiologic mechanisms of AD , allowing for the development of effective treatment strategies. Pathologic studies show that neurodegeneration in AD starts in the entorhinal cortex but in later stages also involves the hippocampus, the limbic system, and neocortical regions. It is characterized by accumulations of β-amyloid plaques and neurofibrillary tangles [2–6], which exert direct and indirect neurotoxic effects by promoting oxidative stress [7,8] and inflammation. In the rare forms of early-onset familial AD, mutations of the amyloid precursor protein and the presenilin genes are identified, which are associated with increased amyloid production and deposition, whereas in late-onset AD, intensive research has led to the identification of several risk factors associated with increased amyloid deposition (eg, allele producing the ε4 type of apolipoprotein E [APOE*E4], hyper-homocysteinemia, hyperlipidemia, and disturbances of the neuronal insulin signal transduction pathway) . This increasing knowledge about the mechanisms in AD facilitates the development of treatments aimed at modifying the disease process [10,11] (eg, anti-inflammatory drugs, statins, antioxidants, acetylcho-linesterase inhibitors, γ- and β-secretase inhibitors , β-sheet disruptors, immunotherapy, neuroprotective agents , and neuroregenerative treatments ). Many of these compounds show promising results in animal models and currently are tested in clinical treatment trials in patients who have AD. There is, however, increasing evidence that the detrimental influences of AD on neuronal function and viability probably start several years before the first clinical symptoms develop. In this preclinical stage, an effective treatment of AD has the most impact, because it can prevent, or at least slow down, the development of clinical symptoms and, thus, preserve cognitive functions at the highest level possible . Consequently, in recent years, there has been considerable interest in characterizing the earliest clinical signs of the degenerative process that are likely to evolve to AD. This effort has led to the development of the concept of mild cognitive impairment (MCI), which represents the transitional zone between normal aging and AD. Subjects who have MCI are not demented but have significant deficits in one or more cognitive domains and have an increased risk for developing dementia . Depending on which cognitive domains are most impaired, different subtypes of MCI are distinguished. The subtype most relevant for AD is amnestic MCI, which is defined by the presence of subjective memory complaints and an objective memory impairment relative to the appropriate reference group but otherwise normal general cognitive functions and largely preserved activities of daily living . The annual conversion rate of amnestic MCI to AD is approximately 12% per year, whereas the conversion rate of age-matched subjects who do not have MCI is approximately only 1% to 2% per year.